It’s an unfortunate fact that chronic illness is poorly served by the acute-care medical model. This is particularly true for thyroid dysfunction and disease where there are many subtleties, complex interconnected interactions within biological systems and shades of grey in the clinical presentation.
The thyroid is intricately involved in the complex web of our metabolism, and is extremely sensitive to even very minor imbalances in other organ systems or areas of physiology.
Low levels of thyroid hormone may lead to the decline of cellular function in all areas of the body.
Every cell in the body has a thyroid hormone receptor and we must consider thyroid dysfunction from a systems-biology approach instead of through a narrow lens.
When we are confronted with sub-optimal or blatant thyroid dysfunction in clinical practice, we must ask two questions:
- What is happening upstream that is disrupting thyroid function?
- What else is going wrong in the body as a result of poor thyroid function?
Simply identifying poor thyroid function and giving the same old nutrients, herbs or hormones to ‘support’ the thyroid gland itself is inadequate in both approach and understanding.
In many cases, it is possible to correct thyroid function without ever targeting the thyroid gland directly with therapeutic interventions, but in order to do so it’s necessary to have a solid understanding of the factors that affect and alter thyroid function and physiology all the way from the hypothalamus to the thyroid hormone receptor on the cell.
The thyroid gland is sensitive to imbalances within the entire endocrine system. Hormones including sex hormones and cortisol have major influences on thyroid enzyme activity including thyroid peroxidase and 5’-deiodinase as well as receptor site sensitivity and thyroid binding globulins.
This means that something like the ubiquitous oral contraceptive pill, providing excess levels of oestrogen activity can affect thyroid in multiple ways such as ‘fatiguing’ the pituitary and altering HPT axis signalling or increasing thyroid binding globulin and therefore decreasing thyroid hormone availability.
Many times endocrine imbalances beyond the well-understood adrenal-thyroid interactions are the culprit in thyroid imbalances. Addressing these issues and restoring hormonal balance to the HPATGG axis as a whole is a more profound and effective way of addressing thyroid metabolism dysfunction.
And this relationship is bi-directional. Hypothyroidism may result in progesterone resistance, which leads to elevated progesterone. These women can present with a complex set of symptoms specific to menstrual disorders, NOT their thyroid, even though the thyroid is actually the problem in these cases.
Mild hypothyroidism may also contribute to ovarian insufficiency, particularly if elevated prolactin or anovulation is part of the clinical picture. Increasing thyroid hormone may actually result in pregnancy in these cases.
Thyroid physiology is very vulnerable to negative influence from many commonly prescribed and widely used medications. These pharmaceuticals may increase or decrease thyroid hormone secretion, decrease absorption of hormones, decrease or increase thyroid-binding globulin production, alter T4 to T3 conversion and alter receptor site responsiveness.
The list of medications that may affect the thyroid includes anti-inflammatory agents, antibiotics, anti-depressants, diabetic and hypertensive medication, antacids, pain medications and cholesterol lowering agents. Many of these meds may disrupt thyroid function but are not identified because they don’t alter serum TSH.
It is very important to understand the thyroid in the context of the immune system, outside of autoimmune presentations.
There is a significant amount of cross-talk that happens between the thyroid and the immune system. Thyroid hormones are considered immune modulators, and
immune signaling mediators such as cytokines have been found to disrupt all aspects of the HPT axis, peripheral metabolism and receptor site transcriptional regulation.
Immune system dysregulation may be very disruptive to thyroid physiology and cellular and metabolic function as a direct result.
As well as immune cell signaling, thyroid hormones have a strong influence on tight junction regulation of the GI mucosa, with low thyroid hormone stimulation leading to intestinal permeability.
Both T4 and T3 have been shown to protect the intestinal mucosal lining from stress and ulceration.
Through an examination of the thyroid needs to include a detailed history, evaluation of drug interactions, physical exam where appropriate and serum laboratory tests.
Serum tests for the thyroid are a very effective way to assess metabolic fluctuations, however there is no set of reference ranges that is accepted by everybody and we need to observe fluctuations outside of the optimal range, not just the disease ranges set by the individual labs to truly be able to identify and understand changes in thyroid function.
Some markers, such as resin T3 Uptake are not commonly included in the standard or even functional thyroid laboratory assessments, but may provide critical insight into thyroid hormone function and therefore guide intervention.
Learning how to assess and understand in more detail seemingly minor fluctuations in thyroid laboratory results will open up a greater understanding of systemic implications and therapeutic strategy that may previously have been overlooked.
This results in more positive clinical outcomes and therefore happier clients/patients and greater job satisfaction for the clinician.