Transforming Fibroid Care

BySandra Ishkanes

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: 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 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. 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. Biomarkers 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…

Manage endometriosis successfully and be pain free

BySandra Ishkanes

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: Presentation and Diagnosis Endometriosis most often occurs on or around reproductive organs in the pelvis or abdomen, including: More rarely, it can also grow on and around the: 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 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. Endometriosis.org 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.  Misdiagnoses Many women with endometriosis who have gastrointestinal symptoms are often misdiagnosed as 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…

Adenomyosis Demystified

BySandra Ishkanes

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: 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…

Come off the pill and the avoid side effects

BySandra Ishkanes

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. The steroids in HBC are not the same as our natural hormones: 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: Medium androgen index: Low androgen index: Mirena coil Side effects of taking HBC 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: 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: Nutritional support Supplement support Individualise supplementation of all the nutrients that HBC depletes including: Test hormones periodically 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. 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.

Reverse PCOS and regain your fertility

BySandra Ishkanes

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

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