Menstrual cycle

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The menstrual cycle plays a role in the variation of symptoms and symptom severity in many immunological, neurological, and female predominant diseases.

Cycles and phases[edit | edit source]

Follicular Phase[edit | edit source]

At the beginning of a woman's cycle, the hypothalamus begins to secrete Gonadotropin Releasing Hormone (GnRH), stimulating the pituitary gland to create Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), which travel to the ovaries. FSH causes follicles in the ovaries to begin to mature. Several follicles, each of which stores an egg, begin to grow as they mature, and in the process release estrogen. This estrogen produces a negative feedback during the first 10 days of the cycle that tells to the pituitary to inhibit the release of LH. It is important to note that low levels of estrogen will inhibit the release of LH from the pituitary, while high levels will stimulate it.[citation needed]

Ovulation[edit | edit source]

As estrogen continues to rise due to the maturing follicles, it also causes FSH levels to fall steadily (low estrogen levels trigger the release of FSH). Around day 10 of the cycle, estrogen levels reach a threshold which stops the negative feedback of LH and begins a positive one resulting in the secretion of LH by the pituitary. The resulting spike in LH triggers the most mature follicle to release an egg (or oocyte); this is called ovulation.[citation needed]

Luteal Phase[edit | edit source]

After ovulation, the empty follicle will begin to die. This dying follicle is called a corpus luteum. As the corpus luteum degrades, it secretes three hormones: estrogen, inhibin, and progesterone. Inhibin provides a negative feedback to the pituitary to suppress the production of FSH. Progesterone provides a similar feedback to prohibit the release of GnRH, which in turn decreases the levels of LH and FSH. It also stimulates endometrial growth (the interior lining of the uterus).

As the corpus luteum degenerates, it will secrete fewer and fewer hormones, and progesterone, estrogen, and inhibin will steadily decrease. In the absence of fertilization, the decreasing levels of progesterone can no longer maintain the lining of the uterine wall, so the wall dies and sheds out of the body, resulting in menstruation. This decrease in progesterone also allows for the secretion of GnRH to begin again, and the cycle repeats.[1]

Immune changes[edit | edit source]

Populations of Tregs increase peak just before ovulation and bottom out during the luteal phase, just before menstruation.[citation needed]

Progesterone and estrogen have anti-inflammatory effects.[citation needed]

Health effects in ME/CFS[edit | edit source]

Women with chronic fatigue syndrome report higher rates of polycystic ovarian syndrome (PCOS) and anovulatory cycles, and higher rates of endometriosis.[2]

Women who develop ME/CFS have higher rates a history of irregular menstrual cycles, amenorrhea, dysmenorrhea, anovolutory cycles and sporadic bleeding between periods.[3][4]

Numerous outbreaks of epidemic myalgic encephalomyelitis noted menstrual irregularities and a tendency toward relapse before or during menstruation.[5][6][7]

Illnesses worsened by the menstrual cycle[edit | edit source]

Mental illnesses or disorders worsened by the menstrual cycle include:

Physical diseases and illnesses worsened by the menstrual cycle include:

Health effects in other conditions[edit | edit source]

The menstrual cycle can have effects on the timing and severity of symptoms of women suffering from many different conditions, including epilepsy, migraines, asthma, rheumatoid arthritis and irritable bowel syndrome.[9]

Many women with epilepsy have patterns of seizure activity linked to their menstrual cycles, called catamenial epilepsy.[10][11][12][13] Seizure activity increases just before ovulation and just before menstruation.[14]

Abrupt estrogen withdrawal, such as what occurs just prior to menstruation, can trigger migraines.[15][9] Women with rheumatoid arthritis experienced reduced symptoms after ovulation, owing potentially to the anti-inflammatory effects of progesterone and estrogen.[16]

In a retrospective study, 72% of women with fibromyalgia reported a worsening of symptoms just before their periods.[17]

Women with these diseases may experiencing a worsening of symptoms at specific points in their menstrual cycle, particularly just before or around their periods.[18]

Managing premenstrual symptoms[edit | edit source]

Nonsteroidal anti-inflammatory drugs are occasionally effective in women with menstrual migraine, as are beta-blockers (e.g. propranolol), calcium channel blockers, ergotamine, antidepressants, estrogen and estradiol.[9]

Pathophysiology of menstrual symptoms[edit | edit source]

Estrogen may directly affect blood vessels by stimulating nitric oxide release. Women with a history of menstrual migraine had a heightened activation of the nitro oxide and L-arginine pathways, especially during the luteal phase.[19]

Notable studies[edit | edit source]

  • 2011, Gynecological History in Chronic Fatigue Syndrome: A Population-Based Case-Control Study[20]

See also[edit | edit source]

References[edit | edit source]

  1. Reed, Beverly G.; Carr, Bruce R. (2000). Feingold, Kenneth R.; Anawalt, Bradley; Boyce, Alison; Chrousos, George; Dungan, Kathleen; Grossman, Ashley; Hershman, Jerome M.; Kaltsas, Gregory; Koch, Christian (eds.). The Normal Menstrual Cycle and the Control of Ovulation. South Dartmouth (MA):, Inc. PMID 25905282.
  2. Allen, Peggy Rosati (July 2008). "Chronic fatigue syndrome: implications for women and their health care providers during the childbearing years". Journal of Midwifery & Women's Health. 53 (4): 289–301, quiz 399. doi:10.1016/j.jmwh.2007.12.001. ISSN 1542-2011. PMID 18586181.
  3. Carruthers, Bruce M.; Jain, Anil Kumar; De Meirleir, Kenny L.; Peterson, Daniel L.; Klimas, Nancy G.; Lerner, A. Martin; Bested, Alison C.; Flor-Henry, Pierre; Joshi, Pradip; Powles, AC Peter; Sherkey, Jeffrey A.; van de Sande, Marjorie I. (2003), "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols" (PDF), Journal of Chronic Fatigue Syndrome, 11 (2): 7–115, doi:10.1300/J092v11n01_02
  4. Komaroff, AnthonyL; Dailey, Christine; Hall, JanetE; Signorello, LisaB; Harlow, BernardL (September 28, 1998). "Reproductive correlates of chronic fatigue syndrome". The American Journal of Medicine. 105 (3): 94S–99S. doi:10.1016/S0002-9343(98)00173-9. ISSN 0002-9343.
  5. Shelokov, Alexis; Habel, Karl; Verder, Elizabeth; Welsh, William (August 1957), "Epidemic Neuromyasthenia — An Outbreak of Poliomyelitis-like Illness in Student Nurses", New England Journal of Medicine (257): 345-355, doi:10.1056/NEJM195708222570801
  6. Albrecht, Robert (March 21, 1964). "Epidemic Neuromyasthenia Outbreak in a Convent in New York State". Journal of the American Medical Association. 187: 904–907.
  7. Poskanzer, David C.; Henderson, Donald A.; Kunkle, E. Charles; Kalter, Seymour S.; Clement, Walter B.; Bond, James O. (1957), "Epidemic Neuromyasthenia — An Outbreak in Punta Gorda, Florida", New England Journal of Medicine (257): 356-364, doi:10.1056/NEJM195708222570802, PMID 13464939
  8. 8.0 8.1 Case, A.M.; Reid, R.L. (2001). "Menstrual cycle effects on common medical conditions". Comprehensive Therapy. 27 (1): 65–71. doi:10.1007/s12019-001-0010-8. ISSN 0098-8243. PMID 11280858.
  9. 9.0 9.1 9.2 Reid, Robert L.; Case, Allison M. (July 13, 1998). "Effects of the Menstrual Cycle on Medical Disorders". Archives of Internal Medicine. 158 (13): 1405–1412. doi:10.1001/archinte.158.13.1405. ISSN 0003-9926.
  10. Herzog, Andrew G. (March 1, 2008). "Catamenial epilepsy: Definition, prevalence pathophysiology and treatment". Seizure - European Journal of Epilepsy. 17 (2): 151–159. doi:10.1016/j.seizure.2007.11.014. ISSN 1059-1311. PMID 18164632.
  11. Herzog, Andrew G.; Harden, Cynthia L.; Liporace, Joyce; Pennell, Page; Schomer, Donald L.; Sperling, Michael; Fowler, Kristen; Nikolov, Blagovast; Shuman, Sevie (2004). "Frequency of catamenial seizure exacerbation in women with localization-related epilepsy". Annals of Neurology. 56 (3): 431–434. doi:10.1002/ana.20214. ISSN 1531-8249.
  12. Herzog, Andrew G.; Klein, Pavel; Rand, Bernard J. (1997). "Three Patterns of Catamenial Epilepsy". Epilepsia. 38 (10): 1082–1088. doi:10.1111/j.1528-1157.1997.tb01197.x. ISSN 1528-1167.
  13. Scharfman, Helen E.; MacLusky, Neil J. (2006). "The Influence of Gonadal Hormones on Neuronal Excitability, Seizures, and Epilepsy in the Female". Epilepsia. 47 (9): 1423–1440. doi:10.1111/j.1528-1167.2006.00672.x. ISSN 1528-1167.
  14. Reid, Robert L.; Case, Allison M. (July 13, 1998). "Effects of the Menstrual Cycle on Medical Disorders". Archives of Internal Medicine. 158 (13): 1405–1412. doi:10.1001/archinte.158.13.1405. ISSN 0003-9926.
  15. Brandes, Jan Lewis (April 19, 2006). "The Influence of Estrogen on Migraine: A Systematic Review". JAMA. 295 (15): 1824–1830. doi:10.1001/jama.295.15.1824. ISSN 0098-7484.
  16. Latman, Neal S. (June 1, 1983). "Relation of menstrual cycle phase to symptoms of rheumatoid arthritis". The American Journal of Medicine. 74 (6): 957–960. doi:10.1016/0002-9343(83)90789-1. ISSN 0002-9343.
  17. Østensen, Monika; Rugelsjoen, Anne; Wigers, Sigrid Horven (January 1, 1997). "The Effect of Reproductive Events and Alterations of Sex Hormone Levels on the Symptoms of Fibromyalgia". Scandinavian Journal of Rheumatology. 26 (5): 355–360. doi:10.3109/03009749709065698. ISSN 0300-9742. PMID 9385346.
  18. Zierau, Oliver (2012). "Role of female sex hormones, estradiol and progesterone, in mast cell behavior". Front Immunol.
  19. Brandes, Jan Lewis (April 19, 2006). "The Influence of Estrogen on Migraine: A Systematic Review". JAMA. 295 (15): 1824–1830. doi:10.1001/jama.295.15.1824. ISSN 0098-7484.
  20. Boneva, Roumiana S.; Maloney, Elizabeth M.; Lin, Jin-Mann; Jones, James F.; Wieser, Friedrich; Nater, Urs M.; Heim, Christine M.; Reeves, William C. (January 2011). "Gynecological history in chronic fatigue syndrome: a population-based case-control study". Journal of Women's Health (2002). 20 (1): 21–28. doi:10.1089/jwh.2009.1900. ISSN 1931-843X. PMC 3017420. PMID 21091051.