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Risk Factors

Endometriosis has a variety of risk factors and these range from things you have no influence over (like genetics and hormone levels in the womb) to diet and what make-up you wear. While progress is slow in finding quick ways to diagnose endometriosis (typically four to eleven years from first reporting problems), we’re learning more about the risk factors for the disease.


The daughters or sisters of women with endometriosis have a significantly greater risk of endometriosis. Women with a first-degree relative with the disease are about ten times more likely to have endometriosis.

Testosterone levels

Endometriosis is defined by excessive, localised levels of estrogen (estradiol, E2) within the endometrial tissue (lesions) outside the womb. However, we’ve recently learnt that testosterone levels, while the baby girl forms in the womb, are crucial for its development. Testosterone levels also determine the development of polycystic ovary syndrome (PCOS), and in PCOS, it remains the defining feature of the condition in adulthood.

Testosterone in the womb affects how the ovaries develop and function, and there are distinct physical and hormonal differences between women with endometriosis and PCOS:

Pattern Endometriosis PCOS
Onset of periods Early Late
Menopause Early Late
Length of menstrual cycles Short Long
Amount of menstrual blood Heavy Light
Testosterone level Low High
Luteinizing hormone (LH) level Low High
Follicle-stimulating hormone (FSH) level High Low
Anti-Mullerian hormone (AMH) level Low High
GnRH secretions from the hypothalamus Low High

Different human populations have broadly different testosterone levels in the womb, which also corresponds to variations in their rates for endometriosis and PCOS: i

Ancestral Pop. Endometriosis rates PCOS rates Testosterone in pregnancy
Asian Highest Lowest Not mentioned
European Average Average >-
African Lowest Highest Higher than European

Testosterone levels vary in both sexes, which creates a range of “feminine” and “masculine” features in the population. In broad terms, the most feminine women are also the most likely to have endometriosis due to their relatively low testosterone levels.

Finger lengths

Differences in finger length are a way to assess the testosterone levels a person was exposed to in the womb. This is known as the 2D:4D ratio, and the connection between finger length and testosterone is due to two genes determining genital and digit growth in the first trimester. The differences in finger length persist into childhood and adulthood.

The more exposure to testosterone in the womb, the greater the difference in length between the second (index) and fourth (ring) fingers. (The measurement is from the middle of the bottom crease to the tip of the finger).

As a rule, the ring finger in men is longer than their index fingers, while in women, they’re roughly the same length. However, some ethnic variations exist (less difference in Chinese and African populations), but the less difference in finger length, the lower the exposure to testosterone in the womb.

Hormones are crucial to sexual development and fertility, and exposure to environmental chemicals is a significant issue for all ages.

Endocrine-Disrupting Chemicals

As endometriosis is an estrogen-dependant disease, there’s significant scope for Endocrine-Disrupting Chemicals (EDCs)) to accelerate its development and severity. There are currently 1500 recognised EDCs that enter our bodies via food, drinks, lungs and the skin. They can accumulate in fat tissue and persist for long periods of time, but avoiding them can have surprisingly quick benefits.

Cosmetics and personal care products contain many EDCs, particularly dioxins, the paraben (PB) and benzophenone (BP) families, and many of the most common EDCs mimic estrogens and increase oxidative stress.

EDCs also disrupt the normal development of follicles and the function of the hypothalamus-pituitary-ovarian axis (HPO), which causes changes to the structure of ovaries and the uterus and an increased risk of retrograde menstruation. ii

Oxidative Stress

Oxidative stress (OS) occurs when there’s an imbalance between the production of “free radicals” and the body’s antioxidant defence. This can be caused by either excessive “free radicals” (a feature of inflammation) or a lack of antioxidant protection.

There’s growing evidence that oxidative stress plays a significant role in the development and progression of endometriosis. iii Low antioxidant levels (including Vitamin D3 and minerals) encourage endometriosis growth, and high oxidative stress levels raise the risk of developing endometriosis.

Antioxidant levels are closely related to diet, which, along with herbs, significantly impacts endometriosis growth and inhibition. Supplementing with antioxidants helps reverse the OS damage

caused to the testis and sperm by the potent hormone disruptor BPA (it’s much easier to measure these factors in male fertility). iv

Body Fat

Studies into body types and endometriosis have found that the women most at risk of endometriosis:  v

  • Were lean as children
  • Were lean in their teens
  • Are relatively tall as adults, especially when sitting

The body shape of adults isn’t an indicator of risk, but the amount of body fat as children was. Adult leg length is linked to childhood BMI, as the earlier a girl starts her periods the less time her femur has to grow.


The traditional view was endometriosis is progressive and that Stage I would become Stage IV at some point. However, this doesn’t appear to be the case, and changes in the opposite direction can naturally occur as women get older. What has also been recognised is that young women can have severe endometriosis, and a recent study found age has no bearing on the severity of the disease: vi

  • Stage I and II are “equally likely to be present in women of all ages”
  • Stage III and IV disease is “not age-dependent”
  • (Stage I and II are considered mild, III is moderate, and Stage IV is severe)

This is important as disabling abdominal pain is often dismissed as “normal” for teenage girls, and a diagnosis is typically delayed for about five years from the onset of symptoms. In many cases, the opportunity to identify a life-changing condition is overlooked and making a diagnosis is also difficult. vii

The signs and symptoms of endometriosis in adolescents often differ from those typically found in adults because in adolescents:

  • The menstrual pain may not be recognisable as part of the menstrual cycle (i.e. the pain occurs throughout the cycle)
  • The pain may be unresponsive to commonly used medications (especially NSAIDs)
  • The images typically seen in adult endometriosis, such as ovarian endometriotic cysts and fibrotic scars, are less common in adolescents
  • Peritoneal lesions (which are less obvious and characteristic of early-stage endometriosis) are commonly found in adolescents


There’s a section devoted to diet and endometriosis, and these broad dietary factors significantly affect the chances of developing the disease and the severity of the condition:

Increases the risk of endometriosis Reduces the risk of endometriosis
Low vitamin A and C Fresh fruit (esp. citrus)
Pesticides Green vegetables
Red meat (processed or unprocessed) A vegetarian diet
Trans-fats (fried foods) Omega-3 fats

These differences and challenges make it especially important to be mindful that teenage abdominal pain may be a symptom of a serious health condition. Following the advice for PFPs and the treatment for endometriosis can significantly affect their health and fertility.

Abdominal interventions

Endometriosis is promoted by three factors: abnormal sex hormones, an imbalanced immune system and inflammation. When women vulnerable to endometriosis experience inflammation, it alters their immune balance and makes disease progression more likely, and two factors that increase the risks of endometriosis this way are:

  1. Contraception with intra-uterine devices (IUDs)
  2. Abdominal surgery


i Crespi, Bernard. (2021). Variation among human populations in endometriosis and PCOS A test of the inverse comorbidity model. Evolution, Medicine, and Public Health. 9. 10.1093/emph/eoab029.
ii Pivonello, C.; Muscogiuri, G.; Nardone, A.; Garifalos, F.; Provvisiero, D.P.; Verde, N.; de Angelis, C.; Conforti, A.; Piscopo, M.; Auriemma, R.S.; et al. Bisphenol A: An emerging threat to female fertility. Reprod. Biol. Endocrinol. 2020, 18, 22.
iii Gennaro Scutiero, et al., “Oxidative Stress and Endometriosis: A Systematic Review of the Literature”, Oxidative Medicine and Cellular Longevity, vol. 2017, Article ID 7265238, 7 pages, 2017. https://doi.org/10.1155/2017/7265238
iv Santiago, J.; Silva, J.V.; Santos, M.A.S.; Fardilha, M. Fighting Bisphenol A-Induced Male Infertility: The Power of Antioxidants. Antioxidants 202110, 289. https://doi.org/10.3390/antiox10020289
v  L.V. Farland, et al., Associations among body size across the life course, adult height and endometriosis, Human Reproduction, Volume 32, Issue 8, August 2017, Pages 1732–1742, https://doi.org/10.1093/humrep/dex207
vi Savaris RF, Nichols C, Lessey BA. Endometriosis and the enigmatic question of progression. J Endometriosis Pelvic Pain Disord. 2014;6(3):121-126.
vii Nakamura, T. Clinical Aspects of Adolescent Endometriosis. Endocrines 20212, 301-310. https://doi.org/10.3390/endocrines2030028

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