How Deiodinase Enzymes Control Thyroid Hormone Levels at a Cellular Level

[Remy]

I wrote this essay to help myself understand why I wasn't having any luck optimizing my thyroid hormones using standard thyroid tests. Hope it helps you too! Read the full piece here: https://9gurus.com/how-deiodinase-e...0i8v0UfqQStXOd09i8KN_VhS2e2eHAzFGZgDCJaM_qYyg

Metabolism is largely dependent on adequate levels of thyroid hormone to create the energy needed by the body to carry out vital functions. Insufficient amounts of thyroid hormone can have broad, non-specific but wide-ranging effects. Such common symptoms of fatigue, brain fog, and weight gain are often associated with hypothyroidism, a condition where not enough thyroid hormone is produced to meet the metabolic needs of the body.

Upon suspicion of low thyroid function, a conventional endocrinologist will typically order a laboratory blood test to measure the amount of thyroid stimulating hormone, or TSH, that is present. TSH is a pituitary hormone that signals the thyroid gland to produce additional thyroid hormone. This is part of a signaling cascade that starts with the production of thyroid releasing hormone (TRH) in the hypothalamus, which then stimulates TSH and ultimately the thyroid gland itself.

Hypothalamus (TRH) -> Pituitary (TSH) -> Thyroid gland (T4 +T3) ->Cell

If the TSH number is “normal” by the typical laboratory range, most conventional doctors will stop investigations at this point. This leaves many people frustrated and confused, still suffering with clear symptoms of hypothyroidism, but without a diagnosis or treatment. That is because most conventional doctors only consider one type of hypothyroidism — as a result of insufficient secretion of thyroid hormone from the thyroid gland itself. If the TSH is normal, the reasoning goes, thyroid hormone production must be sufficient, otherwise, the TSH level would rise. Yet this TSH feedback loop is only one of many ways that thyroid problems can occur, and it is not even the most common source of thyroid problems, especially in those with chronic illness.

Functional medicine practitioners go a step further and will often diagnose hypothyroidism after testing the TSH, but also testing the free thyroid hormone levels, free T4and free T3directly in the blood. When these are found to be low or low-normal in the typical laboratory range, subclinical hypothyroidism may be diagnosed, and thyroid hormone prescribed. This (controversial) method typically improves on that used by the conventional endocrinologist, but still leaves many thyroid patients feeling less than optimal and wondering why.

The answer to that question depends on another aspect of thyroid physiology often overlooked during a clinical thyroid assessment. Blood levels of thyroid hormone are used as a proxy for thyroid function, but these are an indirect measure which may not (and often does not) truly reflect what is happening inside the cell when and where the thyroid hormone binds to the nuclear thyroid receptor and exerts its effects.

Thyroid hormones are not just controlled by the pituitary gland sending TSH to the thyroid gland, but are activated or inactivated locally, at the cell, by a group of enzymes called deiodinases. This local control by deiodinases allows the cell to adjust the amount of thyroid hormone based on the needs of the cell at any given time. The function of deiodinase enzymes varies for every individual based on genetic and environmental factors, which leads to the large variation in treatment response seen clinically to thyroid hormone medication.

 

[cujet]

Hello, I've had Hashimoto's for 25 years. From the instant my thyroid problems started, my problems started. I associate Hashimoto's with a poor quality of life, hypoglycemia, reactive hypoglycemia, weight problems and lack of energy.

Do you have any thoughts as to whether the increased D1, D2 or D3 activity can be controlled or/or if it's necessary?

 

[Remy]

Hello, I've had Hashimoto's for 25 years. From the instant my thyroid problems started, my problems started. I associate Hashimoto's with a poor quality of life, hypoglycemia, reactive hypoglycemia, weight problems and lack of energy.

Do you have any thoughts as to whether the increased D1, D2 or D3 activity can be controlled or/or if it's necessary?

I think that D3 activity can likely be reduced by doing the "normal" things we do to reduce inflammation and balance the immune system when/if infections are present.

But the activity of these deiodinases is based on the body's interpretation of what is best for the system as a whole, given the current circumstances. So I'm not sure there is any real intervention to target them specifically beyond what we do to support health in terms of diet and lifestyle choices. I don't think it makes a lot of sense to try to turn off a protective mechanism, without addressing the original reason, if that makes sense?

Speaking of diet, you might look at Izabella Wentz's books on Hashi's. The first one, which is sadly only available in paperback, is really a wealth of strategies. But the things she discusses can really move the needle for people. Avoiding gluten and taking selenium are two strategies people find particularly helpful.

Good luck!

 

[cujet]

Thanks for the reply. I'm a former athlete, 56, male and exhausted. I've been ultra careful with diet for most of the time. I've followed Wentz's quite excellent book and unfortunately, the guidelines within don't address my current crop of problems (exercise intolerance, crushing fatigue, 6 unwanted naps per day) . Much of what's contained within her book mirror what I've been doing for the last 25 years, through trial and error. I wish I had it years ago.

I'm well into the CFS symptoms now and my life is winding down. Selling my airplane today as I'm too tired, too often to fly anymore. I can't do my job either (aircraft mechanic) . What should take me 1 day takes me 3. I'm the boss, so that's good, but it consumes all my time to finish a task, as I have to keep sitting down. Time to stop.