Autoimmune diseases (AI) are enigmatic. Of the nearly 100 diseases in the AI family, none could really be labeled as prototypical. For years, the diversity of these diseases made it difficult for the medical community to recognize what was happening as autoimmunity grew into an epidemic. The fragmentation and compartmentalization of Western medicine essentially obscured their ability to connect the dots. But now we can see that hormonal birth control is at least partly responsible for the increase in the seemingly disparate group of autoimmune diseases.
Lupus is primarily a rheumatic disease. Multiple Sclerosis attacks the central nervous system. Crohn’s disease goes after the gut. Despite the differences in the broad scope of diseases that fall under the AI umbrella, there is evidence of a robust underlying bond. One in every four autoimmune patients will be diagnosed with another AI disease, and each of these diseases is the product of a renegade immune system attacking the body’s healthy tissue. But the connection expands beyond what’s been labeled as multiple autoimmune syndrome.
The autoimmune disease and estrogen connection
A few years ago I attended a lecture from one of the world’s leading authorities on autoimmune diseases, which would spark my interest in birth control research. During his studies of Hashimoto’s thyroiditis in the late 1950s, Dr. Noel Rose first theorized the idea of the body’s immune system attacking itself and came up with the term “autoimmune” that would lead to him being deemed the Father of Autoimmune Disease. That evening, he told the audience that researchers knew from the beginning that estrogen probably played a critical role in autoimmunity because of the role it normally plays in a woman’s immune system, plus the fact that nearly 80 percent of all diagnoses were (and are) women.
Dr. Rose explained that patients must be genetically predisposed to contract an autoimmune disease, but stressed that environmental triggers are the real key to activating the condition. Studies of identical twins have demonstrated that AIs only strike both twins 24 percent of the time. If an AI were purely genetic and attacked one twin, by their very nature, it would also strike the other sibling. Since that does not always happen, environmental factors play a large role.
As the lecture continued, I was fascinated to learn about T cells. The doctor described them as the soldiers of the immune system. He said that when our body’s natural estrogens attach to receptors on these T cells, it arms the soldiers and gives them their marching orders. Natural estrogen basically points out the invader and triggers the command to attack. But when disruptive agents that mimic natural estrogen enter our body, they attach to the receptors. Suddenly, the soldier is armed but doesn’t know what to attack because the synthetic estrogens don’t carry the code our natural estrogen would have provided. This can cause the armed immune system to battle our body’s healthy tissue, which will result in an AI for those who are genetically predisposed.
The bad news is that a LOT of people are genetically predisposed. In the United States alone, more than 23 million people suffer from an autoimmune disease. Collectively, their incidence is higher than that of cancer or heart disease.
Birth control is an endocrine disruptor
The disruptive agents that mimic estrogen in our bodies are known as endocrine disruptors, and they’ve gained a lot of notoriety in recent years. Unfortunately, news stories in the mainstream media frequently focus on disruptive chemicals such as dioxins, detergents, BPA, even soy. Unfortunately, discussions of endocrine disruptors rarely include the most prolific and potent synthetic chemical explicitly designed to mimic natural estrogen in the body—hormonal birth control.
A conservative estimate of 11 million women in the United States take some form of hormonal contraceptive each day. Given that each molecule of those synthetic estrogens is about 100 times more potent than a woman’s natural estradiol, birth control equates to a powerful form of internal pollution—a physician-prescribed endocrine disruptor. But, how can we be certain they are any more to blame for the rise of AI diseases than of the other chemicals known to disrupt the endocrine system?
The first indication is that the incidence of AI diseases has risen dramatically since the introduction of the Pill. One could argue that a lot of other harmful chemicals were introduced into the environment within the same timeframe, and that’s a valid point; but it doesn’t explain the fact that the gender ratio has also skewed dramatically since the Pill was introduced. For example, twice as many women than men were diagnosed with Multiple Sclerosis (MS) in 1940. By 2000, four out of five MS patients were women. That’s a 50 percent increase over each decade since the Pill was introduced.
Other recent studies found that women who took hormonal birth control were more likely to develop certain autoimmune diseases, including being 35 percent more likely to develop Multiple Sclerosis, 50 percent more likely to develop Lupus, and up to three times more likely to develop Crohn’s disease, when compared with women who never took birth control.
What we know about hormones and autoimmune disease
In the grand scheme of things, scientists still understand very little about the inner workings of autoimmune disease. This we do know: hormones are powerful chemical messengers that play a role in just about every process our bodies perform. Even though we don’t know precisely how these messengers work or exactly what their role is in the immune system, we should know enough by now to try not to throw them out of balance.
References
Click a subtopic below to view scientific references for each of the following autoimmune diseases and their connections to birth control use.
Boyko EJ, Theis MK, Vaughan TL, and Nicol-Blades B. Increased risk of inflammatory bowel disease associated with oral contraceptive use. American Journal of Epidemiology 1994; 140:268–278.
Calkins BM, Mendeloff AI, and Garland C. Inflammatory bowel disease in oral contraceptive users. Gastroenterology 1986; 91: 523–524.
Cornish JA, Tan E, Simillis C, Clark SK, Teare J, and Tekkis PP. The risk of oral contraceptives in the etiology of inflammatory bowel disease: a meta-analysis. American Journal of Gastroenterology 2008; 103:2394–2400.
Corrao G, Tragnone A, Caprilli R, Trallori G, Papi C, Andreoli A, Di Paolo M, Riegler G, Rigo GP, Ferraù O, Mansi C, Ingrosso M, and Valpiani D. Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC). International Journal of Epidemiology 1998; 27:397–404.
García Rodríguez LA, González-Pérez A, Johansson S, and Wallander MA. Risk factors for inflammatory bowel disease in the general population. Alimentary Pharmacology & Therapeutics 2005; 22:309–315.
Godet PG, May GR, and Sutherland LR. Meta-analysis of the role of oral contraceptive agents in inflammatory bowel disease. Gut 1995; 37:668–673.
Halfvarson J, Jess T, Magnuson A, Montgomery SM, Orholm M, Tysk C, Binder V, and Järnerot G. Environmental factors in inflammatory bowel disease: a co-twin control study of a Swedish-Danish twin population. Inflammatory Bowel Disease 2006; 12:925–933.
Han DY, Fraser AG, Dryland P, and Ferguson LR. Environmental factors in the development of chronic inflammation: a case-control study on risk factors for Crohn’s disease within New Zealand. Mutation Research 2010; 690:116–122.
Katschinski B. [Smoking and ovulation inhibitor in inflammatory bowel diseases]. Medizinische Klinik (Munich, Germany) 88 Suppl 1993; 1:5–8.
Khalili H, Higuchi LM, Ananthakrishnan AN, Richter JM, Feskanich D, Fuchs CS, and Chan AT. Oral contraceptives, reproductive factors and risk of inflammatory bowel disease. Gut 2013; 62:1153–1159.
Lashner BA, Kane SV, and Hanauer SB. Lack of association between oral contraceptive use and Crohn’s disease: a community-based matched case-control study. Gastroenterology 1989; 97:1442–1447.
Lesko SM, Kaufman DW, Rosenberg L, Helmrich SP, Miller DR, Stolley PD, and Shapiro S. Evidence for an increased risk of Crohn’s disease in oral contraceptive users. Gastroenterology 1985; 89:1046–1049.
Logan RF and Kay CR. Oral contraception, smoking and inflammatory bowel disease—findings in the Royal College of General Practitioners Oral Contraception Study. International Journal of Epidemiology 1989; 18: 105–107.
Lowe AM, Roy PO, Poulin M, Michel P, Bitton A, St-Onge L, and Brassard P. Epidemiology of Crohn’s disease in Quebec, Canada. Inflammatory Bowel Disease 2009; 15:429–435.
Ng SC, Woodrow S, Patel N, Subhani J, and Harbord M. Role of genetic and environmental factors in British twins with inflammatory bowel disease. Inflammatory Bowel Disease 2012; 18:725–736.
Persson PG, Leijonmarck CE, Bernell O, Hellers G, and Ahlbom A. Risk indicators for inflammatory bowel disease. International Journal of Epidemiology 1993; 2(2):268–272.
Sandler RS, Wurzelmann JI, and Lyles CM. Oral contraceptive use and the risk of inflammatory bowel disease. Epidemiology 1992; 3:374–378.
Vcev A, Pezerovic D, Jovanovic Z, Nakic D, Vcev I, and Majnarić L. A retrospective, case-control study on traditional environmental risk factors in inflammatory bowel disease in Vukovar-Srijem County, north-eastern Croatia 2010. Wiener Klinische Wochenschrift 2015; 127:345–354.
Vessey M, Jewell D, Smith A, Yeates D, and McPherson K. Chronic inflammatory bowel disease, cigarette smoking, and use of oral contraceptives: findings in a large cohort study of women of childbearing age. British Medical Journal (Clinical Research Edition) 1986; 292:1101–1113.
Boyko EJ, Theis MK, Vaughan TL, and Nicol-Blades B. Increased risk of inflammatory bowel disease associated with oral contraceptive use. American Journal of Epidemiology 1994; 140:268–278.
Calkins BM, Mendeloff AI, and Garland C. Inflammatory bowel disease in oral contraceptive users. Gastroenterology 1986; 91:523–524.
Cornish JA, Tan E, Simillis C, Clark SK, Teare J, and Tekkis PP. The risk of oral contraceptives in the etiology of inflammatory bowel disease: a meta-analysis. American Journal of Gastroenterology 2008; 103:2394–2400.
Corrao G, Tragnone A, Caprilli R, Trallori G, Papi C, Andreoli A, Di Paolo M, Riegler G, Rigo GP, Ferraù O, Mansi C, Ingrosso M, and Valpiani D. Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC). International Journal of Epidemiology 1998; 27:397–404.
García Rodríguez LA, González-Pérez A, Johansson S, and Wallander MA. Risk factors for inflammatory bowel disease in the general population. Alimentary Pharmacology & Therapeutics 2005; 22:309–315.
Godet PG, May GR, and Sutherland LR. Meta-analysis of the role of oral contraceptive agents in inflammatory bowel disease. Gut 1995; 37:668–673.
Halfvarson J, Jess T, Magnuson A, Montgomery SM, Orholm M, Tysk C, Binder V, and Järnerot G. Environmental factors in inflammatory bowel disease: a co-twin control study of a Swedish-Danish twin population. Inflammatory Bowel Disease 2006; 12:925–933.
Khalili H, Higuchi LM, Ananthakrishnan AN, Richter JM, Feskanich D, Fuchs CS, and Chan AT. Oral contraceptives, reproductive factors and risk of inflammatory bowel disease. Gut 2013; 62:1153–1159.
Lashner BA, Kane SV, and Hanauer SB. Lack of association between oral contraceptive use and ulcerative colitis. Gastroenterology 1990; 99:1032–36.
Logan RF and Kay CR. Oral contraception, smoking and inflammatory bowel disease—findings in the Royal College of General Practitioners Oral Contraception Study. International Journal of Epidemiology 1989;18:105–107.
Ng SC, Woodrow S, Patel N, Subhani J, and Harbord M. Role of genetic and environmental factors in British twins with inflammatory bowel disease. Inflammatory Bowel Disease 2012; 18:725–736.
Parrello T, Pavia M, Angelillo IF, Monteleone G, Riegler G, Papi G, D’Incà R, Annese V, Tonelli F, Caprilli R, and Pallone F. Appendectomy is an independent protective factor for ulcerative colitis: results of a multicentre case control study. The Italian Group for the Study of the Colon and Rectum (GISC). Italian Journal of Gastroenterology and Hepatology 1997; 29:208–211.
Persson PG, Leijonmarck CE, Bernell O, Hellers G, and Ahlbom A. Risk indicators for inflammatory bowel disease. International Journal of Epidemiology 1993; 22:268–272.
Sandler RS, Wurzelmann JI, and Lyles CM. Oral contraceptive use and the risk of inflammatory bowel disease. Epidemiology 1992; 3:374–378.
Vcev A, Pezerovic D, Jovanovic Z, Nakic D, Vcev I, and Majnarić L. A retrospective, case-control study on traditional environmental risk factors in inflammatory bowel disease in Vukovar-Srijem County, north-eastern Croatia, 2010. Wiener Klinische Wochenschrift 2015; 127:345–354.
Vessey M, Jewell D, Smith A, Yeates D, and McPherson K. Chronic inflammatory bowel disease, cigarette smoking, and use of oral contraceptives: findings in a large cohort study of women of childbearing age. British Medical Journal (Clinical Research Edition) 1986; 292:1101–1113.
Bernier MO, Mikaeloff Y, Hudson M, and Suissa S. Combined oral contraceptive use and the risk of systemic lupus erythematosus. Arthritis and Rheumatism 2009; 61:476–481.
Cooper GS, Dooley MA, Treadwell EL, St Clair EW, and Gilkeson GS. Hormonal and reproductive risk factors for development of systemic lupus erythematosus: results of a population-based, case-control study. Arthritis and Rheumatism 2002; 46:1830–1839.
Costenbader KH, Feskanich D, Stampfer MJ, and Karlson EW. Reproductive and menopausal factors and risk of systemic lupus erythematosus in women. Arthritis and Rheumatism 2007; 56:1251–1262.
Grimes DA, LeBolt SA, Grimes KR, and Wingo PA. Systemic lupus erythematosus and reproductive function: A case control study. American Journal of Obstetrics and Gynecology 1985; 153:179–186.
Sanchez-Guerrero J, Karlson EW, Liang MH, Hunter DJ, Speizer FE, and Colditz GA. Past use of oral contraceptives and the risk of developing systemic lupus erythematosus. Arthritis and Rheumatism 1997; 40: 804–808.
Strom BL, Reidenberg MM, West S, Snyder ES, Freundlich B, and Stolley PD. Shingles, allergies, family medical history, oral contraceptives, and other potential risk factors for systemic lupus erythematosus. American Journal of Epidemiology 1994; 140:632–642.
Zonana-Nacach A, Rodríguez-Guzmán LM, Jiménez-Balderas FJ, Camargo-Coronel A, Escobedo-de la Peña J, and Fraga A. [Risk factors associated with systemic lupus erythematosis in a Mexican population]. Salud Pública de México 2002; 44:213–218.
Alonso A, Jick SS, Olek MJ, Ascherio A, Jick H, and Hernán MA. Recent use of oral contraceptives and the risk of multiple sclerosis. Archives of Neurology 2005; 62:1362–1365.
Hellwig K, Chen LH, Stancyzk FZ, and Langer-Gould AM. Oral Contraceptives and Multiple Sclerosis/Clinically Isolated Syndrome Susceptibility. PLoS One 2016; 11:e0149094. Doi:10.1371/journal.pone.0149094.
Hernán MA, Hohol MJ, Olek MJ, Spiegelman D, and Ascherio A. Oral contraceptives and the incidence of multiple sclerosis. Neurology 2000; 55:848–854.
Kotzamani D, Panou T, Mastorodemos V, Tzagournissakis M, Nikolakaki H, Spanaki C, and Plaitakis A. Rising incidence of multiple sclerosis in females associated with urbanization. Neurology 2012; 78:1728–1735.
Thorogood M, and Hannaford PC. The influence of oral contraceptives on the risk of multiple sclerosis. British Journal of Obstetrics and Gynaecology 1998; 105:1296–1299.
Villard-Mackintosh L, and Vessey MP. Oral contraceptives and reproductive factors in multiple sclerosis incidence. Contraception 1993; 47:161–168.
Champaneria R, D’Andrea RM, and Latthe PM. Hormonal contraception and pelvic floor dysfunction: a systematic review. Int Urogynecol J 2016; 27:709–722.
El Khoudary SR, Talbott EO, Bromberger JT, Chang CC, Songer TJ, and Davis EL. Severity of interstitial cystitis symptoms and quality of life in female patients. Journal of Womens Health (Larchmont) 2009; 18:1361–1368. Doi: 10.1089/jwh.2008.1270.
Gardella B, Porru D, Nappi RE, Daccò MD, Chiesa A, and Spinillo A. Interstitial cystitis is associated with vulvodynia and sexual dysfunction—a case-control study. The Journal of Sexual Medicine 2011; 8:1726–1734. Doi: 10.1111/j.1743-6109.2011.02251.x. Epub 2011 Apr 7.
Konkle K, Berry SH, Elliott MN, Hilton L, Suttorp MJ, Clauw DJ, and Clemens JQ. Comparison of an interstitial cystitis/bladder pain syndrome clinical cohort with symptomatic community women from the RAND Interstitial Cystitis Epidemiology study. Journal of Urology 2012; 187:508–512.
For more on the connections between birth control and autoimmune diseases, see the articles below.