Hypothyroidism - the basics In the next foray into the …
Hypothyroidism - the basics
In the next foray into the exploration of the thyroid, we have to talk about some of the most common disorders that we investigate when it comes to thyroid function and their causes. This is going to be a two-part series – the first being on hypothyroidism and the second on hyperthyroidism.
Hypothyroidism – or slow/underactive thyroid – is typically the diagnosis that’s given when there are lab results that indicate that the thyroid is not producing enough hormone for it to be effective.
When we commonly consider evaluating for hypothyroidism, we’re often seeing symptoms of S-L-O-W
- metabolism (fatigue)
- digestion (constipation)
- heart rate, mood (depression)
- brain function (brain fog, memory)
- movement (with joint or muscle pain)
- menstrual cycles (heavy bleeding that doesn’t stop, irregular, or infertility)
- warming (sensitive to cold)
- taste or smell
- hair growth (thinning, or in the wrong places)
- sleep (insomnia or hypersomnia)
- fluid drainage (swelling, edema)
In typical (non-functional medicine) labs, this is often diagnosed by seeing an elevated TSH (thyroid stimulating hormone), which is a hormone produced by the pituitary gland. When TSH becomes elevated (functional optimal is around 1.0 mIU/L – which is different than lab range), it is assumed that the pituitary is having to work hard to tell the thyroid gland to produce thyroid hormone. Lab ranges for TSH vary wildly – somewhere from .4-4 mIU/L. Remember that this is based purely on statistics and not representative of optimal function and that there is no universal standard of lab ranges – that they can be determined by each specific lab/organization.
Another way that typical (non-functional medicine) labs often determine hypothyroidism is through measuring T4 (usually free T4). You’ll recall from our previous blog that T4 is the highest produced thyroid hormone. It is produced by the thyroid gland itself. The assumption with low T4 is that if T4 is low, then T3 cannot be produced, and the level of thyroid mediated function in the cells will also be low.
In a functional medicine situation, T3 (again, typically free T3) is also measured (see previous blog), and since cellular receptors are for T3, it’s the most accurate measurement of adequate thyroid hormone function. When T3 is low, the cell is not able to metabolize properly, and energy is typically stored – usually as fat – rather than used. Always be mindful that T3 isn’t produced (converted) ONLY in the thyroid gland. In fact, only (depending on which research you read) roughly 7% of T3 is produced in the gland itself. All the rest is produced elsewhere.
Your functional labs will test all 3 of those (and possibly some others – which is for another discussion), to determine whether you are functionally and/or statistically deficient in thyroid function.
Primary or Secondary?
Now, when it comes to the causes of hypothyroidism, we generally consider primary (to do with the thyroid gland/production of thyroid hormones itself) and secondary, or central (dealing with the hypothalamus and pituitary).
Primary:
In primary hypothyroidism, not enough thyroid hormone is produced. Pretty basic. This can be caused by a number of different reasons.
Gland Destruction:
Destruction of the thyroid gland is a factor. Removal, physical injury, radiation, or deficient structure in some way is one aspect. You can’t make thyroid hormone if the structure isn’t there to make it.
Building Blocks:
Then, there’s not enough building blocks for thyroid hormone. In most cases, iodine deficiency is usually considered the problem here. Since T3 stands for tri-iodothyronine, and T4 stands for tetra-iodothyronine (and also known as thyroxine), one can guess that iodine is required and they’d be correct. T4 has 4 iodine molecules and T3 has 3. If there’s a deficiency of iodine in the diet OR a deficiency of iodine absorbed from the gut, it’s possible that there will be reduced production of thyroid hormone (T3 and T4).
Autoimmunity:
Then, there’s autoimmunity. Hashimoto’s thyroiditis is the most common cause of thyroid hormone deficiency and is an autoimmune disorder: i.e. the immune system attacks the body. Either, or both of anti-thyroid peroxidase (anti-TPO) OR anti-thyroglobulin (anti-TG) antibodies can be diagnostic for Hashimoto’s. Since studies seem to indicate that anti-TPO antibodies are present in approximately 90% of cases, many practitioners will only test anti-TPO. Anti-TG is present in about 50-80% of Hashimoto’s cases. And while some practitioners do not test for it, one can have positive anti-TG and negative anti-TPO – and vice-versa. It’s always better to test both. They also indicate different things – as will be explained below.
Thyroglobulin is a protein that is produced by the thyroid gland. Thyroid peroxidase is an enzyme that’s produced in the thyroid gland. It’s responsible for adding iodine molecules to the tyrosine that exists within the thyroglobulin. Remember that we need to add 4 iodine to the thyroglobulin to make it T4. We’re glossing over some heavy science here. The way I generally explain it is that anti-TG antibodies are to the gland (or protein components produced directly within the thyroid gland), and anti-TPO antibodies are antibodies produced to an enzyme in the gland that helps to make thyroid hormones – and in this case, help to produce T4. Antibodies to either will lead to destruction of those chemicals (enzyme or protein) by the immune system, and prevent the adequate formation of thyroid hormones.
Secondary:
Secondary hypothyroidism is caused by damage to the structures that produce or cause the production of TSH (thyroid stimulating hormone). The pituitary gland produces TSH. The hypothalamus produces thyrotropin releasing hormone (TRH). TRH stimulates the pituitary to produce TSH. Any damage/alteration to either of these structures would be considered secondary or “central” hypothyroidism.
A bit of this and a bit of that
Liver:
There are other factors that can contribute to hypothyroidism. And honestly, in conjunction with autoimmunity, this is what is seen clinically most of the time. This is where T4 is not converted to T3. Remember from the last blog that this occurs in the thyroid gland (to produce a small amount of T3), and in other tissues – with the liver being the largest peripheral converter. Any damage to the liver can decrease the conversion from T4 to T3 outside the thyroid gland. This is commonly seen in diabetes, fatty liver disease, and alcoholism.
Gut:
Going back to iodine deficiency and the gut, any malabsorption issue with the gut can also contribute to hypothyroidism. Autoimmune disorders like Celiac disease, Ulcerative Colitis, and Crohn’s, as well as intake of any substance (food or medicine) that causes poor absorption of nutrients can contribute to the development of hypothyroidism. All of these are factors that need to be considered when evaluating for hypothyroidism.
“Subclinical Hypothyroidism?”
Occasionally, the topic of subclinical hypothyroidism gets bantered about. This is often diagnosed when only TSH and T4 are measured and those are “normal” levels, or TSH is slightly elevated, but T4 is “normal”, and the person has symptoms of hypothyroidism. Occasionally, this is in the face of Hashimoto’s – and there are antibodies. But most of the time, this diagnosis is given when T3 isn’t measured (which would clearly indicate that there is OVERT hypothyroidism rather than “subclinical”). On very rare occasion, T3 is converted to rT3 (reverse T3 – a bound form of T3), and that causes a deficiency of free T3 for the cells. Somewhat lastly, is that thyroid hormones will come back at the low end of lab range (vs optimal range) and the individual actually does have hypothyroidism (for their body/functionally). Range for optimal thyroid function is far more narrow than lab range. With this in mind, I have never actually seen a case of legitimate, unexplained “subclinical” hypothyroid. Every case, when tested properly, was diagnosable as actual hypothyroidism.
Lots more to talk about on this topic. See you soon.
Light reading:
https://pmc.ncbi.nlm.nih.gov/articles/instance/371802/pdf/jcinvest00669-0075.pdf
https://pmc.ncbi.nlm.nih.gov/articles/PMC301591/
https://pmc.ncbi.nlm.nih.gov/articles/PMC333152/
https://pmc.ncbi.nlm.nih.gov/articles/PMC7167425/
https://pmc.ncbi.nlm.nih.gov/articles/PMC10579902/
https://pmc.ncbi.nlm.nih.gov/articles/PMC10768172/
https://www.ncbi.nlm.nih.gov/books/NBK544274/
https://www.ncbi.nlm.nih.gov/books/NBK500006/
https://www.ncbi.nlm.nih.gov/books/NBK459262/
https://www.ncbi.nlm.nih.gov/books/NBK285545/
Dr Andrea