Helpful table about hormonal balance symptoms

"Symptoms of Estrogen Deficiency

Physical

·  Hot flashes

·  Fatigue

·  Headaches/migraines

·  Night sweats

·  Vaginal and/or bladder infections

·  Incontinence

·  UTI’s

·  Forgetfulness

·  Difficulty falling asleep

·  Poor concentration

·  Forgetfulness

·  Decreased verbal skills

·  Irregular bleeding

·  Testosterone imbalance

·  Lower libido

·  Painful intercourse

·  Osteoporosis

·  Episodes of rapid heartbeat

Emotional

·  Depression

·  Minor anxiety

·  Emotional instability

·  Feelings of despair

·  Crying easily

Properties of Estrogens

·  Creates endometrium

·  Development at puberty

·  Regulates menstrual cycle

·  Plumps vaginal tissue and reduces vaginal dryness

·  Slows bone loss

·  Can help reduce incidence of heart attacks

·  Anti-aging factor

·  Increases sensitivity of progesterone receptors

·  Affects more than 300 tissue systems of the body

·  Uplifts mood

·  Lowers LDL

·  Increases HDL

·  Decreases lipoprotein(a) and homocysteine

·  Affects every neurotransmitter in the brain; including seratonin, dopamine, GABA

·  Adds moisture to skin

·  Affects brain function responsible for memory and motivation

·  Needed for verbal memory and to learn new concepts, reasoning, and fine motor skills

Symptoms Associated with Estrogen Dominance

·  Breast cyst/breast pain

·  PMS

·  Irregular bleeding

·  Fluid retention

·  Headaches

·  Breast adenomas

·  Gall bladder problems

·  Blood sugar problems

·  Nutrient deficiencies

·  Nervous/Irritability

·  Low libido

·  Fibroids

·  Hormonal cancers

·  Heavy menstruation

·  Bloating

·  Weight gain

·  Nausea

·  Endometriosis

·  Thyroid problems

·  Mood swings

·  Sleep disturbances

·  Sugar cravings

Symptoms of Excess Androgens

Physical

·  Acne/oily skin

·  Facial hair

·  Deepened voice

·  Ovarian Cyst

·  Hypoglycemia

·  Mid-cycle pain

·  Low HDL

·  Thinning scalp hair

·  Breast cancer risk

·  Painful nipples

Emotional

·  Agitated

·  Angry

·  Irritable

Symptoms of Androgen Deficiency

Physical

·  Loss of libido

·  Impaired sexual function

·  Aches/pain/arthritis

·  Incontinence

·  Thinning skin

·  Thin tissue of the vulva and labia

·  Loss of muscle tone

·  Wrinkled skin

·  Lichen slcerosis

·  Hot flashes

Emotional

·  Depression

·  Lack of drive and confidence

·  Demotivation

Properties of Androgens

·  Cardiovascular protection

·  Help with brain function

·  Build bones

·  Enhances libido

·  Build Muscle

·  Anti-aging to skin

·  Antidepressant

Symptoms Associated with Progesterone Deficiency

Physical

·  Fibrocystic breasts or breast pain

·  Anxiety

·  Fluid Retention

·  Stressed Easily

·  Weight gain

·  Irritability

·  Break-though-bleeding

·  PMS

·  Low Body Temperature

·  Hair Loss

·  Headaches/migraines

·  Endometriosis

·  Sleep Disturbances

·  Heavy Periods

·  Cramps

·  Fibroids

·  Hypothyroidism

·  Bone Loss

·  Irregular cycle/spotting between cycles

·  Infertility

Emotional

·  Anxiety

·  Over Reacting

·  Easily alarmed

·  Stressed

·  Feelings of confusion

·  Mood swings

·  Irritability

·  Nervous

·  Jittery

·  Depression

Roles and Properties of Progesterone

·  Decreases menstrual bleeding

·  Decreases fat storage

·  Anti-cancer; especially protective of the breast

·  Increases body supply of oxygen

·  Helps prevent hardening of the arteries

·  Improves brain structure and function, memory

·  Increases metabolic rate

·  Helps regulate water retention

·  Required for conception and gestation

·  Increases intelligence of fetus

·  Mild sedative in large doses

·  Protects against miscarriage

·  Prevents PMS

·  Stimulates new bone formation

·  Anti-aging to skin

·  Inhibits Fibrocystic Breast Disease

·  Natural antidepressant

·  Facilitates thyroid hormone action

·  Normalizes blood sugar levels

·  Reduces spotting

·  Tones blood vessels

·  Reduces irritability and anxiety

·  Reduces testosterone imbalance

·  Prevents endometrial cancer

·  Anti-aging hormone

·  Useful in some cases of seizure disorder

·  Helps prevent high blood pressure

·  Reduces risk of autoimmune diseases

·  Increases (Ig-E) to help prevent sinus, respiratory, vaginal infections and allergic reactions

·  Increases sensitivity of estrogen receptors

·  Natural diuretic

·  Raises HDL, lowers triglycerides

·  Restores sex drive

·  Functions as a precursor to corticosteriods and other steroidal hormones

·  Blocks estrogen’s side effects and excessive estrogen

·  Increases endurance during exercise

·  Calms and protects nervous system

·  Protective effect on brain chemistry

·  Reduces cravings for sweets/carbs

·  Thymus gland depends on progesterone

·  Most protective hormone the body produces

·  Improve efficiency of the heart

·  Basic hormone of adaptation and resistance to stress

·  Restores normal sleep patterns

·  Enhances number of insulin receptors on cells

·  Used by adrenals to produce anti-stress hormones"

from http://www.jacemedical.com/articles/Hormonal%20Health%20and%20Balance%20Information.pdf

Endometriosis Is Associated with Rare Copy Number Variants

"At least one of the 21 risk-associated CNVR is present in 6.9% of the endometriosis cases as opposed to 1.8% of the controls which suggests that CNVs are likely be important markers of endometriosis. This study demonstrates that CNVs are likely to play an important role in endometriosis." http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0103968

Estrogen produced by endometriotic lesions

We have seen before the importance of the role of estrogen receptor alpha in activating endometriosis lesions (see: http://endocomprehensive.blogspot.com/2013/11/estrogen-receptors-importance-in.html). Here we look at estrogen being produced by the lesions themselves:

"Conclusion: Endometriotic lesions have higher production of 17 -estradiol than the eutopic endometrium of patients and controls. This is mostly the result of impaired metabolism....


“It has long been viewed that estrogens are delivered to the ectopic (i.e. outside the uterine cavity) lesions in an endocrine fashion through the circulation, however, there are strong indications that the endometriotic lesions may be a source of estrogens itself. The biosynthesis and bioavailability of estrogens depends on the balance between the production of active estrogens and their inactivation. This balance is determined by the activity of a large variety of enzymes involved in the conversion of androgens to estrogens, oxidative metabolism, the conjugation of estrogens and the conversion of conjugated estrogens into non-conjugated steroid hormones. Most of these processes are present in the human endometrium and some of them appear to be aberrantly regulated in the ectopic endometrium of patients.

“Aromatase is responsible for the conversion of androstenedione to estrone and of testosterone to 17_-estradiol. Although some reports indicated that this enzyme is present in normal endometrium with highest expression during the proliferative phase endometrium (4), other studies showed no aromatase expression in the endometrium of healthy women (5–7). Nobel and co-workers (5) were the first to demonstrate that aromatase mRNA and activity levels are increased in pelvic endometriotic implants, and this has been confirmed by others (8 –10)…. The findings in this study demonstrate the capacity of the endometriotic tissues to produce higher levels of 17-estradiol than the eutopic endometrium. Our findings also indicate that this is more likely the result of a reduction in 17-estradiol inactivation, rather than an increase in 17-estradiol synthesis. We were not able to detect aromatase activity in the tissue. Aromatase activity is in general low in the endometrium and endometriotic tissue (11) and our system is not sensitive enough to detect such low levels. Purohit (11) found activities in the range of 0.1 to 1000 fmol/20 h/g wet weight, whereas the detection limit of our system is around 5 pmol estrone/mg protein/ 24 h. Also Kyama and co-workers (32) recently found low expression of the aromatase at the mRNA level in the endometrium. However, they also found high aromatase mRNA expression in the peritoneum. This suggests a possible explanation to those cases in which the use of aromatase inhibitors efficiently treated endometriosis or its symptoms (12, 13) and poses also the question whether the peritoneum itself, rather than the endometrium implanted at ectopic locations may be the major site of androgens into estrogens conversion….

“In conclusion, we have shown convincingly for the first time that the endometriotic lesions are capable of creating a hyperestrogenic environment. This is corroborated by the enhanced expression levels of TFF1 mRNA in the endometriotic tissues, and is a result of increased reduction of estrone into 17_-estradiol and decreased oxidation of 17_-estradiol into estrone, rather than changes in the activities of aromatase or STS.”  http://www.obgyn.ubc.ca/Education/REI/docs/17beta_000.pdf

(Note for the next study you read below: Aromatase is an enzyme that helps convert testosterone to estrogen, namely estradiol. "Aromatase is located in estrogen-producing cells in the adrenal glands, ovaries, placenta, testicles, adipose (fat) tissue, and brain." http://www.medterms.com/script/main/art.asp?articlekey=15844)

"The mechanism by which endometriosis is able to produce its own estrogen is via the expression of the enzyme aromatase. This enzyme, not expressed in normal endometrium, is stimulated by prostaglandin E2 (PGE2); the resulting estrogen production then stimulates PGE2, further enhancing estrogen." from Modern Management of Endometriosis; edited by Christopher Sutton, G. David Adamson, Kevin D. Jones; CRC Press, Nov 29, 2005

"Aromatase activity is absent in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis, which gives rise to strikingly high levels of aromatase activity in this tissue. Both aromatase expression and activity are stimulated by PGE₂. This results in local production of estrogen, which induces PGE₂ formation and establishes a positive feedback cycle. Another abnormality in endometriosis, that is, deficient 17β-HSD type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE₂ in endometriosis." http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2002.tb02767.x/abstract

(You can see why doctors would then come to the conclusion that prescribing aromatase inhibitors would help. And for some they may. But these drugs have powerful effects on the whole body, some of which can be quite deleterious and permanent. Remember, estrogen has many helpful attributes that helps the function and protection of your bones, brain, heart, and other organs as well as reproductive organs. And it only works as long as one takes the drug. This is why experts today feel that removing the endometriotic lesions in their entirety is the best long term method of treatment. Rather than using a drug that affects your whole system, removing the actual source of the problem is preferred)
 I think that above, in addition to saying that endo produces its own estrogen, is saying that there is an impaired metabolism of estrogen at the endo sites. This puts it well I think:

"Furthermore, two forms of estrogen are altered in women with endometriosis, which is significant because estrogen causes endometriosis tissues to grow.  Estrone is a weak form of estrogen, and estradiol is a much more potent form of estrogen.  Estrone is converted to estradiol and vice versa by two enzymes that work with the help of progesterone.   In a normal endometrium, progesterone is able to increase the conversion of estradiol (strong)  to estrone (weak), thereby keeping the growth effects of estrogen on tissues under control.  In endometriosis, the enzyme which converts estradiol to the weaker form estrone is not at all found in the endometrial tissue.  This causes levels of the stronger estradiol to accumulate.   The enzyme which converts weaker estrone to stronger estradiol, however,  is fully functional. This  results in even higher amounts of more powerful forms of estrogen at the level of the endometrial lesions, causing more and more growth of this tissue outside of the uterus." http://www.whitelotusclinic.ca/endometriosis/
"For decades, scientists assumed that the ovary alone produced steroid hormones during pregnancy. In a new study in mice, however, researchers demonstrate that once an embryo attaches to the uterine wall, the uterus itself actually synthesizes the estrogen needed to sustain the pregnancy....The findings may also be helpful to the study of endometriosis, said molecular and integrative physiology professor Milan Bagchi, an author on the study. This disorder involves the growth of endometrial tissue, which is normally shed during menstruation, at sites outside the uterus, such as the peritoneal cavity and ovaries, producing painful lesions. Endometriosis is spurred, in part, by unusually high levels of estrogen secreted from endometrial tissue growing at these extrauterine sites, he said. Except during pregnancy, "a normal cycling uterus does not make estrogen," he said. High estrogen levels block the activity of progesterone and can cause the non-cancerous growth of tissue seen in endometriosis." http://www.sciencedaily.com/releases/2009/07/090720190724.htm

Also take a look back on progesterone resistance in endometriosis: http://endocomprehensive.blogspot.com/2014/05/progesterone-resistence-2.html

The enzyme aromatase catalyzes the conversion of androstenedione and testosterone to estrone and estradiol. The gene that encodes this enzyme is expressed in several human tissues and cells such as ovarian granulosa cells, placental syncytiotrophoblast, adipose tissue and skin fibroblasts, and the brain.

On the other hand, in postmenopausal women, estrogen formation takes place in extraglandular tissues such as the adipose tissue and skin^[16-18] (Fig. 1). In contrast to cAMP regulation of aromatase expression in the ovary, this is controlled primarily by cytokines [interleukin (IL)-6, IL-11, tumor necrosis factor alpha (TNFα)] and glucocorticoids via the alternative use of promoter I.4 in adipose tissue and skin fibroblasts.^[15] The major substrate for aromatase in adipose tissue and skin is androstenedione of adrenal origin. In postmenopausal women, ~2% of circulating androstenedione is converted to estrone, which is further converted to estradiol in these peripheral tissues. This may give rise to significant serum levels of estradiol capable of causing endometrial hyperplasia or even carcinoma.

Among estrogen-responsive pelvic disorders, aromatase expression was studied in greatest detail in endometriosis.^[6,7,22,23] First, extremely high levels of aromatase mRNA were found in extraovarian endometriotic implants and endometriomas. Second, endometriosis-derived stromal cells in culture incubated with a cAMP analog displayed extraordinarily high levels of aromatase activity comparable to that in placental syncytiotrophoblast.^[22] These exciting findings led us to test a battery of growth factors, cytokines, and other substances that might induce aromatase activity via a cAMP-dependent pathway in endometriosis. Prostaglandin E₂ (PGE₂) was found to be the most potent known inducer of aromatase activity in endometriotic stromal cells.... In fact, this PGE₂ effect was found to be mediated via the cAMP-inducing EP₂ receptor subtype (our unpublished observations). Moreover, estrogen was reported to increase PGE₂ formation by stimulating cyclooxygenase type 2 (COX-2) enzyme in endometrial stromal cells in culture.^[24] Thus, a positive feedback loop for continuous local production of estrogen and prostaglandins (PGs) is established, favoring the proliferative and inflammatory characteristics of endometriosis (Fig. 2). Additionally, aromatase mRNA was also detected in the eutopic endometrial samples of women with moderate to severe endometriosis (but not in those of disease-free women) albeit in much smaller quantities compared with endometriotic implants.^[6] This may be suggestive of a genetic defect in women with endometriosis, which is manifested by this subtle finding in the eutopic endometrium." http://www.medscape.com/viewarticle/473018_3

^^^^A vicious cycle of estrogen stimulating endo, endo with aromatase capabilities, and prostaglandins being produced in this process and then turning around and causing aromatase activity continues. Thus the endo grows and inflammation flourishes.

Immune system and endo

The reaction of the body to endometriosis causes a heightened presence of immune system modulators. In other words, the endo causes your immune system to rev up into overdrive which may cause other issues with the immune system to rev up too (so any auto immune diseases will become exaggerated by the endo revving up the immune system). Endo itself is not thought to be autoimmune as studies have demonstrated it's more of your body's reaction to the activation of endo lesions rather than a deficiency of the immune system to prevent endo. "Peritoneal fluid (PF) in women with endometriosis is marked by increased inflammation, including increased volume of PF, increased concentration of white blood cells and macrophages, and increased activation status of these macrophages (reviewed by D'Hooghe and Hill [12]). These activated peripheral mononuclear cells as well as endometriotic cells in situ are hypothesised to secrete various cytokines with pleiotropic biological activities. Cytokines are low molecular weight proteins or glycoproteins typically synthesised by peritoneal macrophages, lymphocytes, ectopic endometrial implants or mesothelial cells of the peritoneum [13,14]. Usually, inflammatory cytokines and growth factors are secreted and culminate in recruitment of numerous cell types to the peritoneal cavity [15]. Aberrant expression of several cytokines by activated macrophages, such as interleukin (IL)-1, IL-6, IL-8 and TNF-α in peritoneal fluid of women with endometriosis compared to controls [16] may contribute to a peritoneal microenvironment, which favours the implantation of endometrial cells and the establishment of endometriosis [17]. Indeed, as reviewed in the next section, cytokines like IL-8 and TNF-alpha are known to promote endometrial cell proliferation, endometrial adhesion and angiogenesis. Not only peritoneal macrophages, but also endometriotic lesions and mesothelial cells of peritoneal origin may secrete cytokines such as Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-1 (IL-1) in women with endometriosis. These cytokines in turn modulate the stimulation of other cytokines and chemokines such as Interleukin-8 (IL-8) and RANTES (Regulated upon activation, normal T-cell expressed and secreted). RANTES is a potent attractant and activator of macrophages, T-lymphocytes and eosinophils [18,19], while IL-8 promotes angiogenesis [20]. In one study [21],    a positive correlation was found between the rAFS stages of endometriosis and the concentration of TNF-α in PF. The concentration of TNF-α in PF was significantly higher in patients with stage III/IV disease (168 pg/ml) than in women with stage 1/II disease (60.2 pg/ml) or control patients (3.3 pg/ml) [21]. TNF-α and IL-8 concentrations in peritoneal fluid have also been reported to correlate with the size and number of active lesions [22]. The increased concentration of TNF-α reflects enhanced secretory activity of the peritoneal macrophages and not just the mere increase in the number of peritoneal macrophages [20].   Does endometriosis lead to inflammation caused by an inappropriate and exaggerated immune response to ectopic endometrial debris? Or is endometriosis caused by peritoneal inflammation? Obviously, these cause-effect relationships cannot be studied in women for ethical reasons. In baboons, current evidence suggests that peritoneal inflammation is a consequence, not a cause of endometriosis." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC305339/?report=reader   

Estrogen and the thyroid

"Estrogen has a well-known indirect effect on thyroid economy, increasing the thyroxine binding globulin [4], and the need for thyroid hormone in hypothyroid women [5]." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3113168/?report=reader

Interesting- the thyroid has estrogen receptors:

(Note: ER = estrogen receptor)
"Classically, the presence of ER is fundamental for a direct action of estrogen in a given cell. ER has been described in both neoplastic and nonneoplastic human thyroid tissues ....An important role of different patterns of distribution and expression of subtypes ERs in thyroid carcinoma has been proposed: estrogen binding to ERα would promote cell proliferation and growth, and, in contrast, ERβ would promote apoptotic actions and other suppressive functions in thyroid tumors, as reviewed by Chen et al. [40]. Then, ERα:ERβ ratio could have a role in the pathophysiology of thyroid cancer [40], similar to that postulated for breast cancer [41].... Several studies described proliferation of thyroid cells induced by E2... These results, together with the increase in cell growth caused by estrogen, could implicate this hormone in the pathogenesis of goiter and thyroid carcinoma; nevertheless, as just one study evaluated the effect of estrogen on thyroid differentiated proteins in human thyroid tissue, more studies should be done to better understand the role of estrogen in thyroid differentiated protein expression.... There are evidences that estrogen may have direct actions in human thyroid cells by ER-dependent mechanisms or not, modulating proliferation, and function. Different patterns of distribution, expression, and ratios of ERα and ERβ may have a role in thyroid cancer cells proliferation, as well as in the outcome of thyroid cancer. Studying estrogen effects on thyroid cells is a potential tool to better understand the pathogenesis of thyroid diseases, and to develop targets to its treatment. Further studies on the influence of E2 on the growth and function of the thyroid are needed, preferably in primary culture of normal and abnormal human thyroid cells." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3113168/

"Because of its hepatic first-pass effect, oral estrogen therapy, the most commonly used modality of ET/HT, raises the circulating levels of thyroxine-binding globulin (TBG), thereby increasing the bound fraction and decreasing the free (bioactive) fraction of circulating thyroxine (T(4)). As a consequence, oral ET/HT may increase the T(4) dosage requirements of women being treated for primary hypothyroidism as well as alter the pituitary-thyroid axis in euthyroid women." http://www.ncbi.nlm.nih.gov/m/pubmed/15142374/

"But other factors not commonly considered when people think of “stress” place just as much of a burden on the adrenal glands. These include blood sugar swings, gut dysfunction, food intolerances (especially gluten), chronic infections, environmental toxins, autoimmune problems and inflammation. All of these conditions sound the alarm bells and cause the adrenals to pump out more stress hormones. In this context, stress is broadly defined as anything that disturbs the body’s natural balance...

"Cortisol is one of the hormones released by the adrenals during the stress response. Prolonged cortisol elevations, caused by chronic stress, decrease the liver’s ability to clear excess estrogens from the blood. Excess estrogen increases levels of thyroid binding globulin (TBG), the proteins that thyroid hormone is attached to as it’s transported through the body.

When thyroid hormone is bound to TBG, it is inactive. It must be cleaved from TBG to become “free-fraction” before it can activate cellular receptors. (These free-fraction thyroid hormones are represented on lab tests as “free T4 [FT4]” and “free T3 [FT3]“.)

When TBG levels are high, the percentage of free thyroid hormones drops. This shows up on labs as low T3 uptake and low free T4/T3.

Aside from adrenal stress, the most common causes of elevated TBG secondary to excess estrogen are birth control pills and estrogen replacement (i.e. Premarin)."  http://chriskresser.com/5-ways-that-stress-causes-hypothyroid-symptoms

Birth control pills and thyroid:

"In women with hypothyroidism treated with thyroxine, estrogen therapy may increase the need for thyroxine." http://www.ncbi.nlm.nih.gov/pubmed/11396440

"Certain medicines can affect the way thyroid medicines work. People taking the following medicines need to see their doctor often to make sure they are getting the correct dose of thyroid hormone medicine. Some of these medicines include:

• Calcium. Take calcium supplements at least 4 hours before or after taking thyroid hormone medicine.
• Iron supplements.
• Birth control pills or other hormones...."   http://www.webmd.com/women/thyroid-hormone-medications-for-hypothyroidism

"Common laboratory tests used in the assessment and diagnosis of thyroid disorders include measuring the circulating thyroid hormone concentrations, evaluating the integrity of the pituitary negative-feedback system, measuring thyroid antibody concentrations, and evaluating radioactive iodine uptake and scans. Tests to measure circulating thyroid hormone concentrations can include total thyroxine (T₄), total triiodothyronine (T₃), free thyroxine index, free T₄ (FT₄), and free T₃ (FT₃).

Total T₄ and total T₃ measurements are less accurate because several medications can interfere (for example, estrogen and estrogen-containing birth control pills..."  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1070767/?report=reader 

"Anyone who has taken birth control pills, or estrogen, needs to keep in mind that one additional effect of that maneuver is to increase thyroid-binding proteins in the blood. This means that almost any thyroid blood test result is quite suspect, because the regular tests will show plenty of thyroid hormone in the bloodstream, but you may still not have sufficient thyroid hormone in the tissues. In other words, estrogens will make thyroid blood tests even more unreliable than they already are. What this means is that you can be told you don't have a thyroid problem when you really do.

"In addition, if you are taking thyroid medicine, you could be told that you're taking plenty, when in the reality of your tissue levels (not measured on blood tests) you need more. This is not a minor subtlety. It is of critical importance to you. A lack of proper thyroid hormone levels has been implicated in everything from bad PMS to irregular cycles, low libido, infertility, miscarriage, endometriosis, polycystic ovary, uterine fibroids, dysfunctional bleeding, severe menopause, and osteoporosis. With a long list of possible gynecological problems such as this, you are well advised to optimize your thyroid function as much as possible.

"So once again we return to a recurrent theme in our office & coaching practice: if there has been any thyroid, diabetes, migraine, colitis, rheumatoid or other autoimmune problems in your family, then you are likely to have some degree of thyroid involvement yourself. This is especially true approaching and during menopause years. The Journal of Epidemiology in 2001 had a compelling article revealing that as many as 26% of menopausal women were hypothyroid, making their menopause years worse.

"Therefore, you owe it to yourself to do extra diagnostic maneuvers for revealing low thyroid, such as obtaining thyroid antibody testing in addition the routine T3, T4, and TSH. In addition, make sure the T4 determination is the Free T4, and your T3 testing is for both Free T3 and Total T3. Consider asking for a clinical trial of thyroid medicine if you are in the low normal area on these results.
Perhaps even more important is for the person who is already diagnosed and being treated for low thyroid to make sure that your treatment protocol is optimal." http://thyroid.about.com/od/drsrichkarileeshames/a/femalehormones.htm

(Note: gonadotropins are used in infertility treatments)
"Increasing levels of E2 in gonadotropin-treated women stimulated hepatic synthesis of SHBG and TBG, and consequently increases in T4 concentration. Nevertheless, unchanged FTI and TSH suggested that a euthyroid state was maintained. The temporal patterns for the rise in serum concentrations of TBG and SHBG during gonadotropin therapy suggest that the synthesis of these proteins by the liver has different sensitivities to E2." http://www.ncbi.nlm.nih.gov/pubmed/3111894