Hashimoto’s affects so many different systems of the body. One of the main reasons is that thyroid hormone affects so many different activities.
One of the most complex areas of interaction is that of the thyroid and female hormones.
Having some idea of these relationships can be helpful in understanding what is happening in your body. And may help shed light on some symptoms you are having.
Also, once you understand, then you can start working on a plan to fix them.
(But fair warning, your doctor, even your endocrinologist may not understand these interactions and may have even less of idea of what to do about them.)
In the body there are 2 different kinds of feedback loops: positive feedback and negative feedback. These can both play a major role with Hashimoto’s and hypothyroidism.
And the irony is that positive feedback can result in really negative outcomes, while negative feedback generally helps to keeps things in balance which results in positive outcomes.
Positive Feedback Isn’t So Positive
Positive feedback is the feedback of repetition and reinforcement. You get something created from a behavior, habit or health issue and it keeps reinforcing itself.
Take progesterone and Hashimoto’s, for example.
If you take progesterone AND you’ve got Hashimoto’s, taking external progesterone may stimulate your thyroid gland to become more active–increase levels of TPO–and fan the flames of that autoimmune attack on TPO.
What are the signs that progesterone is worsening the Hashimoto’s, or maybe even triggering it?
You could have more fatigue, more hair loss, more depression. You could actually make the symptoms that you thought you were treating with the progesterone worse.
Many women go into a doctor’s office, be it a acupuncturist or a medical doctor or naturopath, complaining of symptoms like depression, hair loss, low libido…and the doctor thinks that that person has a hormonal problem such as a progesterone “deficiency” or “estrogen dominance”.
And the well-meaning practitioner may prescribe creams or oral progesterone and then—the symptoms get worse.
If your symptoms get worse with progesterone that’s a good sign you probably DO NOT have a progesterone deficiency or estrogen dominance.
Instead, it may have caused a flare up of Hashimoto’s.
Adding more progesterone just added to the positive feedback loop.
This whole thing is reinforced and repeated and just builds on itself. This is how vicious cycles are born and how they continue to progress and make things worse. Adding insult to injury.
Negative Feedback Isn’t That Negative
Negative feedback is your body’s way of course correcting.
For example, with thyroid hormone, when too much thyroid hormone is produced, the body responds and signals the thyroid to stop making so much.
Neurons in the hypothalamus secrete thyroid releasing hormone (TRH), which tells cells in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
TSH binds to receptors in the thyroid gland, stimulating the making and release of thyroid hormones, which affect virtually all the cells in the body.
When blood concentrations of thyroid hormones increase above a certain threshold, TRH-secreting neurons in the hypothalamus are inhibited and stop secreting TRH.
One of the things we often see when working with Hashimoto’s people is the complex nature of feedback loops causing a web of problems.
Positive feedback or the feedback of reinforcement leads to one system breaking down and causing a domino effect in others.
The only way to alter these feedback loops is to address all the different parts simultaneously.
That way you can reverse the negative trends and create positive healing momentum.
To add another layer of complication the endocrine system has a number of negative feedback loops that help to regulate and balance other things.
For example, high levels of estrogen suppress the secretion of FSH (follicle stimulating hormone).
So there are naturally occurring positive (reinforcing) and negative (suppressing or counterbalancing) feedback loops happening all the time.
Endocrine function does not go in just one direction. The various female hormones affect thyroid metabolism and thyroid hormone affects how these hormones work in the body too.
So fasten your seat belts because it’s going to get complicated, but I’m going to make as easy as I can.
Let’s Review Some Physiology
First thing we should do before we dive in is to review what happens in a woman’s cycle hormonally. Then we can look how each hormone is impacted by Hashimoto’s and hypothyroidism.
Follicular Phase: Days 1-5: Estrogen Drops and FSH Rises
Menstrual bleeding begins on day 1 and normally lasts about 5 days. During the last few days leading up to day 1 there is a sharp fall in levels of estrogen and progesterone. This signals the uterus that pregnancy has not occurred during the cycle.
This signals starts the shedding of the endometrial lining of the uterus. Since estrogen suppresses FSH, when estrogen levels drop FSH levels rise. Follicle stimulating hormones, stimulate, yup, you guessed it the follicles.
By day 5-7 of the cycle, one of the follicles responds to FSH and becomes the dominant follicle.
When it does it starts releasing lots of estrogen.
Midcycle: Days 6-14: Estrogen Rises and FSH Falls
All good things must come to pass so the large amounts of estrogen released by the follicle during this phase has several important effects.
The endometrial lining of the uterus becomes thicker and is prepared for the fertilized egg. When this happens FSH gets suppressed (through negative feedback).
At about midcycle, this estrogen spike and FSH fall leads to the release of luteinizing hormone (LH).
This is known as an LH surge and this leads to a sudden rise in body temperature which is a sign that ovulation is about to happen.
This LH surge causes the follicle to break and send an egg into the fallopian tube.
Luteal Phase: Days 14-28 Estrogen and Progesterone First Rise, Then Fall
After the follicle frees the egg, its walls collapse and this is called the corpus luteum.
Right after ovulation, the corpus luteum begins secreting large amounts of progesterone, which also helps prepare the lining of the endometrium to accept and nurture the fertilized egg.
If the egg is fertilized, a small amount of a hormone called human chorionic gonadotropin (HCG – the hormone that is used in a popular diet treatment) is released.
HCG keeps the corpus luteum strong so it can keep pumping out estrogen and progesterone. This keeps the endometrial lining strong and intact.
By about week 6 to 8, if pregnancy has occurred then the newly formed placenta takes over and starts secreting progesterone.
Thyroid hormone affects all of this and all of this affects thyroid hormone.
Hypothyroidism Messes with All of This
When women have hypothyroidism, a common problem is an increase of another hormone called prolactin.
This causes less of a release of LH, and a loss of progesterone receptor site sensitivity, and a loss in sensitivity to FSH in the follicle.
All of these losses lead to problems with ovulation, and they also mess with the communication to the pituitary gland.
Hypothyroidism can lead to lower levels of LH. Which means you don’t get an LH surge, which means ovulation may not happen properly.
Using birth control pills on top of this can further harm the communication and feedback loops in this system.
Using herbs to stimulate the ovaries or the reproductive system may also not work unless the hypothyroid issues are corrected.
Studies have found that even mild hypothyroidism may cause ovarian problems.
Testing thyroid function is very important with women who suffer from infertility, especially if they have elevated prolactin or they can’t ovulate.
Also, hypothyroidism can cause the development of ovarian cysts.
We looked at that in detail in a previous post where we look at the connection between PCOS and Hashimoto’s.
Hypothyroidism may also lead to low FSH levels, which may lead to immature follicles and infertility.
Suppressed LH levels will often lead to problems with ovulation in timing or abnormal luteal phase progesterone levels.
These changes may cause miscarriage, depression in the second half of your cycle, or migraines in the second half of your cycle.
To summarize, hypothyroidism can cause:
* A decrease in FSH release and FSH receptor sensitivity, this leads to problems with the development of the follicle and infertility
* Suppressed LH which leads to problems with ovulation and abnormal progesterone levels, this leads to abnormal cycles and infertility
* Progesterone receptor insensitivity which also leads to abnormal cycles and infertility
* Increased Prolactin, which leads to problems with ovulation, abnormal menstrual cycles and infertility
Prolactin has a very close relationship to dopamine, thyroid hormone, progesterone and serotonin.
All of these hormones and neurotransmitters affect each other. For example, low dopamine and progesterone can suppress TSH.
Also, hypothyroidism can affect the adrenals directly. It can cause too much cortisol to be released or over time exhaust the adrenals.
And this also suppresses TSH. So what happens is you get weird mixed test results and symptoms.
Mixed Messages and Confusing Signs
The presentation looks like this: TSH is normal or even slightly low, but you have a ton of hypothyroid symptoms and your T4 is low.
It doesn’t make sense. Everyone is confused. Well, it’s this complex dance of hormones that may be causing this.
Something else that is interesting to note is that high cortisol, which can be caused by hypothyroidism can dampen the activity of the enzyme that converts T4 into T3 (5 alpha deodinase).
So what happens is high cortisol causes low T3.
Estrogen increases thyroid binding globulin levels. These are the proteins that bind to thyroid hormone and keep it from working.
We see this with normal TSH and low free thyroid hormones (free T3 and free T4). This can happen with birth control pills.
This also explains why some women with hypothyroidism and Hashimoto’s experience tachycardia, tremors and hypothermia every month before their cycle.
Progesterone up-regulates TPO (the enzyme thyroid peroxidase). This is why when women ovulate, their temperature goes up.
During ovulation, the surge of progesterone stimulates TPO.
When this happens there is a surge in thyroid hormones produced, that makes the temperature rise.
Women with low progesterone can also have less thyroid hormone than their body needs (even thought this isn’t always visible on a lab test.)
But they might have both low thyroid and low progesterone symptoms.
Symptoms of low progesterone include heavy menstrual cycle, inability to lose weight, mid-cycle luteal phase depression, headaches, etc.
It is interesting to note that problems with progesterone are often not caused by your body being unable to make enough progesterone, rather they are caused by some sort of problem with the pituitary gland.
There are a number of axises involved with the pituitary, the adrenal-pituitary, thyroid-pituitary and ovarian-pituitary connections can all affect each other and can lead to problems with this communication system.
This is always a better place to attempt treatment before adding external progesterone which can actually make Hashimoto’s symptoms worse.
Obviously, this is not something that a single pill is going to correct. Rather than look for the drug or supplement to solve the problem let’s look at how hormones behave and see how we can improve that.
The physiologic effects of hormones depend largely on their concentration in blood and extracellular fluid. Disease and health problems happen when hormone concentrations are too high or too low.
First thing to do is to test to determine whether or not you have enough hormone in your body. As we saw above with progesterone therapy, this can make matters worse if you supplement when you already have enough.
If there isn’t enough, you should consult your physician to help your body get or make more.
This can be done naturally or with supplementation and involves many different treatment options that are beyond the scope of this post.
If there is enough of a given hormone in the body how do we get them to work better?
Well we need to get enough hormone to the target tissue so that it can work. The concentration of hormones is determined by 3 things:
1. The rate of production. How do you improve the rate of production? Well, firstly make sure you have enough of the raw materials in the body to make them.
Many important reproductive hormones are made from cholesterol.
While cholesterol often gets a bad rap, when it comes to hormone production and synthesis it’s critical.
A cholesterol lower than 150 means you may not have enough of the raw materials to make estrogen, progesterone, cortisol and many other important hormones in the body.
Here are some foods high in cholesterol: eggs (especially fish eggs), liver, fish, shellfish, shrimp, bacon, sausages, red meat, and brain which has the highest amounts (all you zombies, take notice).
Then look to improve the feedback mechanisms. Positive feedback can improve this.
2. The rate of delivery. Blood flow makes a huge difference for hormone delivery. If you are anemic and/or have low blood pressure you can pretty much guarantee that you won’t be able to deliver optimal amounts of hormones to your body’s tissues.
High blood flow delivers more hormone than low blood flow. This is a very important fact that is often ignored or disregarded, yet it makes a huge difference physiologically.
3. Rate of degradation and elimination.
Hormones all break down and are reabsorbed by the body, but things like a clogged liver and enhanced negative feedback loops can affect the amount of hormones that are released.
Thyroid hormones are basically a “double” tyrosine with the critical incorporation of 3 or 4 iodine atoms.
The circulating halflife of thyroid hormones is on the order of a few days. They are inactivated primarily by intracellular deiodinases.
Systemic inflammation, out of control blood sugar and high cortisol can all affect the activity of these enzymes.
As we stated above, female hormones like estrogen and progesterone are steroid hormones derived from cholesterol.
The thing that can limit the production of these hormones is the conversion of cholesterol to pregnenolone. Chronic stress can cause something called a “pregnenolone steal” where pregnenolone is siphoned off to make cortisol and is not available for other steroid hormone production.
So reducing stress and balancing blood sugar are also critical for the production of estrogen and progesterone.
Obviously, this is not easy to fix nor is it simple to figure out and correct.
However, doing a proper workup, and working with someone who understands positive and negative feedback interactions and creating an action plan that will use your body’s natural tendencies to your advantage are all important factors in getting better results.
At Hashimoto’s Healing we off a free 30 minute Discovery Session where we’d be happy to discuss this process with you. (Fair warning these are very popular and are currently booked 3 to 4 months out)
If you would like to speak to Marc sooner please contact us here.
http://www.ncbi.nlm.nih.gov/pubmed/25750078 : L/T4 supplementation : These findings suggest that the thyroid gland and peripheral tissues are integrated in the physiological process of T3 homeostasis in humans via a feed-forward TSH motif, which coordinates peripheral and central regulatory mechanisms. Regulatory and capacity deficiencies collectively impair T3 homeostasis in L-T4-treated patients.
http://www.ncbi.nlm.nih.gov/pubmed/1585690 : Higher free T3 levels with birth control?
http://www.ncbi.nlm.nih.gov/pubmed/3107297 : Value of measuring free fractions
http://www.ncbi.nlm.nih.gov/pubmed/23184912: TSH testing not adequate
http://www.ncbi.nlm.nih.gov/pubmed/15588378 : short feedback
http://www.ncbi.nlm.nih.gov/pubmed/15481810: TRH feedback regulation
http://www.ncbi.nlm.nih.gov/pubmed/16876577: TRH Neurons
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520819/ Elevated TSH and elevated cortisol: These studies all taken together suggest a physiologic feedback loop where lower thyroid function increases cortisol, but cortisol feeds back to reduce TSH; this hypothesis is consistent with the observations that in the case of primary hypothyroidism (elevated TSH) cortisol is elevated, but in the setting of primarily elevated cortisol TSH is suppressed.
http://www.ncbi.nlm.nih.gov/pubmed/16793944 – The effects of sex-steroid administration on the pituitary thyroid axis
Ben-Rafael Z, Mastroianni L, Strauss JF, Flickinger GL, Arendasch-Durand B. Changes in thyroid function tests and sex hormone binding globulin associated with treatment of gonadotropin. Fertil Steril. 1987: 48;318-320
Malarkey WB, Strauss Rh, Leizman DJ, et al. Endocrine effects in female weight lifters who self administer testosterone and anabolic steroids. Am J Obstet Gynecology. 1991;165:1385-90
Knopp RH, Bergelin RO, Wahl PW, Walden CE, Chapman MB. Chemical alterations in pregnancy and oral contraceptive use. Obstet Gynecol 1985;5;66:682-90
The Thyroid, A Fundamental and Clinical Text, Ninth Edition, Braverman and Utiger, 2005
Functional Endocrinology, Dr. Datis Kharrazian, 2007