Do you feel fatigued and stressed? If you’re exhausted and can’t seem to catch-up on sleep, you could be suffering from adrenal fatigue. Adrenal fatigue occurs when the adrenal glands are overworked. The adrenal glands produce many hormones including cortisol, the stress hormones. Too much stress leaves you stuck in fight or flight mode which wreaks havoc, inflammation and eventually disease in the body!
Hypothyroidism is when the thyroid gland is not as active as it should be. This means it is not producing enough of the necessary hormones to tell your body what it needs to do. The immune system can then attack the thyroid and the resulting inflammation causes less of the necessary hormones to be produced.
Stress has a major impact on the body. Here are 5 ways stress can cause Hypothyroid Systems.
1) Adrenal stress disrupts the HPA axis
By now many people have heard of the hypothalamic-pituitary-adrenal (HPA) axis. It’s a complex network of interactions between the hypothalamus, the pituitary and the adrenal glands that regulates things such as temperature, digestion, immune system, mood, sexuality and energy usage – in addition to controlling the body’s reaction to stress and trauma.
Countless studies show that chronic adrenal stress depresses hypothalamic and pituitary function. And since these two organs direct thyroid hormone production, anything that disrupts the HPA axis will also suppress thyroid function.
Studies have shown that the inflammatory cytokines IL-1 beta, IL-6 and TNF-alpha, which are released during the stress response, down-regulate the HPA axis and reduce levels of thyroid stimulating hormone (TSH). Another study showed that one single injection of tumor necrosis factor alpha (TNF-alpha), an inflammatory peptide, reduced serum TSH, T3, free T4, free T3 and hypothalamic TRH for 5 days. TNF-alpha was also found to decrease the conversion of T4 to T3, reduce thyroid hormone uptake, and decrease the sensitivity of the thyroid to TSH.
2) Adrenal stress reduces conversion of T4 to T3
We discussed under-conversion of T4 to T3 in a prior article. Remember that although 93% of the hormone produced by the thyroid gland is T4, it is inactive in that form and must be converted into T3 before it can be used by the cells. The inflammatory cytokines I listed above not only disrupt the HPA axis, they also interfere with the conversion of T4 to T3.
The enzyme 5′-deiodinase catalyzes the conversion of T4 into T3 in peripheral tissues such as the liver and the gut. Both Th1 and Th2 inflammatory cytokines – IL-6, TNF-alpha, IFN-gamma and IL-1 beta – have been shown to suppress the conversion of T4 to T3. In patients without thyroid illness, as levels of IL-6 (a marker for inflammation) rise, levels of serum T3 fall. And injections of inflammatory cytokines into healthy human subjects resulted in a rapid reduction of serum T3 and TSH levels, and an increase in the inactive reverse T3 (rT3) form, while T4 and free T4 levels were only minimally changed.
3) Adrenal stress promotes autoimmunity by weakening immune barriers
The GI tract, lungs and the blood-brain barrier are the primary immune barriers in the body. They prevent foreign substances from entering the bloodstream and the brain. Adrenal stress weakens these barriers, weakens the immune system in general, and promotes poor immune system regulation.
As we discussed in my previous article on the gut-thyroid connection, when these immune barriers are breached large proteins and other antigens are able to pass into the bloodstream or brain where they don’t belong. If this happens repeatedly, the immune system gets thrown out of whack and we become more prone to autoimmune diseases – such as Hashimoto’s.
In order for thyroid hormone circulating in blood to have a physiological effect, it must first activate receptors on cells. Inflammatory cytokines have been shown to suppress thyroid receptor site sensitivity.
If you’re familiar with insulin resistance, where the cells gradually lose their sensitivity to insulin, this is a similar pattern. It’s as if the thyroid hormone is knocking on the cell’s door, but the cells don’t answer.
While there’s no practical way to measure receptor site sensitivity in a clinical setting, the research above suggests it is decreased in autoimmune and other inflammatory conditions. A perfect example of this in practice is the Hashimoto’s patient who is taking replacement hormones but still suffers from hypothyroid symptoms – often in spite of repeated changes in the dose and type of medication. In these patients, inflammation is depressing thyroid receptor site sensitivity and producing hypothyroid symptoms, even though lab markers like TSH, T4 and T3 may be normal.
5) Adrenal stress causes hormonal imbalances
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.
Dr. Della treats all types of conditions but has a special interest in digestive problems, chronic fatigue, and thyroid dysfunction. Call 503.344.6631 for a free neural therapy consultation or click to contact Dr. Della Parker today!