7. WOMEN'S HEALTH Flashcards

This module covers: • Sex hormones. • Endocrine disruptors. • Phytoestrogens. • Hormone balancing approach. • Premenstrual syndrome (PMS). • PCOS. • Endometriosis. • Fibrocystic breasts. • Uterine fibroids. • Menopause.

1
Q

What does the hypothalamic-pituitary-ovarian (HPO) axis do?

A

Maintains hormonal balance within the female reproductive system

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2
Q

What does GnRH stimulate to produce and release what hormones?

A

GnRH stimulates the anterior pituitary to produce and release LH and FSH

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3
Q

What do LH and FSH do?

A

support follicle development, ovulation, corpus luteum maintenance and production of progesterone, oestrogen and inhibin

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4
Q

What is pregnenolone?
And what is it a precursor of?

A
  • A hormone synthesised from cholesterol in steroidgenic tissues such as adrenal gland, gonads and the brain
  • synthesised by mitochondrial enzyme CYP11A1.
  • Anti-inflammatory and neuroprotective.
  • precursor of DHEA, testosterone, DHT, oestradiol, progesterone and cortisol
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5
Q

What are the causes low levels of pregnenolone and what are the symptoms?

A

Advanced age (>30) and statin use.

  • Poor memory
  • Declining concentration and attention
  • Fatigue
  • Dry skin, joint and muscle pain
  • Decreased libido
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6
Q

How to support pregnenolone levels

A
  • Improve sleep
  • Manage stress
  • Healthy fats: Avocado, flax and chia seeds, olive oil, walnuts, B vits, Vit K and D3.
  • DHEA balance: maca, rhodiola, magnolia, perilla oil, tribulus.
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7
Q

What is the pregnenolone steal theory?

A

High stress increases the use of pregnenolone for cortisol production, reducing amount of pregnenolone for sex hormone production

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8
Q

What affect does cortisol have on LH and FSH?

A

downregulation, reduces ovulation

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9
Q

Where is progesterone produced?

A
  • In the corpus luteum after ovulation
  • In the adrenal cortex and by the placenta during pregnancy
    (Lack of ovulation=lack of progesterone!)
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10
Q

Functions of progesterone

A
  • Maintains endometrium for implantation and pregnancy
  • Increases cervical mucus
  • Progesterone metabolites potentiate inhibitory actions of GABA by modulating receptors; helps relax smooth muscle
  • Support bone health and mammary development
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11
Q

Low progesterone leads to____ ______.
What are the causes of low progesterone?

A

Oestrogen dominance.
chronic stress, synthetic progesterones, xenoestrogens

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12
Q

Signs and symptoms of low progesterone

A

irritability, mood swings and insomnia.
Also higher risk of breast cancer in premenopausal women

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13
Q

How to balance progesterone

A

Support oestrogen detoxification, increase fibre; 3 balanced meals/day, no snacking, avoid alcohol until balanced, Mg, vit C and B6, Zn. Agnus castus, Aus bush flower essence (she oak), exercise and box breathing (where accompanied by anxiety).

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14
Q

Name the three groups of oestrogen

A

Oestrone (E1), oestrodiol (E2) and oestriol (E3)

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15
Q

How is oestrogen produced and where?

A

By conversion of androgens via aromatase (aromatisation) in ovaries, bone, breast and adipose tissue

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16
Q

How does oestrogens exert their actions?

A

Binds to specific oestrogen receptors: ERa, ERb, and GPER.
Excess oestrogen induces an overexpression of ERa and ERb.

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17
Q

Functions of oestrogen

A
  • reproductive tract development
  • menstrual cycle
  • promotes cell proliferation esp breasts
  • glucose homeostasis
  • immune robustness
  • bone and CV health
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18
Q

What is oestrogen dominance associated with?

A

Fibroids, endometriosis, PMS, fibrocystic breasts, dysmenorrhoea, infertility, miscarriages, perimenopuase, breast/ovarian/endometrial cancers, IR, thyroid dysfunction, brain fog, anxiety, depression

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19
Q

Causes

Oestrogen dominance aetiology

A
  • HRT and OCP
  • xenoestrogens
  • heavy metals
  • obesity
  • poor liver detoxification and methylation
  • constipation
  • genetic mutations (COMT SNP)
  • intestinal dysbiosis
  • chronic stress
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20
Q

How does obesity contribute to oestrogen dominance?

A

increased aromatisation of testosterone to oestrogen

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21
Q

CYP450 enzymes convert E1 into one of three metabolites. Describe 4-OH-E (CYP1B1) metabolite in phase I oestrogen ‘biotransformation’

A

a pro-carcinogenic oestrogen metabolite neautrilsed by COMT into protective 4-MeOE1 metabolites. Oveuse in this pathway=problematic

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22
Q

CYP450 enzymes convert E1 into one of three metabolites. Describe 2-OH-E (CYP1A1) metabolite in phase I oestrogen ‘biotransformation’

A

Weakest, protective form. COMT deactivates 2-OHE1 to protective 2-MeOE1 metabolite

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23
Q

CYP450 enzymes convert E1 into one of three metabolites. Describe 16a-OH-E (CYP3A4) metabolite in phase I oestrogen ‘biotransformation’

A

Highest binding affinity for oestrogen receptors with high proliferative effects.
High levels is associated with higher risk of oestrogen dependent conditions

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24
Q

2-OH-E and 4-OH-E undergo methylation via what gene to become less active?

A

COMT

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25
Q

In phase 2 oestrogen metabolism what may cause 4-OH-E and 16-OH-E levels to elevate?

A

Compromised methylation
(e.g., due to lack of key nutrients or COMT SNP)

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26
Q

Poor methylation increases the conversion of 4-OH-E to _____ which can cause oxidative damage to DNA

A

quinones

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27
Q

In Phase 2 oestrogen metabolism 16a-OH-E metabolises to _____ and undergoes ______

A

E3, sulphation

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28
Q

In phase 2 oestrogen metabolism 2-OH-E and 4-OH-E undergo methylation via COMT and also undergoes _____ and _____

A

sulphation and glucoronidation

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29
Q

Supporting phase I oestrogen metabolism

A
  • Support CYP3A4, CYP1A1, CYP1B1: I3C, cruciferous veg, antioixdants, glutathione (also neutralises reactive quinone species), turmeric, resveratrol, berries, rooibos tea and celery.
  • Support gut microbiome.
  • Avoid CYP450 inducers: paracetamol, PCBs, smoking, grapefruit
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30
Q

Support phase II oestrogen metabolism

A

Include conjugation pathway support - cruciferous veg, allium veg, Mg, antioxidants, glutathione.
Methylation support - folate, B12, B6, SAMe, choline

Avoid - OCP, high alcohol, high cortisol, mould exposure

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31
Q

What is the oestrobolome and what do they produce?

A

A collection of microbes capable of metabolising oestrogens.
They produce beta-glucuronidase.

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32
Q

What does beta-glucuronidase do?

A

It is an enzyme which deconjugates (reactivates) oestrogen that has already been conjugated for elimination. These deconjugated oestrogens can be reabsorbed via the enterohepatic circulation - increasing oestrogen load in the body.

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33
Q

Imbalance of beta-glucuronidase can promote conditions such as…

A
  • endometriosis
  • breast cancer
  • ovarian cancer
  • PCOS
  • endometrial cancer
  • endometrial hyperplasia
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34
Q

advice for high and low levels

How to maintain healthy beta-glucuronidase levels

A

Optimise the microbiome (probiotics, prebiotics)
if high, increase:

  • fibre
  • calcium D-glucarate (inhibitor)
  • glucaric acid-rich foods e.g., mung bean sprouts, apples, cruciferous veg, milk thistle, lactobacilli and bifidum bacteria
    Consider 5R protocol.

if low:
focus on commensal support e.g., probiotics

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35
Q

Testosterone:

  • Produced
  • Converted to
  • Functions
A
  • in the ovaries and adrenal cortex
  • E2 via aromatase (most testosterone) and DHT
  • ovarian density, libido, bone strength, mood, cognition
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36
Q

5a-Reductase:

  • Function
  • Upregulated by
  • Downregulated by
A
  • Function: converts testosterone into more potent form (DHT)
  • Upregulated by: Insulin, inflammation, obesity.
  • Downregulated by: Nettle, saw palmetto, lycopene, turmeric, green tea, zinc, GLA and EPA
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37
Q

Sex hormone binding globulin (SHBG):

  • Produced by
  • Function
A
  • A glycoprotein synthesised by the liver
  • Binds to oestradiol, testosterone, DHT (only unbound hormones are biologically active)
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38
Q

SHBG imbalance:

  • Lower levels
  • High levels
A
  • Lower levels = higher ciculating free/active levels of oestradiol, testosterone, DHT. Associated with hyperinsulinemia, obesity, metabolic syndrome, T2DM, hypothyroidism, PCOS.
  • High levels: Seen in anorexia, pregnancy, androgen deficiency, hyperthyroidism, liver disease
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39
Q

Prolactin:

  • controlled by
  • Functions
  • Increased by
A
  • Oestrogen and dopamine
  • Lactation, breast maturation, inhibits menstruation
  • High cortisol (stress), pituitary tumours, circadian distruption, renal failure, vit D deficiency, drugs e.g., domperidone
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40
Q

When does hyperprolactinaemia occur? What is it assossiated with?

A

Occurs naturally in pregnancy and lactation but can also occur in non-pregnant women.
Associated with: Infertility, menstrual irregularites, low libido, osteopenia, breast pain and vaginal dryness

41
Q

What are endocrine distrupting chemicals (EDC)? Where are they found?

A

Exogenous agents that interfere with the production, release, transport, metabolism, binding, action or elimination of bodily hormones.
Found in BPA, PCBs, phthalates, heavy metals, pesticides, herbicides, fire retardants, dioxins, drugs, tap water

42
Q

Adverse health effects of endocrine disruptors

A
  • Cancer
  • PCOS
  • Early puberty
  • Gynaecomastia
  • Infertility
  • Cognitive deficits
  • Obesity
43
Q

What are xenoestrogens? examples include…

A

Sub-catergory of EDC that are structurally similar to oestrogen and can bind to oestrogen receptor sites with potentially hazardous outcomes.
Examples: pesticides, herbicides, dioxins, parabens, BPAs, phthalates, preservatives, tap water (chlorine, pharmaceuticals etc)

44
Q

How does dairy affect hormones? What steroid hormones are found in milk?

A

Commercial milk is mostly derived from pregnant cows, with increased hormone concentrations in the third trimester - which add to the overall oestrogen load.
E1, E2, and E3 are found in all milk, highest in whole milk

45
Q

What other hormones do dairy products contain apart from E1, E2 & E3?

A

IGF, PCBs, dioxins, insecticides, bovine growth hormone

46
Q

What are phytoestrogens and what do they do?

A

Phytoestrogens are naturally-occuring plant compounds structurally similar to 17B-oestradiol (E2). They produce a weak anti-oestrogenic effect in the presence of high endogenous oestrogen and a weakly oestrogenic effect in the presence of low endogenous oestrogen.
They distrupt aromatase, favouring the 2-OH pathway.
Consider them ‘oestrogen modulators’.

47
Q

Health benefits of phytoestrogens

A

lowered risk of menopausal symptoms, CVD, obesity, metabolic syndrome, T2DM, breast cancer

48
Q

Where are phytoestrogens found?

A

Flavonoids: soybeans, legumes, lentils, chickpeas
Lignans: cereals, linseed, fruit, veg
Flavones: parsley, thyme, celery, chamomile tea

49
Q

What is most sex hormone imbalances driven by?

A
  • Blood glucose dysregulation
  • Chronic low-grade inflammation
  • Poor digestion, microbiome health, detoxification and elimination
  • Thyroid and adrenal dysfunction
  • High toxic load
  • Chronic stress and poor sleep
  • Nutrient deficiencies
50
Q

Hormone balancing approach

A
  • Follow CNM Naturopathic diet
  • Improve blood glucose and weight management
  • Reduce inflammation
  • Support digestion and elimination
  • Build the microbiome
  • Support thyroid hormone synthesis and metabolism
  • Support detoxificaiton and reduce toxic load
  • Managing stress levels, sleep/wake cycle
51
Q

Descibe PMS and its prevalence

A

Symptoms affecting many women a week or two before their period, symptoms may extend into the first few days of menses.
Affects up to 80% of women, peak around 30s and 40s. 50% report that symtpoms follow childbirth and worsen each pregnancy

52
Q

What is PMDD?

A

Prementrual dysphoric disorder- a severe varient affecting 1-10% of women e.g., anger, irritability during the second 1/2 of mentrual cycle

53
Q

Signs and symptoms of PMS

A

Over 150 assossicated.
Non-physical: mood swings, irritabilty, low mood, anxiety, poor concentration, feeling out of control, change in libido, food cravings, reduced cognitive and visuospatial ability, increase in accidents
Physical: Breast tenderness, bloating, headaches, backache, weight gain, acne, GIT upset

54
Q

Name PMS subtypes and their symptoms

A

-PMS-A (Anxiety): High oestrogen:progesterone= irritability, anxiety.
-PMS-C (Cravings): Blood glucose imbalance, hypoglycaemia and low Mg= increased appetite, sugar cravings.
-PMS-D (Depression): Low oestrogen:progesterone and NT imbalance e.g., low serotonin.
-PMS-H (Hyperhydration): Increased water retention secondary to high aldosterone= weight gain, breast tenderness, abdominal bloating, swelling hands and feet.

55
Q

Causes and risk factors of PMS (interactions between oestrogen, progesterone and neurotransmitters)

A
  • Deficient serotonergic functioning: Progesterone and oestrogen can modifty serotonin availability in synapses (consider low tryptophan and gut dysbiosis)
  • Progesterone metabolites bind to GABA receptors and render them resistant to activation. These are often low in PMS due to hormonal contraceptives.
56
Q

dietary and lifetyle

Causes and risk factors of PMS

A
  • Smoking
  • Obesity: BMI>30 assossiated with high risk
  • Alcohol: mood changes, anxiety and headaches
  • High intake of sugar with low protein
  • High omega 6:3 ratio increases inflammatory prostaglandins and induce aromatisation
57
Q

Naturopathic approach for PMS

A
  • CNM Naturopathic Diet with a hormone balancing approach, focus on oestrogen and progesterone balance:
  • Optomise hormone detoxification, elimination, metabolism and hydration
  • Minimise xenoestrogen exposure
  • Adress chronic stress, adrenal support
  • Restore nutritional deficiencies (B vits, Zn, Mg)
  • Balance blood glucose levels
  • Reduce inflamammation
58
Q

Approach to balancing oestrogen:progesterone for PMS

A
  • Support oestrogen detoxification/elimination (B vits, Mg, high fibre, crucifers, borccoli sprouts)
  • Increase phytoestrogens (red clover tea 2 cups/day)
  • Low saturated fat diet reduces oestrogen circulation
  • Remove endocrine disruptors, optimise weight, adress stress
  • Herbal medicine: Agnus castus
59
Q

Approach to balancing neurotransmitters for PMS

A
  • L-tryptophan or 5 HTP
  • Tyrosine, B6, B12, folate, Zn, Mg, L-theanine
  • St. Johns Wort, saffron - serotonergic effects
  • Remove alcohol and caffeine
  • Optimise sleep and exercise
60
Q

Approach to reducing fluid retention for PMS

A
  • Reduce sodium and increase potassium rich foods
  • Vit B6 to regulate aldosterone
  • Seed cycling
  • Duiretics: celery, dandelion, parsley, nettle, Nat. Sulph tissue salt
61
Q

Name the nutrients important for PMS and their mechanisms

A
  • Vit B6: cofactor for GABA, serotonin and dopamine.
    Required for corpus luteum development and supports oestrogen metabolism in the liver.
  • Magnesium: GABA and serotonin synthesis and other cell functions.
  • Calcium: Cofactor for tryptophan => serotonin conversion
  • Vit D: Important role in female reproductive health via cyclic sex hormone flucuations or neurotransmitter function
  • Zinc: Important for proper action of many sex hormones - controls prolactin
  • EFAs: Women with PMS have shown to exhibit EFA and prostaglandin abnormalities e.g., low GLA.
62
Q

What nutrient is typically low when taking the OCP and what might it cause?

A

Vitamin B6.
Low B6 can cause low dopamine which increase prolactin levels, affecting breast tissue and promotes water retention

63
Q

Suggest three herbal medicines for PMS and explain their mechanisms

A
  • Vitex agnus castus: Hyperprolactinaemia can result in irregular cycles and is linked to low progesterone levels. Binds to dopamine receptors and reduce secretion of prolactin. Reduces mood changes, irritability, headaches and breast tenderness
  • Gingko Biloba: Effective against congestive symptoms like breast pain and vascular congestion.
  • Rosemary: neutralising quinones, downregulates CYP3A4 and induces CYP1A1
  • Ashwagandha: adaptogen, nervine, thyroid support
64
Q

Herbal teas for PMS

A

Ginger, green tea, peppermint, St. John’s Worts, chamomile, passionflower

65
Q

Define PCOS

A

Polycystic ovarian syndrome is an endocrine and metabolic pathology (affecting 5-20% of women worldwide) with hallmark features of ovarian dysfunction, hyperandrogenism and polycystic ovaries.

66
Q

Hallmark features of PCOS

A

Ovarian dysfunction, hyperandrogenism, polycystic ovaries

67
Q

Signs and symptoms of PCOS

A

amenorrhoea/oligomenorrhea
weight gain
hirsutism
thinning/loss of hair
oily skin, acne
infertility
increased muscle mass (if severe)

68
Q

Complications of PCOS

A

T2DM, gestational diabetes, hypertension, dyslipidaemia, NAFLD and metabolic syndrome.
Endometrial cancer, anxiety, depression, autoimmunity e.g., hashimoto’s thyroiditis

69
Q

Pathophysiology of PCOS

A
  • Increased amplitude and pulses of LH = anovulation and increased androgens.
  • Increased LH stimulates increased ovarian theca cell production of androgens.
  • Reduced FSH relative to LH reduces aromatisation of androgens to oestrogen leading to anovulation.
  • Follicular development ceases during maturation = anovulation
70
Q

What is the link between IR/hyperinsulinaemia and PCOS?

A

IR is the most common mediator in PCOS:

  • Decreases hepatic SHBG synthesis = high active testosterone and DHT
  • Increases ovarian theca cell androgen production
  • Increases adrenal androgen secretion
  • Leads to leptin resistance, increasing obesity risk.
71
Q

What is the link between obesity and PCOS?

A
  • Consider factors such as overeating, undernourishment, lack of activity, poor sleep, dysbiosis etc
  • High IR and compensatory hyperinsulinaemia which in turn increase adipogenesis and low lipolysis
  • Sensitises thecal cells to LH and increases androgen production
  • High inflammatory adipokines increase IR and inflammation
72
Q

What lifestyle, dietary and/or physiological factors could contribute to chronic low-grade inflammation which is one of the causes for PCOS?

A
  • Western diet, metabolic endotoxaemia, obesity and lack of exercise.
  • All adds to IR and impaired ovulation
  • High levels of oxidative stress are common in PCOS and considered a risk factor. Studies show lower levels of glutathione, vit C and E in PCOS
73
Q

What bacteria have been correlated with PCOS?

A

Proteobacteria, escherichia and shigella

74
Q

How does dysbiosis influence the progression of PCOS?

A

Dysbiosis alters hormone secretions, gut-brain mediators, inflammatory pathways and islet beta-cell proliferation

75
Q

How does HPA-axis dysfunction (chronic stress) relate to PCOS?

A

Increases adrenaline and cortisol production which increases IR. Stimulates production of DHEA/DHEA-S and androstenedione which converts to testosterone in peripheral tissues.

76
Q

PCOS natural approach

A

Support blood glucose balance, insulin sensitivity and weight loss:

  • Limit snacking
  • Quality protein
  • Optimise omega6:3 ratio
  • Chromium rich foods
  • Cinnamon
  • Berberine
  • ALA
  • Magnesium
  • Omega 3
  • CoQ10
77
Q

Herbs to support PCOS

A
  • Saw palmetto
  • Liquorice
  • Spearmint tea
  • Green tea
  • Nettle tea
78
Q

What is endometriosis?

A
  • The presence of endometrial-like tissue outside the uterus
  • Locates in ovaries, fallopian tubes, rectum, pouch of douglas, lungs
  • Tissues responds to natural hormone cycle causing it to grow, break down and bleed
79
Q

Signs/symptoms and complications of endometriosis

A
  • Dysmenorrhoea, heavy menstrual bleeding and deep dyspareunia, chronic pelvic pain, period-related cyclical GI/urinary symptoms, migraines, anxiety, depression
  • Infertility, endometriomas, ovarian cancer
80
Q

Causes and risk factors for endometriosis

A
  • Prolonged oestrogen exposure (OCP, early menarche, nulliparity)
  • Obesity (increased inflammatory cytokines and aromatase activity)
  • Poor oestrogen detoxification
  • Environmental toxin exposure
  • Emotional trauma
  • Microbial infections (EBV, CMV, HSV, E.coli)
  • Dysbiosis
  • Compromised mucosal barrier (increase LPS-immune reactivity)
  • High consumption of sat / trans fats
  • Low vegetables / fibre, omega 3, selenium and vit D
81
Q

Natural approach for endometriosis

A
  • Microbiome support (5R, pro/prebiotics)
  • Liver support (B vits, Mg, glutathione etc)
  • Aromatase inhibitors (cruciferous veg, onions, garlic, chives, scallions, EVOO, olives)
  • ALA
  • Turmeric
  • Ginger
  • Resveratrol
  • Green tea
  • Optimise omega 6:3
  • Quercetin
  • Proteolytic enzymes (serrapeptase)
  • Vit D, C, Mg, Zn, E
82
Q

Herbs for endometriosis

A
  • White willow bark
  • Agnus castus
  • Echinacea
  • Calendula
  • Valerian
  • Dandelion root
83
Q

What are fibrocystic breasts?

A

A common, benign condition characterised by swollen and tender breasts.
Common amongst premenopausal women aged 20-50.

84
Q

Symptoms of fibrocystic breasts

A
  • Cyclical breast cysts; diffuse lumpiness
  • Dull/heavy breast pain (often bilateral) during luteal phase; improves most menses
  • Nipple discharge
85
Q

Causes/risk factors of fibrocystic breasts

A
  • Oestrogen dominance/low progesterone
  • Nulliparty or late menopause
  • Obesity and T2DM
  • HRT
  • Iodine deficiency
  • Methylxanthines (found in coffee, tea, cola, chocolate and some drugs)
  • Low fibre
86
Q

Natural approach to fibrocystic breats

A
  • CNM diet with hormone balancing approach
  • Evening primrose oil (1000mg 3x/day)
  • Agnus castus
  • Vitamin E and omega 3
  • Remove methylxanthines and caffeine, stop smoking
  • Seed cycling
  • Restore iodine balance
  • Castor oil packs
87
Q

What are uterine fibroids?

A

Benign tumours that originate from the myometrium and connective tissue.
Most common age 35-49y/o

88
Q

Signs and symptoms of fibroids

A
  • Heavy/prolonged menstrual bleeds
  • Pelvic discomfort/pain
  • Abdominal bloating
  • Frequent urination/constipation

*50-80% are asymptomatic

89
Q

Complications of fibroids

A
  • Iron deficiency anaemia
  • Infertility
  • Miscarriage
  • Pre-term labour
  • Obstructed labour
  • Foetal abnormalities
  • Postpartum haemorrhage
90
Q

What is the link between fibroids and oestrogen?

A
  • Fibroids are oestrogen dependent.
  • Oestrogen receptors are over expressed in fibroid tissue.
  • Oestradiol concentration increases, which increases progresterone receptor availability.
  • Progesterone completes fibroid development.
  • Excess aromatisation is also seen
  • IGF and cytokines can also promote fibroid growth
91
Q

Causes and risk factors for fibroids

A
  • Genetics: SNPs on CYP1A1, MED12
  • Hypertension: may cause smooth muscle cell injury / cytokine release
  • Poor oestrogen metabolism/clearance, EDCs, OCP, obesity
  • Chronic stress
  • Heavy metals: cadmium and lead activate oestrogen receptors
  • Diet/lifestyle: low fibre, low activity, high sat fat, refined carbs, caffeine, alcohol
  • Vit D deficiency: shown to increase fibroid cell proliferation
92
Q

Natural approach to uterine fibroids

A

CNM diet with hormone balancing approach.

Support oestrogen balance and detoxification:

  • Avoid xenoestrogens/endocrine distruptors
  • Eliminate caffeine and alcohol
  • Address stress (reduce cortisol)
  • Increase phyto-oestrogen foods/herbs (chickpeas, sage, flaxseed, red clover)
  • Green tea (epicatechins inhibit fibroid cell growth)
  • Agnus castus (prolactin inhibitor)
  • Support liver detoxification (cruciferous veg, B vits, Mg, NAC, choleretic / cholagogues)

Regulate excessive bleeding:

  • Astringent herbs - yarrow, cranesbill, shepherd/s purse.
  • Check iron / ferritin levels: deficiency = increased risk of heavy bleeding.

Reduce inflammation:

  • Omega-3, curcumin, ginger, green leafy veg, vit D, proteolytic enzymes, castor oil packs.
  • Optimise weight and address IR to reduce inflammation and aromatisation.
93
Q

What are the stages of menopause?

A
  • Early menopause (40-45yo): Cessation of ovarian function without identifiable underlying secondary cause
  • Perimenopause (45-50yo):
    Begins from onset of irregular mentrual cycles and ends 1 year after final period
  • Menopause (50-55yo):
    after 12 months of amenorrhea
  • Postmenopause (55 onwards):
    Periods cease and generally the worst of hormonal symptoms subside
  • Premature menopause (<40yo):
    Permanent bilateral oophectomy or due to ovarian insufficiency
94
Q

What are the hormonal patterns in perimenopause, menopause and postmenopause?

A
  • Peri: Ovarian follicular activty starts to fail. FSH/LH rises due to reduced negative feedback. O:P fluctuates.
  • Menopause: low oestrogen, persistently high FSH and LH
  • Post: 65% produce sufficient testosterone in adrenals to sustain libido
95
Q

What factors may leads to early menopause? Name other factors affecting menopause transition

A

Associated with early menopause:

  • Smoking
  • Long term lead exposure
  • Family history
  • Hypertension

Other factors:

  • Obesity (can exacerbate symptoms)
  • Chronic stress (associated with menstrual irregularity)
  • Gut microbiome changes (‘oestrobolome’)
96
Q

Signs and symptoms of menopause

A
  • Hot flashes/flushes
  • Weight gain and obesity
  • Sleep disturbance
  • Genitourinary symptoms: dry/sore vagina, dyspareunia
  • Mood disturbances
  • Hair loss, joint/muscle pains, headaches, itchy skin, fatigue, low libid, low self-esteem
97
Q

What is the mechanism of vasomotor symptoms (VMS) in menopause?

A

Oestrogen is a neuromodulator and changes in levels can impact temperature homeostasis

98
Q

Natural approaches to menopause

A
  • CNM diet with hormone balancing approach
  • Increase antioxidants and fibre
  • Include phytoestrogen foods daily
  • Choose more plant than animal proteins, organic where possible (reduce endrocrine distruptors)
  • Pre/probiotic foods
  • 1.5l water daily
  • Low GL, high omega 3 diet
  • Avoid caffeine, coffee, spicy foods, alcohol
99
Q

Herbs for menopause

A
  • Black cohosh: oestrogen-modulating & energetically cooling
  • Shatavari: reproductive tonic (testosterone-like effects), adaptogen. Relieves vaginal symptoms.
  • Nervines: valerian root, passionflower, chamomile
  • St. John’s Wort extract: reduces hot flashes, improves sleep, mood, relieves anxiety
  • Liquorice root: mildly oestrogenic
  • Maca: improves libido, mood and hot flushes