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Conditions explained

Hormone imbalances, PCOS, endometriosis, fertility challenges, uterine fibroids, even breast and endometrial cancer, are more than just bad luck and faulty genes – they are the result of living in a chaotic environment.

Unbalanced nutrition, a sea of toxicity and unrelenting stress are the 3 horsemen of the hormonal apocalypse that women are facing today.

The approaches described here address these root causes and form my foundation to help you reimagine your relationship with your body and hormones, empowering you to take control of your health and your life.

  • Navigating Endometriosis: Latest Insights and Natural Treatment Strategies from Functional Medicine

    Endometriosis is a complex and often misunderstood condition that affects millions of women worldwide. It occurs when the tissue similar to the lining of the uterus, known as the endometrium, grows outside the uterus. This misplaced tissue can be found in various areas of the body, such as the ovaries, fallopian tubes, pelvic lining, and even distant organs like the bladder or intestines.

    Unlike the normal endometrial tissue that sheds during menstruation, the displaced endometrial tissue has no means of exit from the body. This can lead to the formation of painful adhesions, scar tissue, and the development of cysts, causing a range of symptoms and complications.

    Early warning signs

    It is often difficult to evaluate endometriosis by physical examination and clinical history review. The warning signs include:

    • The first sign is unbearable period pain from the very first period. The typical symptoms in teenage girls include:
      • Avoidance of exercise during the period, particularly if due to excessive pain or heavy flow
      • Increased anxiety, depression and/or fatigue in relation to pain
      • Nausea with pelvic pain, especially if it is non-cyclic pain
      • Period pain or pelvic pain so severe it interferes with school/socialising/work/daily activities
      • Gastrointestinal problems such as diarrhoea/constipation particularly around the time of the period and in relation to period pain
      • Pelvic pain/period pain that does not respond to treatment with painkillers or hormonal treatments like the pill
    • Heavy or irregular periods
    • Pain during intercourse
    • Digestive problems – the endo belly – pronounced bloating or swelling of the abdomen, which can often be uncomfortable or painful, often accompanied by a feeling of ‘fullness’ in the abdomen. This bloating may occur at certain points of the menstrual cycle or randomly at other points of the month.

      One of the common symptoms of endometriosis is very painful bowel movements specially during the menstrual cycle. But the bowel symptoms are not only limited to painful defecation, but it can include the following:
      • Constipation
      • Diarrhea
      • Bloating
      • Rectal bleeding
      • Nausea and vomiting
    • Infertility and furthermore, studies on IVF have shown that women with endometriosis have higher rates of pregnancy loss, complication of preterm delivery, pre-eclampsia and infants small for gestational age.

    Presentation and Diagnosis

    Endometriosis most often occurs on or around reproductive organs in the pelvis or abdomen, including:

    • Fallopian tubes
    • Ligaments around the uterus (uterosacral ligaments)
    • Lining of the pelvic cavity
    • Ovaries
    • Outside surface of the uterus
    • Space between the uterus and the rectum or bladder

    More rarely, it can also grow on and around the:

    • Bladder
    • Cervix
    • Intestines
    • Rectum
    • Stomach (abdomen)
    • Vagina or vulva

    Endometrial tissue growing in these areas does not shed during a menstrual cycle like healthy endometrial tissue inside the uterus does. The buildup of abnormal tissue outside the uterus can lead to inflammation, scarring and painful cysts. It can also lead to adhesions – the buildup of fibrous tissues between reproductive organs that causes them to “stick” together.

    Diagnosing endometriosis requires a combination of medical history, physical examination, and imaging tests such as ultrasound or MRI. A definitive diagnosis can only be made through laparoscopy, a surgical procedure in which a thin tube with a camera is inserted through a small incision in the abdomen to view the pelvic organs and remove any abnormal tissue for biopsy.

    Some of the procedures to diagnose a suspected case of endometriosis are

    1. Laparoscopy:  It is a surgical process. A camera is utilized to have a look into the abdominal cavity and estimate the severity of the condition. It visualizes the externally visible lesions.  If the lesions are not visible, a biopsy can be drawn. This process of diagnosis also allows for surgical treatment through laparoscopy.  6 to 13 percent of women have shown the invisible lesions of endometriosis in the biopsy.
    2. Ultrasound: a pelvic ultrasound detects the larger endometriotic cysts as in ovaries called endometriomas. However, it has no role in diagnosing smaller implants. Vaginal ultrasound is used in detecting deeper endometriomas and before operating on them. This is one of the most easily accessible, inexpensive and required no preparation.
    3. Magnetic resonance imaging:  it is a noninvasive technique. But due to its limited availability and cost, it is not widely recommended. But it precisely and accurately diagnoses smaller lesions.

    Diagnosis delays – it’s something else

    A US survey found that 75.2% of endometriosis sufferers were initially misdiagnosed as either having another physical disorder or mental health issue and many doctors choose to go down the route of symptom management like pain relief or hormonal medication without any formal diagnosis. 

    For those that insist on finding an answer to their debilitating symptoms, pursuing the issue takes time and patience. A US study found that 23.5% of endometriosis patients see 5 or more physicians before receiving a diagnosis. And the more physicians patients saw, the longer the diagnostic delay. Those that only saw 1 to 2 doctors received a diagnosis in 1 to 2 years, while this increased to 7 to 8 years for those that saw 5 to 9 physicians.

    Why is there such a delay in the diagnosis of endometriosis? Studies have found that women are less likely to feel listened to and taken seriously, and are assumed to have a higher pain threshold. One of the main side effects of endometriosis is chronic pain, and because endometriosis patients don’t receive a definitive diagnosis until they’ve had laparoscopic surgery, not having their pain believed can be particularly harmful.

    Activists have used the term ‘gender health gap’ to bring together evidence that would suggest that your gender has a bearing on your experience with doctors and the healthcare you receive. Studies that point out that women are 25% less likely than men to receive pain relief have been used to back up the notion of gender bias in medicine. 

    In a study published in 2018, entitled “Brave Men” and “Emotional Women”, researchers concluded that pain experienced by women was often described as medically inexplicable, as there was often no visible cause for their pain. As a result, healthcare professionals often attributed the pain to a psychological rather than physical cause. This was due to the absence of any visible or diagnostic evidence of illness. 

    Studies have found that in addition to medical professionals assuming that women have higher pain thresholds, there is also an assumption that they are more emotionally unstable. Research published in 2001 found that when women came to their doctors with legitimate concerns of chronic pain, they were more likely to be described as “emotional”, and their pain to be “psychogenic”, and “not real” by their medical expert. This is especially harmful for endometriosis patients who already face long diagnosis waiting periods and may not feel like they’re listened to. 

    The gender health gap, especially as it relates to endometriosis, has historical roots in medical practice. explains that pain associated with endometriosis is often dismissed because “‘women’s problems’ perplexed nineteenth-century doctors, who saw them as indicative of unstable and delicate psychological constitutions. Even though attitudes […] have improved during the twentieth century, some of the old beliefs still linger unconsciously, and affect the medical profession’s attitudes towards complaints including period pain.”

    In 2014, Brigham and Women’s hospital in the U.S. said that medical developments that look into the way conditions are treated and diagnosed “routinely fail to consider the crucial impact of sex and gender. This happens in the earliest stages of research when females are excluded from animal and human studies or the sex of the animals isn’t stated in the published results.” This would suggest that in order to tackle the gender health gap and improve medical understanding of conditions like endometriosis, medical research that includes and prioritizes the experiences of people who identify as women need to take place in higher numbers. 

    The lack of medical research on endometriosis leads to less medical education on the disease, and can result in serious delays in the period of time it takes to receive an endometriosis diagnosis and how much your doctors understand about the condition. 


    Many women with endometriosis who have gastrointestinal symptoms are often misdiagnosed as

    • Inflammatory bowel disease
    • Crohn’s disease
    • Appendicitis

    If symptoms are cyclical in nature, it’s a sign indicating endometriosis. Some women may have symptoms throughout the cycle in chronic cases but the symptoms do aggravate during menstruation

    Origin of Endometriosis

    The origin of endometriosis is still not well defined. Many hypotheses have been proposed to explain the development of endometriosis and Dr David Redwine has proposed the most viable theory – Mulleriosis – that appears to cover all the salient features of endometriosis. His theory favours a genetically-driven embryonic origin of endometriosis. Müllerian tissue is tissue in a female embryo that eventually develops into the fallopian tubes, uterus, cervix and the upper part of the vagina. Mulleriosis indicates a problem of differentiation and migration of any Mullerian tissue during the formation of the embryo which results in patches of this tissue being laid down in abnormal locations in the pelvis or elsewhere in the body. Later in life, these misplaced patches of tissue develop into endometriosis when they are exposed to oestrogen.

    To support his theory, Dr Redwine described a case of fingertip endometriosis, where surgical excision brought complete relief. He posits that that’s because the entire tract of Mulleriotic tissue that had been laid down in the dermis or nail bed had been removed by excision.

    Via Dr David Redwine:

    The cause of endometriosis is a subject of continued debate. My best guess is that it is a disease that the woman is born with because of a process called embryologically patterned metaplasia. At the moment of conception, a woman is dealt three cards.

    1. The first card is that she will have endometriosis.
    2. The second card is where in her body the disease will be.
    3. The third card is how biologically active the disease will be in each area.

    And depending on these various cards, which can be quite different from patient to patient, endometriosis, or areas that will become endometriosis, are laid down in the woman’s pelvis or elsewhere in the body during foetal formation. When oestrogen production begins at puberty, the tracts of tissue that were laid down can become painful and can begin to change into endometriosis. Men can also develop endometriosis for somewhat the same reasons.

    Excision is the only cure

    Going by Dr Redwine’s theory, excision of the lesions is the only cure for endometriosis, however it needs to be done by a surgeon who is specialised at removing the lesions ‘from the root’ otherwise they will grow back. The recurrence of endometriosis after ovarian endometrioma excision has been evaluated at 24, 36, 60, and 120 months as 5.8%, 8.7%, 15.5% and 37.6% respectively.

    Development and Progression of Endometriosis

    Endometriosis is driven by oestrogen that may come from the ovaries or from within the lesions themselves. Women with endometriosis tend to to have higher ovarian production of oestrogen and this combined with lesional oestrogen can result in high levels that make symptoms worse.

    The central driver connecting oestrogen to symptoms is the high production of prostaglandin E2 (PGE2). PGE2 is a regulator that makes the environment inside the body more favourable for endometriosis to develop and progress by affecting various cellular activities and immune responses. Specifically, it:

    1. Promotes cell growth (cell proliferation): PGE2 makes cells multiply faster, which can contribute to the growth of endometrial tissue where it shouldn’t be.
    2. Prevents programmed cell death (antiapoptosis): Normally, cells have a built-in process of dying when they are damaged or not needed, called apoptosis. PGE2 stops this process, allowing potentially harmful cells to survive longer.
    3. Weakens the immune system’s response (immune suppression): It hinders the body’s immune system from effectively responding to these abnormal cells.
    4. Stimulates the formation of new blood vessels (angiogenesis): PGE2 encourages the growth of new blood vessels, which can supply more nutrients to the endometrial tissue growing outside the uterus, allowing it to grow more.

    Feedback loop between oestrogen and PGE2 promotes growth and inflammation

    Two basic pathologic processes, namely growth and inflammation, are responsible for chronic pelvic pain and infertility, which are the primary devastating symptoms of endometriosis. Estrogen enhances the growth and invasion of endometriotic tissue, whereas PGE2 and cytokines mediate pain, inflammation and infertility.

    Estradiol (E2) is produced locally in endometriotic tissue. The precursor, androstenedione of ovarian, adrenal or local origin becomes converted to estrone (E1) that is in turn reduced to E2 in endometriotic implants.

    Endometriotic tissue is capable of synthesising androstenedione from cholesterol via the activity of steroidogenic acute regulatory protein (StAR) and other steroidogenic enzymes also present in this tissue. E2 directly induces cyclo-oxygenase-2 (COX-2), which gives rise to elevated concentrations of PGE2 in endometriosis. The cytokine Interleukin-1β (IL-1β), vascular endothelial growth factor (VEGF) and PGE2 itself are also potent inducers of COX-2 in uterine cells. PGE2, in turn, is the most potent known stimulator of StAR and aromatase in endometriotic cells. This establishes a positive feedback loop in favour of continuous oestrogen and PG formation in endometriosis.

    Feeding into this loop is arachidonic acid which is synthesised from omega-6 fats commonly found in foods. COX-2 converts arachidonic acid to to PEG2 which directly increases COX-2, creating another feedback loop.

    PEG2 increases the rate of the enzyme aromatase, increasing E1, and because the enzyme 17β-HSD is low in edometriotic tissue, this then increases the production of E2.

    Women with endometriosis produce more lactate which stimulates an environment that promotes invasion of endometrial cells into the peritoneum so that they form lesions.

    PGE2 prevents the macrophages of the immune to do a clean up job

    Abnormal hormone production by endometriotic lesions is a significant factor that helps endometriotic tissues survive and grow. However alongside this is a critical issue in immune system dysfunction, particularly the reduced ability of immune cells to consume and remove unwanted materials, a process known as phagocytosis. This dysfunction is largely due to macrophages, a type of immune cell responsible for cleaning up debris, not working properly.

    In cases of endometriosis, these macrophages are attracted to the peritoneal cavity, an area inside the abdomen, because of inflammation. Ideally, they should remove abnormal endometrial tissue that is present in the peritoneal cavity. However, they often fail to do this effectively in endometriosis, allowing the endometriotic tissue to grow.

    The way macrophages function involves two main methods. Firstly, they produce zinc-based enzymes called matrix metalloproteinases (MMPs) to break down the surrounding material of foreign entities. Secondly, they use scavenger receptors (CD36) to enhance the uptake and destruction of cell debris. In endometriosis, however, the function of these macrophages is impaired. In the presence of a high concentration of PGE2, the expression of MMP-9 and CD36 is suppressed. This significantly inhibits the phagocytic ability of macrophages. As a result, the endometrial tissues proliferate in the peritoneal cavity, maintaining and progressing endometriosis.

    In essence, the development of endometriosis is not just about the abnormal production of hormones by the lesions but also involves significant dysfunction in the immune system, especially in macrophages. This dysfunction is characterised by a reduced capacity to remove unwanted materials and impaired production of important enzymes and receptors, influenced by PGE2 in the peritoneal fluid.

    PGE2 is the likely master of endometriosis

    In women with endometriosis, there are two self-reinforcing cycles that keep the levels of PGE2 high in the peritoneal fluid.

    • PGE2 – COX-2 – PGE2 pathway in macrophages: In peritoneal macrophages (immune cells in the abdominal cavity), PGE2 increases the activity of an enzyme called COX-2, leading to more production of PGE2.
    • PGE2 – Estrogen – COX-2 – PGE2 pathway in lesions: In ectopic endometriotic lesions (abnormal tissue growths), PGE2 boosts estrogen production, which then increases COX-2 activity, resulting in more PGE2.
    • High PGE2 Levels then lead to:
      • Abnormal steroid production: PGE2 leads to unusual production of steroidogenic proteins, like StAR and aromatase. This results in excess production of estradiol, a key hormone for endometrial tissue survival.
      • Stimulation of growth factors: The estradiol produced by ectopic tissues increases growth factors (like VEGF and FGF), promoting cell growth (proliferation) and new blood vessel formation (angiogenesis).
      • Direct impact on cell growth: PGE2 directly causes endometriotic and blood vessel cell growth through increased levels of FGF and VEGF.
      • Reduced macrophage function: PGE2 inhibits the expression of MMP-9 and CD36 in macrophages. This diminishes their ability to clean up debris, aiding the survival and growth of endometriotic lesions.

    In essence, elevated PGE2 in the peritoneal fluid maintains a cycle that encourages the development and persistence of endometriosis by influencing increased hormone production and cell proliferation, and immune cell dysfunction.

    Additional sources of inflammation

    Interactions with gut bacteria, blood debris, iron overload, anti-oxidant deficiencies, increased nitrites/nitrates and gene expression of oestrogen metabolism also play a part in maintaining endometriosis.

    • Bacterial contamination from the gut creates more inflammation and make endometriosis worse via PGE2
      Researchers have found that some of the gut microbes linked to bowel problems also feature prominently in endometriosis. When they treated the mice with the broad-spectrum antibiotic metronidazole, the lesions became smaller. Inflammation also was reduced.

      Additional research found that the menstrual blood was highly contaminated with E. coli and that the endometrial samples were colonised with other bacteria. The concentration of bacterial toxins – endotoxin – was four to six times higher in the menstrual blood of women with endometriosis compared to those without endometriosis. Treatment with GnRH agonist further worsened the colonisation of the uterus by bacteria potentially leading to endometriosis. 

      There appears to be an additive effect between estradiol and endotoxin on the proliferation endometrial cells and that an immune-endocrine cross-talk between oestrogen and endotoxin in the pelvic ecosystem creates an inflammatory environment leading to growth of endometriosis. The connection appears to be PGE2: PGE2 is increased by endotoxin, and PGE2 also stimulates increased growth of bacteria that produce endotoxin.

      Further, endotoxin promotes the polarisation of macrophages from M1 to M2, increasing the progression of endometriosis.

      Therefore, as well as considering oestrogen/hormone biotransformation in endometriosis, we should also be looking at the gut and vaginal microbiomes for endotoxin-producing bacteria, modulation of the gut ‘oestrobolome’ (bacterial recycling of oestrogen in the gut), endotoxin clearance by the liver and liver support.
    • Blood debris causes oxidative stress which promotes inflammation
      It is now widely accepted that oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity. ROS are intermediaries produced by normal oxygen metabolism and are inflammatory mediators known to modulate cell proliferation and to have negative effects.

      The body’s complex antioxidant system is influenced by dietary intake of non-enzymatic antioxidants such as manganese, copper, selenium and zinc, beta-carotenes, vitamin C, vitamin E, taurine, hypotaurine, and B vitamins. On the other hand, the body produces several antioxidant enzymes such as catalase, super- oxide dismutase, glutathione reductase, glutathione peroxidase, and molecules like glutathione and NADH. Glutathione is produced by the cell and plays a crucial role in maintaining the normal balance between oxidation and antioxidation. NADH is considered as an antioxidant in biological systems due to its high reactivity with some free radicals, its high intracellular concentrations and the fact that it has the highest reduction power of all biologically active compounds. When the balance between ROS production and antioxidant defence is disrupted, higher levels of ROS are generated and oxidative stress may occur, leading to harmful effects. Oxidative stress is implicated as a major factor involved in the pathophysiology of endometriosis.

      Macrophages, red blood cells, and apoptotic endometrial tissue are well known inducers of oxidative stress; therefore, peritoneal production of ROS may be involved in endometriosis. Indeed, activated macrophages play an important role in the degradation of red blood cells that release prooxidant and proinflammatory factors such as heme and iron, implicated in the formation of inflammatory ROS.
    • Inflammation from excess iron
      Higher levels of iron, ferritin, and haemoglobin have been found in the peritoneal fluid of affected women than controls. The stroma of endometriotic lesions and peritoneum also revealed the presence of iron conglomerates. Iron overload acts as a catalyst to generate a wide range of ROS, inducing injury to cells.

      Oxidative stress destroys tissue which produces adhesions. Iron-binding protein haemoglobin has been identified as one of the factors potentially leading to adhesion formation.

      ROS production by iron overload induces an increase of NF-kappa B in peritoneal macrophages, leading to pro-inflammatory, growth, and angiogenic factors.

      Iron, heme, and hemoglobin accumulation leads to oxidative stress causing DNA hypermethylation and histone modifications. DNA hypermethylation is linked to defective endometrium development in endometriosis.

      Treatment with an iron chelator could thus be beneficial in endometriosis, to prevent iron overload in the pelvic cavity, thereby diminishing its deleterious effect.
    • Inflammation from deficiency of Superoxide Dismutase (SOD): SOD is an important antioxidant system. It catalyses the dismutation of superoxide into hydrogen peroxide and oxygen. SOD shows a decreased activity in the plasma of women with endometriosis, suggesting a decreased antioxidant capacity. SOD requires manganese as a cofactor (see the section on interventions).
    • Inflammation from deficiency of Glutathione Peroxidase:
      Glutathione peroxidase is an antioxidant enzyme class with the capacity to scavenge free radicals. This is in turn helps to prevent lipid peroxidation and maintain intracellular homeostasis as well as redox balance. Glutathione peroxidase is localised in the glandular epithelium of normal human endometrium and reaches a maximum level in the late proliferative and early secretory phases of the menstrual cycle.

      A study on endometriosis-associated infertility demonstrated a lower mean activity of glutathione peroxidase and increased lipid peroxidation in infertile women with endometriosis compared to women without this disease. This suggests that low level of antioxidant enzymes in the peritoneal fluid plays an integral role in the development of endometrial pathology. Furthermore, in women with endometriosis, abnormal expression of glutathione peroxidase in eutopic and ectopic endometrium has been reported. Overall, this aberrant change in antioxidant enzyme level can be one of the many contributors of the oxidative damage seen in endometriosis (see the section on interventions for approaches to manage glutathione levels).
    • Inflammation from Nitrates and Nitrites
      The concentrations of nitrates and nitrites are higher in endometriosis and are higher in women with deep infiltrating endometriosis, especially those with intestinal involvement. The higher concentration of nitrates probably derives from the augmented nitric oxide (NO) activity of the peritoneal macrophages and a higher activity of nitric oxide synthase 2 (NOS 2). A significant correlation between pelvic pain symptom scores and peritoneal protein oxidative stress markers was observed in women with endometriosis.

      This suggests that NO plays a role in the pathogenesis of endometriosis, especially in the most aggressive form with intestinal involvement. Additionally, peritoneal macrophages in endometriosis produce more NO in vitro after endotoxin treatment.

      NO may contribute to painful symptoms, and reduction of blood nitric oxide levels is associated with clinical improvement of the chronic pelvic pain related to endometriosis.

      NO activates COX-2, which in turn increases the levels of PGE2, thereby causing the levels of aromatase, the enzyme necessary for estrogen production. The resultant estrogen elevation stimulates further eNOS gene expression in a positive feedback loop (see the section on interventions for approaches to manage nitric oxide production).
    • Gene Expression of Oxidative Metabolism of Estrogens – methylation, COMT and liver detoxification
      Increased expression of CYP1A1, CYP3A7, and COMT was observed in endometriosis. Expression of SULT1E1, SULT2B1, UGT2B7, NQO1, and GSTP1 was decreased. These findings exhibit a disturbed balance between phase I and II liver metabolising enzymes in endometriosis, leading to excessive hydroxy-estrogen and altered ROS formation, and stimulation of ectopic endometrium proliferation.

      This model suggests increased 2-hydroxylation and 16α-hydroxylation and high 4 hydroxylation of estrogens together with high methylation, lower sulfatation and glucuronidation of CEs and 16α-OH-estrogens in endometriosis. This imbalance between phase I and II metabolic enzymes can result in excessive 2- and 16α-OH-estrogen and corresponding oestrogen quinone formation. The first could be involved in maintaining strong oestrogen agonistic activity in endometriotic tissue, while the second might be a source of excessive ROS generation. Moreover, altered NQO1 isoform distribution could result in impaired detoxification of toxic quinone oestrogens and may contribute to over enhanced ROS production in endometriosis. Apart from E2, 4-OH-, 16α-OH-estrogens and ROS can also be responsible for excessive growth of ectopic endometrium in ovarian endometriosis. ROS scavengers, or even antioxidant nutrients, might, therefore, influence the proliferation of ovarian endometriotic cells.

    Disrupting the feedback loops, reducing PEG2 and supportive anti-oxidants are effective treatments for endometriosis

    Understanding the biochemical pathways involved in the maintenance and progression pf endometriosis provides targets for interventions to reduce and manage inflammation and lesion growth.

    Arachidonic acid inhibitors

    • EPA:GLA ratio of 8:1
      Essential fatty acids (EFAs) are biologically active fats which the body requires to support several important functions from blood clotting to inflammation; differentiating them from other fats which are either stored or used for energy. EFAs are deemed ‘essential’ because humans and other animals cannot produce them; meaning that they must be consumed from food.

      The two types of fatty acids which are essential to the body are omega-3 (ALA) and omega-6 (LA). Other fatty acids such as EPA, DHA and GLA are considered ‘conditionally essential’ as they may become essential under certain developmental or disease conditions. 

      Arachidonic acid, derived from LA is found in meat, eggs and dairy, and is needed to support muscle growth, brain development and a healthy nervous system. However, we only require very small amounts of this fatty acid and when consumed in excess, it can promote inflammation.

      Human studies have revealed that when EPA is introduced in a balanced ratio to GLA, elevations in serum arachidonic acid are prevented leading to a reduction in levels of pro-inflammatory PGE2. This conversion requires adequate zinc, magnesium and vitamin B6 as cofactors.

      The ideal ratio of EPA to GLA to suppress arachidonic acid is 8:1 and should be combined with the cofactors.
    • Quercetin
      Quercetin is found many fruits and vegetables including citrus fruits, apples, onions and strawberries, and is known to reduce inflammation. It does this by interfering with the production of arachidonic acid. Specifically, quercetin stops the creation of inflammatory mediators like PGE2 and leukotrienes. These mediators are not only involved in causing inflammation but also play a role in controlling how the uterus contracts. Quercetin has been shown to significantly reduce endometrial lesions.

    COX-2 inhibitors

    IL-1, VEGF and oxidative stress inhibitors

    Lactate inhibitors

    StaR inhibitor

    Aromatase inhibitors

    Reducing systemic oestradiol (from the ovaries, gut and adrenals)

    • Vitamins B1 and B2 maintain oestrogen detoxification by the liver, and a deficiency can lead to excess estradiol. Alcohol and high carbohydrate diets increase the need for vitamin B1 and supplementation would be required.
    • Calcium D-glucarate is a natural compound found in fruits and vegetables. It works by inhibiting the activity of beta-glucuronidase made by gut bacteria, an enzyme that helps to circulate oestrogen back into the body from the gut.


    There has been extensive data over the past decades indicating endometriosis may be linked to select co-morbid conditions in some individuals with the disease as well, including but not limited to a low/modest association between certain pigmentary traits and melanoma;  pain syndromes (interstitial cystitis/painful bladder syndrome, irritable bowel syndrome/inflammatory bowel disease, chronic headaches, chronic low back pain, vulvodynia, fibromyalgia, temporomandibular joint disease, chronic fatigue syndrome, etc.) as well as mood conditions (defined as depression and anxiety) and asthma; select infections and endocrine disordersheadaches and migrainesthyroid disease and others. Similarities in the clinical and epidemiological features of the associated disorders may be at the root of their co-morbidity, and further investigation is needed.

    There is a very strong association with many autoimmune diseases and endometriosis, Hashimoto’s thyroiditis probably being the most prevalent, as well as lupus, antiphospholipid syndrome, scleroderma and multiple sclerosis. 3 common gene fingerprints – known as haplotypes – are prevalent with women with endometriosis. One of these haplotypes accounts for about 90 percent of all autoimmune disease an includes celiac disease, which is why cutting out gluten can have a tremendous benefit symptomatically (see the section on interventions for dietary recommendations).

    The other haplotypes are associated with antiphospholipid syndrome, Hashimoto’s thyroiditis, autoimmune hepatitis and are antibody mediated. The antibodies can react to paternal antigens in pregnancy and can lead to pregnancy loss. This may be a cause of repeated miscarriages and multiple IVF failures, and may point to ‘silent endometriosis’ where endometriosis exists, but does not present with any of the common symptoms.

    Endometriosis is often associated with Restless Leg Syndrome (RLS) an irresistible urge to move the legs due to an unpleasant non-painful sensory disturbance, described in a variety of ways for example as crawling, creeping and pulling. RLS is associated with dopamine deficiency. Dopamine is a neurotransmitter which mediates multiple functions in the body and its deficiency is associated with

    • low moods
    • depression
    • fatigue
    • lack of motivation
    • inability to experience pleasure
    • insomnia
    • trouble getting going in the morning
    • mood swings
    • forgetfulness
    • memory loss
    • inability to focus and concentrate
    • inability to connect with others
    • low libido
    • sugar cravings
    • caffeine cravings
    • inability to handle stress
    • inability to lose weight

    Research shows that women with moderate to severe endometriosis have a higher than normal frequency of genes which show mutations – polymorphisms – in dopamine receptors – dopamine receptor D2 (DRD2). The presence of polymorphism 2 could cause a defect in a post-receptor signalling mechanism, resulting in a mild increase in serum prolactin levels. Prolactin has angiogenic activity which may promote implantation of ectopic endometriosis tissue.

    Studies with the dopamine agonist – a drug that promote a dopamine response – quinagolide, have shown a 69.5% reduction in the size of the lesions, with 35% vanishing completely. By interfering with angiogenesis, enhancing fibrinolysis, and reducing inflammation, quinagolide reduces or eliminates peritoneal endometriotic lesions in women with endometriosis.

    Women receiving Carbegoline – another dopamine agonist – experienced considerable pain relief, through the lowering of prolactin.

    Pentoxifylline, which can act as a dopamine agonist, has also been shown to increase pregnancy rates in women with endometriosis

    The use of high doses of dopamine agonists may cause an increase in the number of receptors that can make the post-receptor signalling mechanism work properly with this compensation, despite the presence of the polymorphism.

    Dopamine can be increased naturally with the use of the amino acid l-tyrosine.

    Contraindications for Endometriosis

    Women with endometriosis should not use the copper coil because its side effects include longer, heavier and more painful periods.

    Studies analysing the impact of hormone replacement therapy (HRT) for menopausal with endometriosis are conflicting, with some research showing that oestrogen therapy could reactivate endometriosis. A systematic review of the literature suggested that the malignant transformation of the ectopic endometriotic tissue is related to oestrogenic stimulation. Women who are suffering with hot flushes, night sweats, brain fog, weight gain, anxiety and fatigue can reverse all these symptoms within 6 weeks with the Menopause Core Nutrition Solution.

    My approach to Managing Endometriosis – A pain-free Life is Possible

    The biggest breakthroughs in the management of endometriosis has come studies showing that nutrition, detoxification and supplements can effectively and significantly reduce pain and inflammation.


    While there is no one-size-fits-all diet for endometriosis, there are certain foods that can exacerbate inflammation and make symptoms worse, and others that can help reduce inflammation and promote healing.

    As an oestrogen-driven condition, nutrition has to focus on preventing excess oestrogen and other hormone intake. For this reason I recommend:

    • avoiding red meat and focusing on seafood for protein. Protein is important for tissue repair and hormone balance, but it’s important to choose lean sources to avoid excess saturated fat. Omega-3 fatty acids, found in fatty fish like salmon and sardines can help reduce inflammation and promote hormonal balance. A diet high in fish and seafood is ideal for endometriosis.
    • avoiding cow’s dairy
    • avoiding soya
    • avoiding high sugar foods. High sugar drives insulin which can increase oestrogen.

    For lowering inflammation I recommend:

    • avoiding gluten and all grains
    • avoiding all processed foods. These are often high in sugar, salt, and unhealthy fats, which can exacerbate inflammation and worsen symptoms.
    • avoiding artificial sweeteners, which disturb the gut microbiome.
    • avoiding pro-inflammatory seed oils like sunflower oil and focusing on monounsaturated fats, found in foods like avocado and olive oil.
    • avoiding coffee. Caffeine can worsen symptoms, so it may be worth experimenting with avoiding or reducing this to see if it helps.
    • include vegetables with every meal. These are rich in fibre, vitamins, minerals, and antioxidants, which can help reduce inflammation and promote healing. Choose a variety of colourful fruits and vegetables, including leafy greens, berries, citrus fruits, and cruciferous vegetables like broccoli, cauliflower, and Brussels sprouts.

    Include plants that help to detoxify oestrogen via the liver:

    • Artichoke hearts
    • Bok choy
    • Broccoli
    • Brussels sprouts
    • Cabbage
    • Cauliflower
    • Greens: beet greens, kale, chard, collard, mustard greens and rocket
    • Onions, garlic, and scallions
    • Oregano
    • Rosemary
    • Sage
    • Thyme

    Gut and Vaginal Microbiome Restoration, and Detoxification

    • Healing intestinal and vaginal microbiome imbalance and supporting liver detoxification restores hormone balance and remove sources of inflammation.


    • The nutrients discussed above support hormone metabolism and reduce inflammation, but I just want to note that 4 supplements have made the most difference in my clinical experience: vitamin E, vitamin D, NAC and methylated B complex in high doses.
    • In a 2017 study a cohort of endometriosis patients was treated for three months with a composition including quercetin, curcumin, 5-methyltetrahydrofolate and omega 3/6 displayed a significant reduction of the symptoms at the end of the treatment:
      • headache from 14% to 4%
      • cystitis from 12% to 2%
      • muscle aches from 4% to 1%
      • irritable colon from 15% to 6%
      • period pain from 62% to 18%
      • pain with sex from 30% to 15%
      • chronic pelvic pain from 62% to 18%
      • PGE2 from 3404ng/l to 137 ng/l
      • CA-125 from 61.4 U/ml to 38 U/ml
      • 17 Beta Estradiol on day 21 of the cycle from 184pg/ml to 171 pg/ml.



    Endometriosis is a complex condition that involves immune dysregulation, inflammation, gut and microbiome imbalances, and a dominance of local and circulating oestrogen.

    • Endometriosis most likely starts with differentiation and migration of any Mullerian tissue during the formation of the embryo resulting in patches of this tissue being laid down in abnormal locations in the pelvis or elsewhere in the body. Later in life, these misplaced patches of tissue develop into endometriosis when they are exposed to oestrogen.
    • Silent endometriosis may be a cause of infertility
    • The maintenance of endometriosis is largely mediated by prostaglandin E2 which leads to increased growth of lesions and inflammation
    • High levels of prolactin mediate pain and can be reduced with dopamine boosters
    • Increased risk with chemicals commonly found in plastic and cosmetics.
    • Increased risk with imbalanced gut and vaginal microbiomes
    • Increased risk with genetic variants of COMT and MTFHR genes
    • A hormone balancing diet is essential
    • Multiple supplements are supportive in prevention and treatment particularly vitamin E, NAC, vitamin D and methylated B vitamins
  • Adenomyosis Demystified: Functional Medicine Strategies for Relief and Recovery

    Adenomyosis is a condition where the tissue that normally lines the inside of the uterus is found within the muscular layer of the uterus. It is common in women who are of childbearing age, and can develop at any age. The most common symptom of adenomyosis is unrelenting pain, throughout the cycle, on the top of the uterus. Severe period pain is common and there may be heavy bleeding.

    Adenomyosis can occur alongside endometriosis. Although endometriosis can be found in about 1 in 10 women of reproductive age,  it is impossible to know how many women are affected by adenomyosis. That is because diagnosis of adenomyosis is often difficult. The gold standard tool for diagnosing adenomyosis is by histopathological examination of a womb which has been removed by hysterectomy, which of course is not an option or preferred choice for everyone. In contrast, the gold standard tool for diagnosing endometriosis is a laparoscopy (keyhole surgery), which does not necessitate removal of any organ. Up to 1 in 5 women attending a gynaecology clinic with heavy periods, pelvic pain or infertility, were found to have evidence of adenomyosis on ultrasound scan.

    Studies using imaging to diagnose adenomyosis have reported an association between adenomyosis and an increased risk of preterm birth, small for gestational age, and pre-eclampsia among pregnant women who conceive spontaneously. Among women undergoing in vitro fertilisation and intracytoplasmic sperm injection treatment, adenomyosis is associated with a reduced rate of pregnancy and live births as well as an increased risk of miscarriage.

    Presentation and Diagnosis

    To understand adenomyosis, it is necessary to understand that the uterus has different layers. The innermost layer, which lines the uterine cavity, is called the endometrium. An embryo implants in the cells of the endometrium. The endometrium is what is shed each month when a woman has a period. Moving outward, the next layer is composed of mostly muscle and is called the myometrium. The myometrium can be further divided into an inner layer which is also called the junctional zone and an outer layer. The outermost layer of the uterus is a very thin covering called the serosa. In normal women, the “dividing line” between the endometrium and the junctional zone is clear and distinct and is thin.

    In 80% of cases with histological adenomyosis (hysterectomy specimens), the junctional zone can be seen to be enlarged or thickened on an MRI scan:

    • less than 5mm thickening: normal uterus;
    • 6-12mm thickening: diagnosis is unclear and could represent developing adenomyosis that not yet reaching diagnostic criteria. The test should be repeated within 12 months;
    • more than 12mm: proven adenomyosis.

    Another important clue to the diagnosis of adenomyosis, especially in the younger (smaller) uterus, is the ratio of the junctional zone to the myometrium. In the absence of adenomyosis this ratio is less than .4 (40%).  Greater than 40% is usually, but not always, also found where the junctional zone thickness is more than 12mm. 

    In teenage girls with adenomyosis the uterus is not yet matured, so if their junctional zone is in the 5 to 12mm range (strictly not diagnostic), but the ratio of the junctional zone to the myometrium is greater than 40% (in a small uterus), they should be treated as if they have adenomyosis. 

    This is particularly important where symptoms of endometriosis have led to a laparoscopy but no endometriosis was found. It is usually the case that adenomyosis is present.

    Dr Tronc uses this diagnostic table to identify adenomyosis, specifically whether the junctional zone is more than 12mm and whether there is an associated increase in the percentage thickness of the junctional zone amongst other features.

    Dr Tronc reports that his choice of scanning techniques for the confirmation of adenomyosis is the MRI scan, not the ultrasound scan, because unless the radiologist is experienced in the diagnosis of early adenomyosis, an ultrasound scan may not give adequate results. In order to get the most accurate diagnosis, women should have the test performed in the “late proliferative” phase, usually on days 10 to 13 of a 28 day cycle.  If someone is on the oral contraceptive pill, it seems not to matter when it is done.

    It is important to know however that the relationship between JZ thickness and adenomyosis itself is poorly understood, and in about 20% of premenopausal women, the JZ is undefinable on MRI.

    Fibrosis is one important feature of adenomyosis. Elastography is a relatively new type of imaging technology that has become available for commercial use. It works by creating images that show how stiff different tissues are. There are two main types: ultrasound elastography (UE) and magnetic resonance elastography (MRE). Ultrasound elastography uses sound waves, while magnetic resonance elastography uses magnetic fields and radio waves.

    This technology is similar to the traditional method of feeling for lumps or hardness in a clinical exam (palpation) but offers several advantages. Elastography is less subjective, meaning it doesn’t rely as much on the individual judgment of the clinician. It also doesn’t require as much experience to use, and it provides more precise information about where in the body the stiffness is located.

    As of now, the use of MRE in the field of gynecology has been limited. However, ultrasound elastography is becoming more popular in this field. One of the biggest benefits of elastography is that it can detect a wider range of tissue stiffness in adenomyosis compared to other imaging methods like CT scans, standard ultrasounds, and MRI scans.

    Early adenomyosis usually evolves in the central part of the fundus in the uterus. Even in more advanced cases of adenomyosis the expansion of the junctional zone in MRI often shows concentration of lesions at this location. During menstruation the muscular waves of contraction start in the cervical canal and rapidly move in the fundal direction, exerting their strongest power at the upper level of the uterus, which is where the most trauma will then occur, causing the intense pain of adenomyosis.

    Development and Maintenance of Adenomyosis

    The most comprehensive theory of of the development of adenomyosis involves the traumatisation of the uterine tissue followed by the initiation of the mechanism of tissue injury and repair (TIAR).

    In essence, adenomyotic lesions experience cyclic bleeding and are fundamentally wounds undergoing repeated tissue injury and repair (ReTIAR), which progress to fibrosis, fusing into existing myometrium, and causing an enlarged uterus. The enlarged uterus is likely to result in increased magnitude of uterine contraction, especially when oxytocin receptor (OTR) is overexpressed. In addition, due to the fusion into the myometrium, the uterine contraction is likely to be out of synchronisation, resulting in abnormal and painful muscle contractions.

    Wounds may be caused by:

    As long as the endometrial–myometrial interface disruption (EMID) is severe enough, it will cause adenomyosis. Lesional progression can be facilitated by psychological stress, and a history of adverse early life events.

    Injury resulting EMID leads to platelet aggregation, inflammation, and hypoxia (low oxygen), causing the release of copious inflammatory cytokines such as IL-1β and growth factors such as TGF-β1, increased local oestrogen production, as well as nerve damage.

    Local oestrogen production

    Oestrogen is critical to tissue repair, however it can disrupt the normal control that the ovaries have over the uterine muscle movements. As a result, the uterus starts to contract more frequently and intensely than usual, a condition known as hyperperistalsis. This excessive muscular activity can further harm the uterus, creating a cycle where the condition keeps getting worse on its own. Essentially, the ongoing damage leads to more inflammation and hormonal imbalances, which then causes even more damage, continuing the cycle of the disease.

    Estradiol’s repair effects are primarily executed through the estrogen receptor-beta (ER2). Research, including animal experiments and studies on various body tissues like astroglia, bladder tissue, fibroblasts, and cartilage, has shown that healing after tissue injury involves locally produced oestrogen.

    When tissue is injured, a substance called interleukin-1 activates the cyclooxygenase-2 (COX-2) enzyme, leading to the production of prostaglandin E2 (PGE2). PGE2 then activates the steroidogenic acute regulatory protein (STAR) and the P450 aromatase enzyme. This process facilitates the movement of cholesterol to the inner mitochondrial membrane, where testosterone is produced and subsequently converted into estradiol.

    Intriguingly, studies with fibroblasts have shown that even minor physical strain can initiate this healing process.

    The similarity of the molecular biology of TIAR in various tissues with that described in endometriosis strongly suggests that this represents the common underlying mechanisms of both diseases.

    An increase in nerve fibres and pain

    Ectopic endometrial stromal cells, which are cells from the uterus lining found outside their normal location, secrete neurotrophic factors such as NGF, NT-3, TrkB, TXA2, and GDNF, as well as axon guidance molecules like Semaphorin 3E and SLIT/ROBO. These substances stimulate the growth of nerve fibers in the lesions, resulting in an increased density of nerves, known as hyperinnervation.

    Additionally, the normal endometrial tissue can promote the growth of both nerves and blood vessels (neuroangiogenesis) through the release of tiny particles called exosomes. This increased nerve presence in the endometrium and the muscle layer of the uterus (myometrium) makes these areas highly sensitive. Therefore, even minor pain signals, changes in pain mediators, or abnormal muscle movements in the uterus can be significantly amplified. These signals are transmitted from the nerves in the uterus to the spinal cord and then to the brain, leading to the perception of pain. The situation is further worsened by the loss of GABAergic inhibition in the nervous system, a mechanism that usually blocks the transfer of pain signals to the brain.

    Moreover, with more nerve fibers, especially an elevated density of sensory nerve fibers, there is an increase in the secretion of neuropeptides. However, some neuropeptides, such as substance P and calcitonin gene-related peptide (CGRP), can trigger changes in the ectopic endometrial cells that accelerate the formation of fibrous tissue (fibrosis) in the lesions.

    In essence, the interplay of ectopic endometrial cells, increased nerve fibers, and altered neuropeptide levels in adenomyosis synergistically contribute to the pain experienced by women with this condition. This complex interaction involves nerve growth, heightened pain signal transmission, and tissue alterations in the uterus.

    Heavy menstrual bleeding, lower PEG2?

    In adenomyosis, the tissue becomes stiffer and more fibrous, leading to a decrease in COX-2 activity and lower PGE2 production. The reduction in PGE2 levels disrupts the hypoxia in the endometrium, impairing its ability to repair itself, which contributes to heavy menstrual bleeding. Studies have found that women with adenomyosis who experience heavy menstrual bleeding tend to have greater fibrosis in their lesions, accompanied by lower levels of HIF-1α, COX-2, and other related substances, indicating disrupted prostaglandin signalling and impaired endometrial repair.

    Additionally, glycolysis, a process where glucose is broken down to produce energy, plays a crucial role in endometrial repair. The endometrium shifts to glycolysis during repair to meet increased energy demands and reduce oxidative stress, which can damage cells and tissues. However, reduced hypoxia signaling in fibrotic adenomyotic lesions, as seen in decreased levels of HIF-1α, can impair glycolysis. This impairment further disrupts endometrial repair, contributing to heavy menstrual bleeding in adenomyosis.

    These findings provide a good explanation as to why different subtypes of adenomyosis have different symptoms. An early study indicated that adenomyosis lesions that penetrate less deeply into the myometrium, the muscular layer of the uterus, are more likely to be associated with heavy menstrual bleeding. This is because lesions closer to the lining of the uterus can more easily affect this area due to their physical proximity, thereby increasing the likelihood of heavy menstrual bleeding as the lesions progress. Additionally, internal adenomyosis, where lesions are within the muscle layer of the uterus, is commonly linked with heavy menstrual bleeding, whereas external adenomyosis, with lesions on the outer part of the uterus, often correlates with deep endometriosis and associated pain.

    Heavy menstrual bleeding might further worsen the impairment of endometrial repair. The bleeding could lead to an accumulation of iron in the local area, potentially reducing the growth of endometrial stromal cells by inducing autophagy, a process where cells break down their own components. This could further hinder the endometrium’s ability to repair itself.

    A vicious cycle of adenomyosis–pain–stress–lesional progression–more pain

    Pain, heavy menstrual bleeding, and infertility can trigger various degrees of anxiety, discomfort, depression, and stress. When stress is chronic or persistent, it activates the Hypothalamic-Pituitary-Adrenal and Sympathetic-Adrenomedullary axes in the body, leading to the release of hormones called catecholamines, including adrenaline and noradrenaline. These hormones act on specific receptors and proteins in the ectopic endometrium (uterine lining cells found outside the uterus), notably adrenergic β2 and cAMP-responsive element-binding protein, accelerating the progression of lesions associated with the condition.

    Chronic stress can also diminish the presence of dopamine receptor D2 in the ectopic endometrium. Dopamine is a neurotransmitter involved in mood regulation and other bodily functions. In contrast, positive stress, known as eustress, increases DRD2 presence in the lesions and slows their progression. This finding is consistent with research showing that dopamine or drugs activating DRD2 can hinder stress-related increases in blood vessel formation and cell growth in cancers.

    Low dopamine levels can increase prolactin, a hormone important in the reproductive system. High prolactin can disrupt the secretion of gonadotropin-releasing hormone (GnRH), essential for reproductive health, leading to decreased levels of luteinizing hormone and follicle-stimulating hormone, affecting hormone production and fertility.

    Prolactin’s elevated levels have been linked to the development of adenomyosis, appearing to encourage the growth and function of cells in the uterus.

    In mouse studies, implanting part of the pituitary gland (which produces prolactin) into the uterus induced adenomyosis. Also, higher prolactin levels in the bloodstream were associated with increased adenomyosis incidence. This evidence points to prolactin’s potential role in triggering adenomyosis. Treatment with bromocriptine, a dopamine agonist that reduces prolactin, completely halted adenomyosis development in some studies.

    Another aspect of prolactin’s impact is its role in angiogenesis, the formation of new blood vessels. Vascular endothelial growth factor (VEGF) promotes angiogenesis. Dopamine agonists, like cabergoline, hinder VEGF from binding to its receptor on blood vessel cells, thus reducing angiogenesis. Animal studies on endometriosis showed that cabergoline treatment significantly decreased endometriotic lesion size and activity and VEGF production.

    A self-perpetuating cycle emerges in adenomyosis, where the condition leads to pain and stress, which then accelerates lesion progression, resulting in more pain. This cycle highlights the intricate interplay between emotional and physical stress and the biological processes in adenomyosis, exacerbating the disease through a combination of hormonal and neurotransmitter effects.

    My approach to resolving adenomyosis


    • Avoiding gluten, dairy, alcohol, soy and sugar can make a significant difference to reducing pain and inflammation


    • Vitamin E has been shown to prevent adenomyosis in a study that used Fluoxetine to induce it. Fluoxetine is an antidepressant from SSRI group having effect on reproductive organs by increasing oxidative stress. Administering vitamin E to fluoxetine-induced adenomyosis prevented the rise of prolactin and the development of adenomyosis.
    • L-tyrosine increases the production of dopamine and can reduce uterine pain.
    • L-arginine can prevent hypoxia and reduce uterine pain and heavy bleeding.
    • Agnus castus can reduce prolactin.
    • DIM and Myomin can improve the overall balance of oestrogens.
    • Quercetin can inhibit the proliferation of ectopic endometrial stromal cells in adenomyosis and reduce their mobility and invasiveness.

    Vaginal microbiome swab testing


    • Adenomyosis is characterised by a constant pain on the top of the uterus.
    • Adenomyotic lesions are fundamentally wounds undergoing repeated tissue injury and repair, which progress to fibrosis, with ensuing greater tissue stiffness, resulting in impaired endometrial repair and eventually causing heavy menstrual bleeding.
    • Wounding may be caused by medical uterine procedures, imbalance vaginal microbiome leading to uterine infections and/or excess oestrogen causing strong muscle contractions.
    • A high level of prolactin can induce adenomyosis.
    • Adenomyosis can be managed by avoiding gluten, dairy, alcohol, soy and sugar.
    • Helpful supplements include vitamin E, l-tyrosine, l-arginine, Agnus castus, DIM, Myomin and quercetin.

  • Transforming Fibroid Care: Exploring Functional Medicine Approaches for Natural Relief

    Fibroids are the most common growths in the uterus. Their growth is stimulated by oestrogen and progesterone, causing uterine collagen to cross-link and harden, creating  a stiff mass of collagen fibres. Fibroids tend to develop in early perimenopause, when oestrogen levels increase and regress in menopause as oestrogen declines. Fibroids tend to have more oestrogen receptors, so this may be one reason oestrogen disproportionately affects the growth of these solid tumours. More than 80% of Black women and nearly 70% of white women have fibroids by age 50. Sometimes these growths are harmless and can even go undetected, but in many cases they cause symptoms ranging from pain and bleeding to infertility.

    Early warning signs

    The symptoms of fibroids are relatively common and can be associated with other factors or diseases, such as ovulatory dysfunction, endometriosis or endometrial polyps. Many women do not connect their symptoms to fibroids, so can go undiagnosed for some time, and some fibroids can be asymptomatic, thereby avoiding detection.  Many women have uterine fibroids and don’t even know it. Small fibroids don’t often cause symptoms and don’t regularly affect your life. However, larger fibroids may lead to several warning signs, including:

    • Heavy bleeding: you can experience heavy menstrual bleeding, large clots, and bleeding between cycles when you have one or more uterine fibroids. This is the most common symptom. Excessive bleeding can lead to the development of anaemia (low red blood cells) causing ongoing tiredness and weakness.
    • Pelvic pressure or pain, lower back pain: pelvic pain and low back pain are common early symptoms of uterine fibroids. The pain may be sharp or feel similar to your menstrual cramps but worse.
    • Full feeling in the abdomen: as uterine fibroids grow, they occupy more space in your uterus and pelvic area. You may feel like your belly is full, as if you’ve eaten a large meal.
    • Increased urination: you might feel like you have to urinate more often when you have uterine fibroids. This happens when the fibroid is big enough to put pressure on your bladder. Although rare, fibroids can also cause obstruction of the ureter, which might require treatment if this progresses to severe hydronephrosis.
    • Pain during sex: the fullness in your abdomen that fibroids cause can also lead to discomfort during sex. Not everyone feels this, but if you have pain with intercourse, getting evaluated for uterine fibroids is a good idea.
    • Gastrointestinal symptoms: constipation or the recurrent need to void bowels can also be caused by fibroids. 
    • Rarely, a fibroid can cause sudden, serious pain when it outgrows its blood supply and starts to die. Get medical care right away if you have severe bleeding from the vagina or sharp pelvic pain that comes on fast.

    There are long-term complications that can affect the integrity of the endometrium, the uterine lining. This means it can be difficult getting pregnant. During pregnancy, women with fibroids have an increased risk of complications compared with women without fibroids, including

    • preterm delivery (16.7% versus 6.3%) and
    • premature rupture of membranes (14.3% versus 2.1%)
    • risk of placental abruption (7.5% versus 0.9%)
    • fetal malformation (6.2% versus 3.3%)
    • caesarean section (70–76% versus 32.8%)
    • postpartum haemorrhage (33% versus 6%) and
    • foetal malpresentation (19% versus 4.4%) are increased in women with fibroids

    Fibroids can also be associated with miscarriage. 

    The symptoms of fibroids are relatively common and can be associated with other factors or diseases, such as ovulatory dysfunction, endometriosis or endometrial polyps. Many women do not connect their symptoms to fibroids, so can go undiagnosed for some time, and some fibroids can be asymptomatic. Lack of symptoms does not necessarily mean lack of inflammation, so women experiencing infertility should be evaluated to the presence of fibroids.

    Presentation and Diagnosis

    Diagnosing fibroids is usually done by transvaginal ultrasound, although this is limiting if the uterus extends beyond the pelvis, a common problem with this disease. Abdominal ultra-sonography might be required to diagnose fibroids that extend beyond the effective range of the trans-vaginal probe, but then MRI is generally preferred. 

    Women often have more than one fibroid. They can be different in size and in their location. The location of fibroids directly affects the symptoms they induce, as well as the time to the manifestation of such symptoms. For example, submucosal fibroids that bulge into the uterine cavity seem to have more of an effect on abnormal menstrual bleeding and pregnancy problems. This is independent of fibroid size as small fibroids that protrude into the uterine cavity can also induce menstrual irregularities. Conversely, subserosal fibroids that form on the outside of the uterus are slow growing and considerable time is needed before they are of a sufficient bulk to cause symptoms, such as back, leg or pelvic pressure and abdominal and pelvic pain. 

    The International Federation of Gynecology and Obstetrics (FIGO) has established a classification system which uses an 8-point numerical system to describe the location of fibroids relative to the endometrium (submucosal surface) and the serosal surface, with low numbers indicating a central location.

    • Type 0: pedunculated fibroid, which is localized in the submucosa and extends inside the uterine cavity 
    • Type 1: submucosal fibroid, with <50% in an intramural location 
    • Type 2: submucosal fibroid, with ≥50% in an intramural location 
    • Type 3: contacts the endometrium, with 100% in an intramural location 
    • Type 4: intramural fibroid
    • Type 5: subserosal fibroid, with ≥50% in an intramural location • 
    • Type 6: subserosal fibroid, with <50% in an intramural location •
    • Type 7: subserosal pedunculated fibroid
    • Type 8: other (for example, cervical or parasitic) 

    Recently, shear wave elastography (SWE) has been developed as a potential screening tool for the early identification of women at risk for developing fibroids. This provides the option of preventative treatment to delay or even arrest or reverse fibroid progression.

    Proposed application of SWE as a screening tool for identification of women at risk of fibroid development and corresponding preventive measures to be taken. MyoN: normal non-fibroid myometrium; MyoF: at risk-myometrium, EGCG: Epigallocatechin Gallate.

    The principle of SWE is to use sound waves to produce images. The sound waves can give an indication of how stiff the uterine tissue is: soft, firm, solid or hard. The stiffness indicates the progression of fibroid growth, as well as the use of appropriate therapies.


    In urine

    As oestrogen can fuel the growth of fibroids, it can be helpful to identify whether oestrogen is elevated, and how it’s metabolised. DUTCH urine testing is unique because it helps identify symptoms of hormonal imbalances by providing a complete picture of hormone levels which cannot be seen in testing serum (blood) alone. The DUTCH test can measure the levels of the 3 types of oestrogen, oestrone (E1), oestradiol (E2) and oestriol (E3) and how they are metabolised.

    Estradiol (E2) is the most biologically active estrogen in the body. However, estrone (E1) and the phase 1 estrogen metabolites (2-OH, 4-OH, 16-OH) can also bind to estrogen receptors. Thus, it is possible that elevations in any of these markers may contribute to fibroid growth.

    The phase 1 metabolite, 16-OHE1, tends to bind more tightly to oestrogen receptors than the 2-OH and 4-OH metabolites (but not nearly as tightly as E2), and is known to cause tissue groeth. If too much oestrogen is metabolised into the 16-OHE1 form, it may contribute to increased fibroid growth. 

    Having this information is extremely valuable, because it means that as a practitioner I can first reduce the amount of oestrogen and alter the metabolism of oestrogen in a more favourable way.

    In blood

    The CA-125 blood test measures the amount of CA125 protein that both women and men have in their blood. CA-125 is elevated in cases of fibroids, endometriosis and adenomyosis, as well as ovarian cancer. This means that it can’t be used to identify any one of these conditions, but it can be used to monitor progression.

    Development and Progression of Fibroids

    Fibroids are associated with high oestrogen levels, or oestrogen dominance. Obesity and the perimenopausal state are often associated with higher oestrogen levels. Studies have shown that oestrogen levels are actually higher in perimenopausal women, and fat is  hormonal organ capable of producing oestrone, a strong oestrogen. The inflammatory mediators interleukin-2 (IL-2), IL-6, tumor necrosis factor-alpha (TNF-alpha), and leuko- triene B4 (LTB4) are also produced in the adipocyte and contribute to fibroid formation.

    MED12 gene mutations created by high oxidative stress in the uterus drive fibroid formation

    Nearly 70 percent of uterine fibroids are linked to a mutation in the MED12 gene but recreating this problem in the lab has proven to be difficult because when cultured, the mutant cells in the fibroids do not survive. This year scientists used CRISPR-based genome editing technology (for which 2 women scientists won a Nobel prize in 2020) to precisely engineer cells that have the same mutation in the MED12 gene. After successfully culturing the mutated fibroid cells in 3D spheres, it was found that the cells produced heightened levels of collagen, a key feature of uterine fibroids, as well as other chromosomal abnormalities commonly seen in uterine fibroids. 

    A clear connection has been made between MED12 mutations and high levels of oxidative stress in the uterus. The direct connection between oxidative stress and MED12 is not yet clear however almost all the risk factors below can drive oxidative stress.

    Risk Factors

    Anything that increases oestrogen:

    • Age
      Increasing age is a significant risk factor for uterine fibroids, especially among women at the premenopausal stage and those ≥ 40 years of age. For instance, 60% of African American women aged 35-49 years reported uterine fibroids, whereas 80% of those aged ≥ 50 have uterine fibroids. Among White women, 40% of those aged ≤ 35 years and 70% aged ≥ 50 years developed uterine fibroids. Rapid growth of fibroids after the age of 30, especially in perimenoause, is consistent with age-related changes in oestrogen and progesterone. Fibroids have not been detected in prepubertal girls, and only sporadic cases have been reported in adolescents. However, the factor(s) involved in their development at such an early age is unknown. Due to the slight difference in biochemical pathways, uterine fibroids in young women do not exhibit typical uterine fibroid biology. In several cases, adolescent patients had a translocation between chromosomes 12 and 14, which is a confirmed risk factor for uterine fibroids. Women at the menopausal stage have shrunk uterine fibroid lesions and decreased sex hormones.
    • Early first period
      Women with an earlier age at menarche had higher levels of estradiol and estrone and lower levels of sex hormone-binding globulin than women with a later age at menarche.
    • Early use of oral contraceptives
      Use of oral contraceptive for the first time between 13 to 16 years of age increases the risk of fibroids
    • Excessive sugar
      Elevated 2-hour glucose post-challenge, an indicator of diabetes, is found to be associated with an increased risk of fibroids. Sugar boosts oestrogen levels and is strongly associated with a higher risk of breast cancer.
      Sugar boosts insulin which can increase the conversion of testosterone to oestrogen via the enzyme aromatase. Fibroids express three times higher aromatase levels than surrounding tissues, increasing active estradiol promoting growth of fibroids.
    • Soy
      Babies fed soy formula within 2 months of birth and for more than 6 months had an elevated risk of fibroids incidence in comparison with those never fed soy formula. Additionally soya is associated with an increased risk of uterine fibroids in premenopausal women.
    • Red meat?
      A diet higher in protein is protective however there has been a question mark around the risk of red meat increasing oestrogen. A study measuring the concentrations of oestrogen in American and Japanese beef found that the median concentrations of E2 and E1 in USA beef fat  were 140 times and 11 times, respectively, higher than those in Japanese beef fat. In red meat, E2 and E1 levels of USA beef were ∼600 times and 10 times, respectively, higher than those of Japanese beef. It’s likely that the very high levels of E2 and E1 in American beef derive from the steroids given to the cattle. On the other hand, nearly zero level of E2 seen in Japanese beef was considered to be the natural endogenous status in beef without steroids. The go on to say “Accordingly, it is our intuitive feeling that the increasing consumption of oestrogen-rich beef following steroid implantation might facilitate oestrogen accumulation in the human body and could be related to the incidence of hormone-dependent cancers”, and very likely fibroids.
    • HRT
      A state-of-the-art literature review found that some combinations of oestrogen and progestin have exhibited a significant influence on fibroids enlargement, as well as in frequency of newly detected fibroids in menopause. By contrast, several studies failed to demonstrate a significant increase in fibroids size, although a trend towards enlargement was noted. Women should have regular thorough follow-up, including trans-vaginal ultrasound for the monitoring of fibroid size, and HRT should be discontinued if an increase in size of uterine fibroids is documented.
    • Obesity
      Fat tissue, has been proven to play hormonal, metabolic, and immune regulatory roles in the body. Fat cells make leptin, a hormone which in excess can promote inflammation driving fibroid growth. Additionally fat cells create a fibroid-friendly micro-environment that can induce fibrosis and fuel fibroid growth by increasing blood supply to it. Each kilogram of excessive body weight is correlated with an increased risk of uterine fibroids development. A study conducted in the United States found that women diagnosed with uterine fibroids are heavier than those without uterine fibroids. Moreover, an increase in the body mass index (BMI) by one unit, higher waist-to-hip ratios, and body fat percentage exceeding 30% increase the risk for uterine fibroids. Abdominal visceral fat also enhances this risk. Obesity and particularly excess visceral fat may be complemented with the reduced production of the sex hormone-binding globulin (SHBG), which binds circulating hormones, disrupting the hormonal activity toward sensitive tissues, and thereby influencing the delicate hormonal balance in the body.
    • Alcohol
      Alcohol and especially beer are known to increase oestrogen. A recent Korean study assessed alcohol consumption and the risk of new-onset fibroids in 2.5 million Korean women aged 20 to 39 years concluded:
      • Mild-to-Moderate Drinkers vs. Heavy Drinkers: Women who consumed alcohol had a higher chance of developing uterine leiomyomas. The increase in risk was between 12% and 16%. Specifically, women who drank alcohol mildly to moderately had about a 12% higher risk, while heavy drinkers had about a 16% higher risk.
      • Frequency of Drinking: The risk of developing these tumors increased with the frequency of alcohol consumption. Women who drank once a week had an 11% increased risk, while those who drank three or more times a week had a 15% increased risk.
      • Amount of Alcohol per Session: The risk also increased with the amount of alcohol consumed per session. Drinking seven or more glasses of alcohol in one session was associated with a 17% increased risk.
      • Sustained Drinkers vs. Sustained Non-Drinkers: Women who consistently consumed alcohol over a period of time (referred to as “sustained drinkers”) had a 20% increased risk of developing these tumors compared to women who consistently did not drink alcohol (referred to as “sustained nondrinkers”).
      • Change in Drinking Habits: Women who stopped drinking alcohol showed a small increase in risk (3%), whereas women who started drinking who previously did not have a 14% increased risk.

        In summary, the study found that drinking alcohol is associated with a higher risk of developing uterine leiomyomas, and this risk increases with the amount and frequency of alcohol consumption. Women who consistently drink have a notably higher risk compared to those who don’t drink or those who stopped drinking.
    • An imbalanced gut microbiome
      The estrobolome is a collection of bacteria in the gut which is capable of metabolising and modulating the body’s circulating oestrogen. The gut bacteria regulate oestrogens through secretion of β-glucuronidase, an enzyme that splits detoxified oestrogen, releasing free oestrogens that are then reabsorbed into the bloodstream and repeatedly circulated through the body, increasing oestrogen levels. The genes for β-glucuronidase are widely found in Firmicutes (which are increased in the vaginal microbiome in women with fibroids, see below).

    Possible mechanisms that could link gut dysbiosis and the development of uterine fibroids.

    A dysbiotic gut results in an altered microbiome which triggers the following pathways

    1. interferes with the estrobolome functioning and results in hyperestrogenic state leading to uterine fibroids
    2. altered levels of gut metabolites such as short chain fatty acids (SCFA) which triggers immune dysregulation and induce inflammation and also leads to hyperestrogenic state
    3. interferes the gut permeability leading to a leaky gut and toxicity which could dysregulate the immune function.

    • COMT
      Catechol-O-methyltransferase (COMT) is an enzyme that triggers enhanced transformation of 2-hydroxyestradiol (anti-estrogen) into 2-methoxyestradiol (pro-estrogen) with resultant hyperestrogenic environment that may contribute to cell proliferation and increase in fibroid development. High COMT activity has been found in fibroids. Women with the high-activity COMT Val/Val genotype are 2.5 times more likely to develop fibroids than women with other genotypes. The prevalence of this genotype was significantly higher in African American women (47%) compared with white (19%) or Hispanic (30%) women. 
    • MTFHR
      Methylenetetrahydrofolate reductase (MTHFR) plays a key role in the enzymatic process in the folate metabolism pathway, which converts folic acid (obtained from food and/or supplements) into methyl-folate (the form of folate used by your body), and then participates in DNA synthesis, modification and methylation. The mutation of the MTHFR C677T gene leads to the disorder of folate metabolism, the decrease of antioxidant capacity, the increase of uterine related oxidative stress, and the proliferation of uterine smooth muscle cells, thus leading to the formation of fibroids. Additionally MTHFR mutations can cause high blood pressure via increased homocysteine. Vitamin B2 (riboflavin) is a required cofactor for MTFHR and higher vitamin B2 levels are associated with increased MTHFR enzyme activity, lower homocysteine and improved blood pressure.

      Genetic testing has identified:
      • The wildtype (non-variant) MTHFR 677 shown as “CC”. This is associated with 100% enzyme activity and does not increase risk for higher homocysteine or high blood pressure.  
      • A single MTHFR 677 variation shown as “CT”. This results in 30-35% reduction in enzyme activity and can slightly increase risk for higher homocysteine levels and blood pressure.  
      • A double MTHFR 677 variation shown as “TT”. This results in 60-70% reduction in enzyme activity and increases the risk for higher homocysteine and high blood pressure.  


    Fibroids are associated with high prolactin levels, originating from the fibroid itself or from the pituitary gland. High prolactin can cause infertility and fibroid progression.

    Blood pressure (hypertension)

    A study this year reported that women with untreated hypertension faced an 18% higher risk of developing uterine fibroids when compared to those without hypertension. Conversely, women with hypertension who were using blood pressure medications had a 37% lower risk of developing uterine fibroids, with the use of angiotensin-converting enzyme inhibitors associated with a 48% lower risk. Interestingly, women with new-onset hypertension had a 45% greater risk of uterine fibroid diagnosis, while those with pre-existing hypertension had little additional risk. The formation of fibroids is attributed to the chronic destruction of the uterine lining due to increased blood flow and inflammation.

    Vitamin D deficiency

    A systematic review last year concluded that 100% of all research studies identified vitamin D deficiency in women with uterine fibroids. The best estimate of the effect of hypovitaminosis D on fibroid development found that deficient vitamin D (< 20 ng/mL) increased the risk of uterine fibroids by 32%. The importance of this relationship is underscored by the prevalence of vitamin D deficiency, a condition which affects approximately 80% of Black American women, a population disproportionately affected by fibroids.

    Further, a case-control study this year found that  vitamin D supplementation reduces fibroid growth and development, perhaps partly because it reduces COMT activity.

    Further, vitamin D recovers the damaged DNA repair system, thus inhibiting fibroid progression.

    Women at risk for deficiency should be screened and those with deficiency should take supplements. The functional range for vitamin D is 125-150. I usually recommend 10,000 IU a day at deficiency below 60 and test serum levels regularly to avoid any overdose-related toxicities. Routine vitamin D supplementation for women with insufficiency may provide effective treatment and prevention of fibroids.

    Imbalanced vaginal microbiome

    A recent study showed that an increased level of the bacterial phyla Firmicutes was observed in both the cervical and vaginal microbiome of women with fibroids. An increased level of Firmicutes is associated with obesity. Firmicutes include Lactobacillus, Streptococcus, Clostridia, and can be reduced with high animal protein diet.

    Uterine infections 

    Fibroids are associated with Chlamydial infection, and pelvic inflammatory disease. The risk of fibroids is increased 5x when infections are associated with the copper coil.

    Copper Intrauterine Devices (IUD)

    The copper coil may be a cause of uterine fibroids. Intrauterine devices can cause local irritation, pressure, inflammation, and tissue changes in the uterus. Copper IUDs in particular impact cellular mechanisms in the endometrium. There may be oedema, vascular congestion, cell death, and other cytological alterations. These effects involve inflammatory cytokines and changes in cell proliferation and activity that have been associated with fibroids: Interleukin 1 beta (IL-1β) and tumour necrosis factor-alpha (TNF-α) levels were high in the late secretory phase and IL-6 levels were high in the proliferative early secretory phase in IUD-subjected endometrial samples. The expression of IL-1, IL-6, and TNF-α was found to be associated with the pathophysiology of uterine fibroids. A study concluded that the use of copper IUDs for more than 2 consecutive years should be avoided in order to prevent oxidative damage. 

    Copper T380A is one of the most commonly prescribed IUDs and has been shown to significantly increase copper levels. The use of copper T-200 IUD for 12 months significantly increased copper levels and significantly decreased zinc and iron levels. It is suggested that the low zinc status was probably responsible for the heavy bleeding which was common among the study group using copper IUDs, which in turn was responsible for the anaemia seen in more than 50% of the IUD users. 

    The adverse effects of copper intrauterine devices (IUDs) such as abnormal bleeding, pain and cramps may be due in part to the burst release of copper ions during the first few months of usage. Copper can then continue to build up slowly in the body. reports: “For many women, symptoms often first begin appearing 2 or 6 months after insertion.  For others, the time period may be much longer, years to decades, before they notice anything, or connect the dots. Side effects of the copper IUD as copper accumulates usually begin with increasing brain fog and fatigue, often paired with a racing mind.  Eventually, once the liver is overloaded, copper will then start accumulating more in the brain, and severe shifts in personality can occur as a result of increasing bio-unavailable copper and calcium and changes in neurotransmitter production. The period 2 to 5 months post-insertion is a common time for many women when metabolism begins slowing and energy, behaviour, and reactions begin changing, especially with a tendency towards increasing depression and irritability.”

    Zinc was found to be decreased and copper increased in the blood serum of women with diagnosed uterine fibroids compared to the control tissues, which may be associated with PMS in the luteal phase of the menstrual cycle.

    Estrogen is known to increase copper absorption vice versa. Having an excess of copper in the body has been linked to being one of the key underlying drivers of anxiety, oestrogen dominance, painful periods, heavy periods, irregular periods, mental health issues, and overall hormonal imbalances.

    Toxic pollutants

    Common chemicals called phthalates found in hundreds of household products have been linked to fibroids. Phthalates are present in many household items ranging from food packaging and processing equipment to shower curtains, building materials, and car interiors. Phthalates are also used as solvents in cosmetics and other personal care products and to coat or encapsulate certain pharmaceutical pills and dietary supplements. The chemicals can leach out of these products and enter food, air, and water, meaning you can swallow, inhale, or absorb these phthalate particles through direct skin contact. The body then metabolises these chemicals, yielding byproducts that several studies have detected in human urine, breastmilk, and blood.

    DEHP, a phthalate that’s commonly added to plastics to make them flexible has been found to foster the survival and growth of fibroids, helping them grow to large sizes. DEHP has been found to enhance MED12, triggering fibroid formation.

    Studies connect in utero exposure of those women who are going to develop uterine fibroids while the foetus is still in the uterus. When those women are exposed to endocrine-disrupting chemicals — compounds you can find in plastics, beauty products — those endocrine-disrupting chemicals can disrupt the hormonal signalling. And, later in life, the children of those women who are exposed to endocrine-disrupting chemicals have a higher chance of developing uterine fibroids.

    In the meantime, in November this year L’Oreal announced that one of the recipients of its 2023 For Women in Science Fellowship program is Joscelyn Mejías, whose research in biomedical engineering at John Hopkins University focuses on studying uterine fibroids. She hopes her research will lead to new and better treatment options for targeting uterine fibroids and fibrosis. Perhaps L’Oreal should also focus on removing toxins from their products.

    Racial Disparities

    A systematic review and application of social, structural, and political context to racial disparities in uterine fibroids found that Black women face worse clinical and surgical outcomes than their white counterparts. The differences in gene expression in fibroids from Black and white women, as well as racial disparities in fibroid prevalence, they say, may reflect that Black individuals disproportionately experience exposures linked with increased risk for uterine fibroids.

    This includes a higher risk of chronic psychological stress, adverse childhood experiences, perceived racism and environmental contaminant exposures like air pollution among Black women, which have all been associated with a higher risk for developing and experiencing severe symptoms from fibroids.

    Racial disparities may also stem from other social determinants of health such as a higher fat diet, lower levels of physical activity, vitamin D deficiency, as well as individual behaviours such as use of chemical hair relaxers that contain chemicals that are associated with increased risk of uterine fibroids. Studies have also suggested racial disparities in uterine fibroids and endometriosis can be linked to a lack of adequate access to health care, authors note, including minimally invasive gynecologic surgeons, interventional radiologists, and bias and discrimination within the health care system.  “Black women may be more likely to have symptoms dismissed, report negative experiences with the health care system and wait too long to see a specialist, which delays diagnosis and treatment,” the author said. “These significant differences in experiences, access and dismissal or misattribution of symptoms may lead to worse outcomes.”

    While some women with fibroids don’t have symptoms, others have significant pain, anaemia, heavy menstrual bleeding, increased urinary frequency, fertility problems and pregnancy complications. Black women are diagnosed with fibroids roughly three times as frequently as white women, develop them earlier in life and tend to experience larger and more numerous fibroids that cause more severe symptoms. The author of the study said “If we are sincere about striving for health equity, then we have to look at the underpinnings of inequity in our healthcare system and in society. Solutions need to address root causes of disparities through policy, education and programs that ensure all patients receive competent care.”


    Association with Breast Lumps (fibroadenoma)

    The same mutated MED12 gene that is found to cause fibroids is also found in 59% of breast fibroadenomas. This indicates that benign tumours of the breast and uterus, both of which are key target tissues of oestrogen, may share a common genetic basis underpinned by highly frequent and specific MED12 mutations. Interestingly supplementing with iodine resolves breast lumps and breast pain which may indicate that iodine deficiency is also a driver for fibroid development.

    Tissues that store iodine include the thyroid, breasts, ovaries, uterus and placenta. While the thyroid tends to concentrate a higher percentage of iodide (I¯), other tissues tend to utilise a greater percentage of molecular iodine (I₂), which exerts multiple and complex actions related to its role as an antioxidant, an anti-inflammatory, a pro-inflammatory, an inducer of cell death, an immune modulator, and a promotor of cell differentiation. Importantly, iodine helps to maintain the oestrogen balance in favour of estriol which has been shown to protect against oestrogenic cancers and decrease the risk of fibrocystic changes in the breasts.

    High oestrogen levels can prevent the absorption of iodine, which may be an additional cause of fibroid development. Iodine deficiency has been associated with fibrocystic breast disease and, more recently, with the development of distant metastatic breast cancer in young women aged 25-39. This trend toward the development of breast cancer in younger women has been associated with the reemergence of iodine deficiency in the U.S. since the 1970s. Since iodine protects against abnormal cell development and proliferation, adequate iodine levels may prevent fibroids from occurring.

    Association with Breast Cancer

    Both the uterus and breasts have sex hormone dependence, and this year a study involving over 630,000 women concluded that women with fibroids have a higher risk of breast-related diseases, including cancer:

    • Benign breast disease: 33.5% higher risk
    • Carcinoma in situ : 79.6% higher risk
    • Breast cancer: 30% higher risk

    Women with fibroids should be more vigilant about breast cancer, having regular breast exams and ultrasound for early detection of breast cancer.

    Advances in Surgical Treatment

    Traditional surgical treatments for fibroids are:

    • Removing the whole womb including the fibroids (a hysterectomy). This is an option for
      women who do not want to have any (more) children.
    • Removing the fibroids only (called myomectomy). This type of operation is suitable for women
      who want to keep their uterus – mainly to preserve the chance for future pregnancy.

    More recent surgical treatments for fibroids include:

    • Removing the fibroid through keyhole surgery (laparoscopic myomectomy).
    • Blocking the blood vessels feeding the fibroids (uterine artery embolization) which does not
      remove fibroids but can cause them to shrink and reduce heavy periods.
    • Some fibroids that are growing inside the the womb can be removed through a hysteroscope passed inside the womb through the cervix.

    There are many factors to consider when deciding the best way of removing fibroids. These include the number of fibroids, their size and exactly where they are in the womb. There can also be other issues to consider like whether you have had any operations on the womb in the past. For example, some of the fibroids that grow inside the womb can be removed by using hysteroscope operations. The fibroids that are more embedded in the womb itself cannot be removed this way.

    In the last few years some hospitals have been offering SONATA: Sonography-Guided Transcervical Fibroid Ablation. It is an incisionless, uterus-preserving, transcervical approach, with real-time visualisation using intrauterine ultrasound guidance, and combines ultrasound imaging with radiofrequency energy.

    Recently scientists have been developing a new therapeutic treatment using a drug capable of breaking fibroids down inside the body. Since fibroids are collagen-based, the key ingredient in this intervention is collagenase, an enzyme that digests collagen, and it is combined with LiquoGel™, which is liquid at room temperature, and becomes a gel at body temperature. Because of that, once it gets injected into a fibroid, it becomes a gel. Over time, collagenase will degrade the fibroid and LiquoGel™ will degrade, allowing the body to get rid of it. Much work remains before the treatment can reach patients.

    Tests to Consider for Evaluation Fibroids

    Transvaginal and abdominal ultrasonographyTo determine the size and location of fibroids and rule out ovarian tumors
    Progesterone/estradiol ratio (100–300:1) Luteal phase progesterone measurementLow luteal phase progesterone level support oestrogen dominance and fibroid growth
    Vitamin D testLow levels increase fibroid growth by several mechanisms
    Vitamin A testLow levels shown to increase heavy bleeding
    Iron or total iron-binding capacity
    measurement, ferritin tests
    Low iron stores reduce uterine contractions and increase menstrual blood loss
    Zinc and copper testsAn imbalanced copper:zinc ratio can lead to fibroids
    Thyroid function testingHypothyroidism associated with menstrual dysfunction
    MTFHR testing35% weakness in methylation, increased oestrogen dominance
    DUTCH testing for Phase 1 and Phase 2 oestrogen detoxification evaluationUnhealthy oestrogen metabolism contributes to oestrogen dominance
    Comprehensive digestive stool analysisIntestinal dysbiosis is a cause of oestrogen dominance through several mechanisms
    Vaginal microbiome testingAn unbalanced vaginal microbiome has been associated with fibroids
    Testing for celiac disease (antigliadin antibodies)Gluten grain sensitivity common in fibroid sufferers and can lead to further oestrogen dominance

    My approach to treating fibroids

    My personal experience with fibroids, and supporting women with fibroids, clearly shows that nutrition, supplements and lifestyle changes can make a significant impact on fibroid size, heavy bleeding and pain to the point of not creating any symptoms. I initially ask clients to commit to a 3-month trial period, during which they will do as much of their protocol as possible. At the end of these first 3 months, we assess symptoms, such as heavy bleeding and pain, and any growth or shrinkage of the fibroids. The protocol is considered successful if the client perceives a reduction in symptoms and no further fibroid growth has occurred. We then continue the program for 3-month periods while continuing to monitor symptoms and uterine size. If at any time symptoms recur or worsen or the fibroids begin to grow, other more aggressive measures must be considered.


    Women with fibroids begin a hormone-balancing diet involving foods with low inflammation effects, low acidity, and a low glycemic load.

    Reduce foods that increase oestrogen dominance:

    • Foods that are acidic and inflammatory, like red meat, poultry, and dairy, contain arachidonic acid. This acid can increase inflammation and help fibroids grow. Avoiding commercial meat products also reduces exposure to added hormones. Small amounts of range-fed meats can be added back once inflammation goes down.
    • Sweets and high glycemic foods can cause stress and raise insulin. This can increase oestrogen dominance and help fibroids grow. Eating breakfast with protein, fat and quality carbs prevents drops in blood sugar. This avoids spikes in cortisol and adrenaline, which break down muscle and raise insulin resistance.
    • Gluten grains like wheat, rye and barley contain a strong gluten that is genetically engineered. This gluten can raise oestrogen by blocking the detoxifying cytochrome P450 3A4 enzyme system. It can also affect thyroid hormones. Anyone with high oestrogen should be tested for gluten sensitivity.
    • Alcohol, dairy, coffee, artificial ingredients, colours, flavours and preservatives should be avoided. Also avoid margarines and foods with trans fats or hydrogenated oils.

    Include foods that reduce oestrogen dominance:

    • Cruciferous vegetables such as broccoli, Brussels sprouts, cabbage, and cauliflower support healthy oestrogen metabolism.
    • 3 cups of green tea daily are helpful (to reduce COMT activity).

    Gut and Vaginal Microbiome Restoration, and Detoxification

    • Healing intestinal and vaginal microbiome imbalance and supporting liver detoxification restores hormone balance and remove sources of inflammation.


    These nutrients to support hormone metabolism and reduce inflammation:

    • Vitamin B complex, methylated
    • Vitamin D
    • Vitamin A
    • Indole-3-carbinol or diindolylmethane (DIM) to reduce estrogen dominance
    • Aromatase inhibitors such as Myomin can reduce oestrogen dominance
    • Calcium D glucarate can reduce increased recirculation of oestrogens from the gut back into the body
    • Iodine
    • Calcium: significant negative associations have been found between low serum calcium levels and uterine fibroids, uterine size and the number of fibroid nodules, possibly reflecting associated low vitamin D levels
    • Selenium has been shown to reduce fibroid size, possibly because it is an integral part of the antioxidant enzymes glutathioneperoxidase, catalase, and superoxide dismutase (SOD) which neutralise oxidative toxic intermediates, and of which there is a deficiency in fibroids.
    • Iron, copper/zinc, and manganese are also required for optimum antioxidant activity.


    • Support for weight loss to maintain an appropriate weight.
    • Avoidance of toxic xenoestrogens (dioxins, polychlorinated biphenyls) by eating organic foods and avoiding plastics
    • Having regular exercise


    • Being over 40 with heavy periods may be a strong sign of having fibroids, and the risk is higher in Black women
    • Silent fibroids may be a cause of infertility
    • Oestrogen and progesterone are drivers of fibroid onset and growth
    • Fibroid growth is largely mediated by high levels of oxidative stress in the uterus via the MED12 gene
    • DUTCH testing can identify elevated oestrogen and unbalanced oestrogen metabolism
    • Increased risk with obesity (more than 30% body fat increases risk), drinking alcohol, having high blood pressure
    • Increased risk with chemicals commonly found in plastic and cosmetics.
    • Increased risk with imbalanced gut and vaginal microbiomes
    • Increased risk with genetic variants of COMT and MTFHR genes
    • A hormone balancing diet is essential
    • Multiple supplements are supportive in prevention and treatment particularly iodine and methylation support
    • Routine vitamin D supplementation for those with insufficiency provides effective treatment and prevention
    • Women with fibroids should be more vigilant about breast cancer, having regular breast exams, or ultrasound for early detection of breast cancer
    • HRT and the copper coil may increase the risk of fibroid onset and progression
  • Reverse PCOS and regain your fertility

    Polycystic ovaries contain about twice as many small cysts as normal. These cysts are egg-containing follicles that have not developed properly. PCOS is the leading cause of infertility in women, and it comes in 4 types.

    Underlying causes:

    • high insulin
    • high testosterone
    • low serotonin and dopamine
    • a disturbance in the gut bacteria

    Polycystic ovary syndrome (PCOS) is a relatively common and frequently misunderstood condition with variable clinical presentation. Its key features are irregular or absent menses often followed by episodic heavy and prolonged menses; infertility; central obesity; androgenisation (acne, male pattern hair loss, and hirsutism); and multiple ovarian cysts. It is estimated to affect 5-10% of women and is thought to have both genetic and environmental roots.

    Most women with PCOS will present with only two or three of the clinical features of PCOS:

    • Approximately 70% will have missed periods (oligomenorrhea) or lack of periods (amenorrhea).
    • Obesity is present in 70%.
    • Hirsutism to a varying degree is present in roughly 75%
    • Ovarian cysts – unilateral or bilateral- are present in 90%.

    Ethnicity plays a role in the presentation of PCOS. For example, women of Asian descent are less likely to have hirsutism. The variability in presentation of PCOS reflects heterogeneous causative factors. Thus, the approach for each woman needs to be individualised based on her particular presenting symptoms and laboratory findings.

    PCOS types

    The ovarian “cysts” of PCOS are unique in that they appear as multiple (10-20) small cysts, often forming a bubbly ring around the ovary on ultrasound. These cysts are easily distinguishable on ultrasound from benign solitary ovarian cysts that occur in up to 20% of women and from complex cysts and ovarian cancer that are also usually solitary. The numerous PCOS cysts are actually ovarian follicles that have been halted in their monthly march toward ovulation. These cysts develop a “thick skin” (thecation) under the stimulation of luteinising hormone (LH).
    When a woman presents with any two features of PCOS, further evaluation for PCOS is warranted.

    There are a variety of definitions of PCOS but the two most accepted ones are:

    • NIH consensus: A woman should have all of the following: oligoovulation, signs of androgen excess (clinical or biochemical), other entities are excluded that would cause polycystic ovaries.
    • Rotterdam consensus: Any 2 of the following: oligoovulation and/or anovulation, excess androgen activity, polycystic ovaries (12 or more S-7mm follicles) by ultrasound (Hart et al, 2004).

    By the Rotterdam criteria, a woman can have one of four PCOS syndromes:

    • PO: polycystic ovaries with anovulation
    • PH: polycystic ovaries with hyperandrogenism and normal ovulation
    • PHO: polycystic ovaries with hyperandrogenism and anovulation
    • HO: hyperandrogenism and anovulation with normal ovaries on ultrasound

    Research has shown that women with the PO syndrome do not show a tendency toward insulin resistance and metabolic syndrome in contrast to women who have all three features of PCOS.

    Underlying causes of PCOS

    Insulin resistance

    The most common underlying cause of PCOS is insulin resistance, which is observed in both normal weight and overweight women with PCOS. Insulin resistance occurs at some level in 50-80% of women with PCOS.
    Insulin resistance can occur through multiple mechanisms including genetic predisposition and lifestyle impact. Obesity has a well-known correlation with insulin resistance and plays an increasing role in PCOS given the current obesity epidemic in the Western world and much of the developed world. Overweight and obese women with PCOS are more likely to have glucose intolerance than normal weight women with the syndrome.

    However, even normal weight women with PCOS tend to have altered body fat distribution with more central (visceral) obesity that is associated with elevated insulin levels and insulin resistance.

    Insulin resistance in at least 50% of PQQ women appears to be related to inflammatory pathways that block insulin receptors, resulting in less glucose uptake by muscle cells, increased glucose in the blood and increased insulin levels. High circulating insulin then appears to increase ovarian and adrenal hormone production and pituitary LH release directly through the insulin receptor.

    Inflammatory pathways also appear to modulate the activity of the key regulatory enzyme of androgen biosynthesis, shedding light on the co-occurrence of insulin resistance and androgenisation commonly seen in the syndrome.

    Deficiency of Glucose Transporters

    Another mechanism for insulin resistance in PCOS is decreased glucose transporter- GLUT-4activity. GLUT-4 is instrumental in fat cell responsiveness to insulin. Thus, the GLUT-4 deficiency results in elevated glucose levels leading to a compensatory increase in circulating insulin levels.

    Ovarian Sensitivity to Insulin

    Why the ovaries are so sensitive to insulin when the rest of the body’s cells are resistant to it? Research shows that insulin action in the ovaries is mediated by different mechanism to the rest of the body, involving inositol. Thus, the high circulating insulin levels have more influence on the ovaries than on other tissues in the body.

    Disordered Function of the Pituitary Gland

    Insulin also has a direct impact on the pituitary gland. The elevated insulin increases the pulse frequency of the gonadotropins which results in LH dominance over FSH, increased ovarian androgen production, decreased follicular maturation, and decreased sex-hormone-binding. This means that ovarian follicles are stimulated to be released, but not not mature. In a positive feedback loop, increased androgens increase insulin resistance.

    Oestrogen Dominance

    Oestrogen dominance and unopposed oestrogen are issues that pose additional health risks in PCOS. Higher levels of oestrone and oestradiol are derived from increased aromatase activity in the excess visceral fat tissue. Increased oestrogen feeds back to the pituitary to reduce follicle stimulating hormone (FSH), resulting in arrest of ovarian follicle development (the “cysts” seen in the ovaries are actually arrested follicles). Arrested follicles prevent ovulation, with the subsequent failure of ovarian progesterone production that follows normal ovulation.

    Early on, prolonged unopposed oestrogen produces episodes of irregular, heavy, prolonged bleeding (dysfunctional uterine bleeding). Over time there is an elevated risk for uterine hyperplasia and cancer due to persistently unopposed oestrogen.

    Increased Testosterone Production

    Another route to PCOS is thought to be through a primary disturbance in testosterone production. Increased testosterone alone can contribute to the cascade of PCOS through increasing visceral fat, leading to insulin resistance, elevated circulating insulin levels, and ovarian dysfunction. In normal ovarian physiology androgens produced by LH-stimulated theca cells undergo aromatisation to oestrogens by FSH-stimulated granulosa aromatase.

    As aromatase activity increases and oestrogen levels increase, ovulation usually follows. In some PCOS patients, the ratio of follicular androstenedione (theca cell androgen) to estradiol is elevated and a mutation in the P450 aromatase gene has been found to be a cause of this shift.

    Increased Prolactin Production

    Elevated prolactin levels have been shown to correlate with PCOS. While very high prolactin levels are usually caused by a prolactin-secreting pituitary tumour, mildly elevated prolactin levels can be triggered by stress.

    Increased prolactin levels can also be caused by the persistently elevated oestradiol levels seen in PCOS. An overly sensitive pituitary has been implicated as women with PCOS have been shown to have a more vigorous and/or prolonged prolactin response to infusions of TRH (thyroid releasing hormone). PCOS is also associated with a more vigorous prolactin response to dopamine blockers.

    Prolactin promotes insulin resistance, so again the final common pathway is in part through the insulin receptors on the ovaries. In addition, elevated prolactin levels are known to promote excess hair growth.

    Lab Tests for PCOS

    Serum LH and LH/FSH ratio are significantly higher in women with PCOS, but these tests are abnormal in only about 40% of patients with PCOS. Mean serum total testosterone concentration is significantly higher in about 70% of women with PCOS.

    Androstenedione is significantly higher in about 50% of women with PCOS. When testing for all of the above, an abnormality will be detected in about 80% of women with PCOS.

    If serum testosterone levels exceed 150ng/dL a virilizing tumor of the ovaries should be ruled out with pelvic ultrasound.

    Other laboratory tests that may be indicative of other diagnoses or of co-morbid conditions include:

    • serum prolactin
    • HCG
    • fasting glucose and insulin
    • lipid profile
    • DHEA-S- levels greater than 700 suggest adrenal dysfunction warranting adrenal imaging
    • 17-hyd roxyprogesterone
    • elevated LH, estrone, and testosterone in the presence of normal estradiol (in idiopathic hyperprolactinemia, estradiol levels are suppressed)
    • 24 hour urinary oestrogen levels are increased in PCOS

    Ultrasound can identify polycystic ovaries, typically bilaterally enlarged ovaries with more than eight follicles per ovary, with follicles less than 10mm in diameter. More than 90% of women with PCOS have this finding, although this also occurs in 25% of normal women.

    My Approach to PCOS

    Women who seek support for PCOS are primarily concerned with correcting abnormal periods (particularly when it evolves into dysfunctional uterine bleeding), infertility, weight gain, hair growth, and acne.

    Additional preventive interests include associated increased risks for endometrial cancer and cardiovascular disease from hyperinsulinism. The risk of endometrial cancer is three times higher in women with PCOS. There is also conflicting evidence for a three-fold increased risk for breast cancer in the postmenopausal years with chronic anovulation.

    The functional medicine approach to a woman with PCOS takes into consideration the unique pathophysiology of each woman, addressing as required:

    • Dietary measures focused on weight loss and reduction in circulating insulin levels through carbohydrate restriction, particularly refined carbohydrates, unless the lean type of PCOS is presenting
    • Insulin resistance
    • Elevated ovarian and adrenal androgens
    • Elevated oestrogen
    • Elevated LH
    • Insufficient progesterone
    • Elevated prolactin
    • Lack of ovulation
    • Inflammation
    • Oxidation
    • Underlying stress
    • Obesity and metabolic syndrome

    In addition, frequently associated co-morbidities such as fatty liver, hypertension, depression with anxiety, cardiovascular disease, and dyslipidemia are also addressed.

  • Come off the pill and the avoid side effects

    Hormonal birth control (HBC) is a double edged sword.

    Women have fought long and hard for contraception, so that all of us could have control over our reproductive health. Birth control has always been a major part of this fight because it is an important tool in allowing us agency over our health and bodies as well as providing protection from unwanted pregnancy.

    However the problem with hormonal birth control (HBC) is that it is prescribed for women for all sorts of hormonal health issues that are completely unrelated to contraception including period pain, heavy periods, no periods, irregular periods and acne which masks those issues, and it can have significant side effects.

    It takes 12 years for a woman to mature her HPA axis – the communication pathway between the brain, the pituitary and the ovaries. So if you start your period at 14, it will take until you’re 26 to have established a healthy, normal, ovulation cycle, it is no wonder then, that many women who have been on the pill since their teens and stop in their 30s to try for a baby, have fertility issues.

    Are you having problems coming off the pill?

    The medical approach to period problems shuts ovulation with contraceptives such as the Pill, implants, injections and Nuvaring.
    As ovulation stops, so the production of DHEA, oestrogen, progesterone shuts down as well. It causes the ovaries to shrink by almost 50%, to the same size that they shrink to at menopause.

    When HBC is discontinued, the ovaries previously suppressed with synthetic hormones fail to return to healthy function, often leading to irregular periods, heavy bleeding and acne.

    In the meantime the hormonal imbalances cause troubling and potentially serious side effects such as depression, weight gain, microbiome disturbance, and loss of libido. Emerging research is also suggesting long term impacts on insulin resistance, fat mass, diabetes and bone mass.

    What is hormonal birth control?

    Our natural hormones oestrogen, progesterone an DHEA are required to make a healthy brain, bones, muscles and metabolism.

    • Estradiol (the main oestrogen) plays a key role in insulin signalling;
    • Estradiol and progesterone influence the release of neurotransmitters- serotonin, dopamine, GABA- to keep your mood stable throughout the cycle;
    • Progesterone converts to alloprogesterone and interacts with the brain and nervous system to relax and keep your mood stable coming up to your period.

    The steroids in HBC are not the same as our natural hormones:

    • Natural oestrogen is replaced by Ethinyl estradiol which worsens insulin sensitivity, causing insulin resistance and weight gain.
    • Natural progesterone is replaced with a variety of progestins
    • Levonorgestrel causes abortions -it is used in the Plan B abortion pill
    • Many synthetic progestins have a similar structure to testosterone, and are androgens i.e. they work as testosterone
    • Natural progesterone is a calming hormone which converts to allopregnenalone, which is a strong modulator of the GABA receptors in the brain. It is hormonal valium. Progestins don’t convert to allopregnenalone and so don’t support mood or brain function. Levonorgestrel dramatically reduces progesterone and therefore allopregnenalone, and does the opposite, reducing GABA receptors, leading to anxiety.

    Synthetic Progestins increase testosterone

    Progestins have an androgen index, indicating how close their effects are to testosterone.
    Androgenicity is described as the progestin’s affinity for and binding to the androgen receptor, an( it’s effect on the sex hormone binding globulin (SHBG). SHBG binds testosterone and estrogen making the sex hormones unavailable for use at the receptors.

    Levonorgestrel and dl-norgestrel have a high affinity for sex hormone binding globulin and decrea free sex hormone binding globulin levels by binding it and displacing testosterone, consequently increasing free testosterone levels. (PMID: 15802398)

    High androgen index:

    • Causes acne, weight gain, anxiety and hair loss (can be devastating)
    • Older progestins are made from testosterone
    • Progestins include: Levonorgestrel, Norgestrel, Medroxyprogesterone
    • Included in: Levelen, emergency contraception, Mirena, Depo-provera

    Medium androgen index:

    • Norethindrone, Desogesterel, Etonogestrel
    • Included in: Loestrin, Implanon, Nova ring

    Low androgen index:

    • suppresses DHEA, higher risk of fatal blood clots, depression and anxiety, loss of libido
    • Drospirenone – derived from a diuretic drug – anti-androgen – reduces acne but causes more depression, anxiety and clot risk than the high androgen progestins
    • Cyprotenone – Yaz and Yasmin, Brenda

    Mirena coil

    • Is an intrauterine Levonorgestrel releasing intrauterine device (IUD)
    • Works locally in the uterus, prevents fertile mucus, impairs sperm and thins the uterine lining.
    • Blood levels of progestins are at 10% compared to Levonorgestrel pill, but this is still enough to cause androgen side-effects in some women such as acne and hair loss.
    • Allows normal estradiol and some ovulation.

    Side effects of taking HBC

    • Altered microbiome of gut
    • Altered microbiome of vagina
    • Altered brain structure
    • Altered sleep architecture
    • Reduced bone density
    • Gallbladder disease
    • Increased risk of cervical dysplasia
    • Increased risk of autoimmune disease
    • Zinc deficiency
    • 3-fold higher risk of breast cancer
    • Digestive bloating
    • Recurrent bladder infections
    • Thrush
    • Vaginal dryness

    Side effects of stopping HBC

    A real period is about the healthy functioning of the ovaries and the healthy production of oestradiol and progesterone via ovulation. A pill bleed suppresses those hormones and instead is a bleed from the withdrawal of the drugs. So the timing of the pill bleed is about the dosing of the drug.

    There is no medical reason to bleed monthly on HBC. Hence HBC does not regulate periods. It stops periods altogether, and a bleed only occurs when HBC is paused which causes a drug deficiency.

    Once HBC is stopped, the most common symptoms are:

    • Irregular or skipped periods
    • Heavy menstrual bleeding
    • Ovulation pain and menstrual cramps
    • Acne breakouts
    • Bloating
    • Mood swings

    My approach to coming off HBC and avoiding side effects

    I support women in coming off hormonal birth control to minimise unwanted side effects such as rebound acne, irregular periods or no periods. Additionally she provides support for weight loss and hair growth.

    My approach is tailored to each woman. Hormonal birth control does not fix period problems, only masks them so support is customised depending on the health issues before starting hormonal birth control.

    My approach to coming off the pill consists of consecutive stages, and ideally should begin 2-3 months before HBC is stopped:

    Address health issues masked by HBC

    Individualised support, with 4 distinct strategies, depending on how periods were before HBC started:

    • PLAN A: normal periods
    • PLAN B: irregular periods
    • PLAN C: acne
    • PLAN D: heavy bleeding and/or period pain

    Nutritional support

    • Individualised recommendations for appropriate nutrition, including avoiding sugar and dairy increasing healthy fats, protein, fibre and phytonutrients.
    • Full blood tests including: liver function, thyroid metabolism, iron levels, vitamin D, vitamin B]2, folate, cholesterol, zinc levels.

    Supplement support

    Individualise supplementation of all the nutrients that HBC depletes including:

    • B vitamins: loss of B vitamins can lead to depression, which then leads women to be prescribed anti-depressant medication (if you would like support with coming off antidepressants then please mention this at your discovery call).
    • Magnesium
    • Zinc
    • Vitamin D, which declines once off HBC, and is required for ovulation
    • Support the hypothalamic pituitary ovarian axis with glandulars to revive the ovaries, restore ovary-brain communication and support fertility.

    Test hormones periodically

    • 3 months after coming off HBC, testing for oestradiol, progesterone and testosterone is recommended, to make any further adjustments to your protocol
    • Some women may need cortisol tests.

    Support you while your periods normalise and side effects reverse

    How long it takes for periods to resume and normalise depends on which HBC was taken, how long it was taken for, what it was taken for originally and your age.

    • Stopping the Pill should allow the ovaries to return to their normal size within 3 months, and AMH levels to normalise within a year. Which means that conception can be delayed for over a year.
    • It can take up to ! 8 months for cycles to return after Depo-Provera discontinuation
    • IUD can allow a quick return of fertility, but progestin-based IUDs can take longer.

    The wonderful news is that I can guide and support you with nutrition, supplements and lifestyle changes to restore ovarian function and get you back to your natural flow.