That’s the number of Hashimoto’s thyroiditis diagnoses in the US alone.
If you suffer from hypothyroidism, you’re at a big risk of developing Hashimoto’s thyroiditis too.
It’s a big problem that just keeps getting bigger.
Yet, here’s the biggest problem…
…most doctors don’t have a clue as to how to treat it properly.
And that’s really bad news for you and your thyroid.
(Hashimoto’s thyroiditis s an autoimmune form of hypothyroidism that involves the production of autoimmune thyroid antibodies.)
In this post, I’m going to explain how Hashimoto’s thyroiditis develops and one way we help our clients to get their life and health back on track.
Remember, this isn’t only about the research.
We work with a lot of Hashimoto’s clients and we do see consistent improvements in thyroid antibody numbers.
Some of our clients have even had their antibody tests come back in the clear, which is always amazing to see.
But remember, in order to understand how to overcome this disease, we need to understand how it develops and what exactly it is doing to your body.
As you’ll see, Hashimoto’s is not what a lot of people think it is…
How Hashimoto’s Thyroiditis Is Diagnosed (and Misdiagnosed)
Let’s start with the diagnosis.
That’s the first place where many doctors get it totally wrong.
The problem here is that doctors and the medical system simply just test for so-called ‘anti-thyroid antibodies’, and if they find the presence of these antibodies over a certain level, they diagnose the patient with Hashimoto’s.
The two antibodies of concern are:
- Thyroid Peroxidase Antibody (TPOAb).
- Thyroglobulin Antibodies (TgAb)
But true Hashimoto’s is when these anti-thyroid antibodies are actually infiltrating the gland and causing destruction or damage to the thyroid tissue.
Where doctors can go wrong is that the presence of these antibodies in the blood is not necessarily an indication of the thyroid gland actually being harmed or damaged.
Though certain antibodies have names associated with the thyroid, they have many functions unrelated to the thyroid.
In some cases, people have high levels of antithyroid antibodies in conjunction with other autoimmune diseases, for example: arthritis, Sjögren’s syndrome, or other autoimmune cases where we see elevated levels of antithyroid antibodies, yet we see no damage to the thyroid gland.
Thyroid hormone autoantibodies in primary Sjögren syndrome and rheumatoid arthritis are more prevalent than in autoimmune thyroid disease, becoming progressively more frequent in these diseases.
“We conclude that prevalence of THAb in the 2 non-thyroid autoimmune diseases is greater than in the 2 thyroid autoimmune diseases. In addition, prevalence of THAb is increasing over time regardless of disease.”
So, just seeing the presence of the anti-thyroid antibodies isn’t enough to confirm a diagnosis.
The only way to determine that is to do a fine needle biopsy of the actual thyroid tissue to look for physical signs that the thyroid tissue itself is being infiltrated or damaged.
Now, let’s take a closer look at how Hashimoto’s thyroiditis develops.
Here’s an overview, but we’ll get into the details below…
Hashimoto’s Thyroiditis, Hypothyroidism, and Estrogen Dominance
It all starts with hypothyroidism.
In fact, Hashimoto’s thyroiditis stems directly from hypothyroidism, which is why we address the two conditions very similarly.
If you’re a frequent reader here at Forefront Health, then this is going to sound a little familiar.
It’s something that we see all the time with clients, and something we’ve talked about in lots of other articles.
I’m talking about estrogen dominance.
People who are hypothyroid both overproduce estrogen and cannot detoxify it, causing it to accumulate in their body.
Needless to say, both of these problems tend to cause estrogen to build up to dangerous levels.
Unfortunately, this isn’t caught through blood testing because estrogen tends to accumulate in the tissue, not in the blood.
This is important to point out, because many times, when people are tested for estrogen, the blood tests are normal or even low, when tissue levels can be up to 50 times higher.
Regardless of the mechanism, you end up with long term exposure to high levels of estrogen.
And prolonged exposure to excess estrogen is shown to significantly increase the production of Hashimoto’s thyroiditis TPO antibodies.
2-Methoxyestradiol, an endogenous estrogen metabolite, induces thyroid cell apoptosis.
“Prolonged exposure to 2-ME led to apoptosis and to increased release of the autoantigen thyroid peroxidase (TPO).”
And get this…
There’s also empirical evidence that further implicates estrogen’s role in Hashimoto’s thyroiditis.
Considering that women produce far more estrogen than men, one would expect that women would experience a higher incidence of Hashimoto’s thyroiditis.
Not only is the incidence of Hashimoto’s thyroiditis in women higher than men, it’s 20 times higher.
And what’s more, women are more likely to be diagnosed during times of their lives when estrogen dominance is most severe.
Now, don’t get me wrong.
Men produce estrogen and men can greatly overproduce estrogen through aromatization as well.
So this can definitely happen to men, but Hashimoto’s is an issue that affects women to a much greater degree.
For all intents and purposes, this points to estrogen as being a big part of the problem.
(Note: Want to learn more about how to correct estrogen dominance? See this article: “3-Step Plan Can Lower Hidden Hashimoto’s Hormone by More than 55% In 10 Weeks”.)
So, how does this all happen?
Hashimoto’s and Your Thymus: The Autoimmune Connection
We’ve already established that estrogen dominance plays a central role in the development of Hashimoto’s thyroiditis.
And it stems from estrogen’s effects on your thymus gland.
The thymus gland sits right behind your breastbone and it plays the important role of regulating your immune system.
You see, estrogen (and cortisol, which is also overproduced in hypothyroidism) causes involution, or degeneration, of the thymus gland.
Not only does estrogen damage your thymus gland, it also increases the production of autoimmune antibodies.
As Dr. Raymond Peat points out…
“While this is happening [degeneration of the thymus gland], the B cells, which normally are under the control of the thymus cells, are not killed by estrogen, and actually seem to be stimulated by estrogen to produce certain types of antibodies, but they are more likely to produce autoimmune antibodies.”
So, for people who are having issues with Hashimoto’s thyroiditis or other autoimmune conditions, and want to help regulate their immune system… restoring the thymus gland is essential.
Interestingly, progesterone (and thyroid hormone), which opposes estrogen very strongly, has been shown to reverse damage to the thymus gland.
But, that’s not all estrogen does to your thyroid…
Hashimoto’s Thyroiditis and Your Thyroid Gland: Goiters and Nodules
Estrogen disrupts your entire Thyroid Hormone Pathway in many ways…
…but with respect to Hashimoto’s thyroiditis, estrogen directly affects the thyroid gland in a very dangerous way.
Estrogen is known to increase Thyroid Stimulating Hormone (TSH), while also inhibiting the proteolytic enzymes that are needed for the gland to release thyroid hormone into your bloodstream.
In other words, estrogen stimulates your thyroid gland to produce more thyroid hormone… yet, at the same time, it also inhibits your thyroid gland from releasing that thyroid hormone.
This causes a buildup of thyroid hormone (colloid) within your thyroid gland.
And this is a big reason today why Hashimoto’s sufferers develop goiters or soft nodules on their thyroid gland.
(NOTE: We’ll be covering this in more detail in an upcoming post.)
It’s important to point out that if you do have a goiter or enlarged thyroid nodules, then it’s often best to begin with supplementing thyroid hormone, rather than progesterone to help lower your TSH first.
Other Factors for Hashimoto’s Thyroiditis
While prolonged exposure to estrogen is a primary factor in the development of Hashimoto’s thyroiditis, it’s not the only one.
Other known factors include:
- Physical injury to the thyroid tissue
- Radiation to the thyroid gland (i.e. X-rays)
- Bacterial endotoxin (SIBO)
- Vitamin D deficiency
(NOTE: Want to see how Vitamin D can lower your Hashimoto’s antibodies? Take a look at this article on “How Hashimoto’s Patients Lowered TPO Antibodies by 46.7% with Vitamin D and Calcium”)
So there you have it.
That’s the basis for how Hashimoto’s develops.
It’s development follows a path from:
- Hypothyroidism to the…
- Overproduction of estrogen, which causes the…
- Degeneration of the thymus gland, and increases the production of…
- Autoimmune antibodies by estrogen’s effects on B-Cells and often the…
- Development of goiter and nodules.
And unfortunately, the development of one autoimmune disease, including Hashimoto’s thyroiditis, puts you at a much greater risk for developing other autoimmune diseases such as:
- Multiple Sclerosis
- Sjögren’s syndrome
Most people with Hashimoto’s thyroiditis are not addressing the estrogen concern.
They’re not addressing the thymus gland.
Ultimately, what this boils down to is, if you have Hashimoto’s, you have to address the underlying cause.
In other words, you must address the estrogen issue.
There’s no other way around it.