Hypothyroidism reflects the far-reaching biological effects of thyroid hormones in the body.
Although many individuals with hypothyroidism can be asymptomatic, such clinical features can occur in the gastrointestinal (constipation, reduced appetite, difficulty swallowing); integumentary (dry skin, hair loss, loss of outer eyebrow third, puffy face and eyes); neurological (poor attention and memory, anxiety, low mood); musculoskeletal (cramps, stiffness, weakness, fatigue); endocrine (menstrual irregularities, reduced libido, increased serum cortisol); and metabolic (increased oxidative stress, systemic inflammation) systems
How do we test and track outcomes?
Pathology: Blood tests relevant to thyroid dysfunction
Clinicians have a panel of assays available to assist in the diagnosis of suspected thyroid dysfunction and the identification of underlying causes (Table 2). Whilst comprehensive testing of all markers arguably provides a more valuable and complete picture of thyroid function and underlying causes, testing Thyroid Stimulating Hormone (TSH) is the recommended first step in the Australian medical field. TSH is the only test funded by the Medicare Benefits Scheme to screen for thyroid disease when there is no history of thyroid problems.
Thyroid Stimulating Hormone
TSH is a sensitive marker of thyroid function as it is infuenced by slight changes in T4 levels. If the initial TSH reading is elevated (> 4.0 mU/L), it is repeated after 6-8 weeks together with free T4 to confrm the diagnosis. Considerable debate exists regarding the appropriate upper limit of the TSH reference range. Reference ranges are altered by factors such as the prevalence of autoimmune diseases, age, iodine status, smoking and ethnicity. Including subjects with these risk factors in the assessment to determine reference ranges has reportedly led to a raised ‘normal’ upper limit. In individuals without these factors, a more appropriate lower upper limit is likely to be 2.5 mU/L.
Measuring antibodies assists in determining the cause of dysfunction and whether thyroid autoimmunity is present. In 95% of patients with autoimmune thyroiditis, antithyroid peroxidase (TPO) and antithyroglobulin antibodies are present. As anti-TPO is the most sensitive biochemical marker of autoimmune thyroid disease, it is usually the only thyroid antibody test recommended for monitoring treatment.
Free Thyroxin (free T4) & Free Tri-iodothyronine (free T3)
Raised TSH with low free T4 is indicative of primary hypothyroidism, typically due to autoimmune thyroid disease, though it may also be caused by previous surgeries or exposure to radioiodine. Subclinical hypothyroidism (sHT) presents as raised TSH with normal free T4 levels which in most cases, is still suggestive of autoimmune thyroid disease. This subclinical picture is more likely to progress to overt hypothyroidism in the presence of autoantibodies and higher levels of TSH.
Reverse T3 (rT3) can also be a useful test in suspected thyroid disorders. The conversion of T4 to T3 (the more biologically active thyroid hormone) is facilitated by 5-‘deiodinase, a selenium-dependent enzyme; in the absence of selenium, rT3 is produced at the cellular level. Unlike free T3, rT3 is metabolically inactive. Elevated rT3 with low T3 and TSH may indicate impaired conversion (deiodination) of T4 to T3 and subsequent hypothyroid-related symptoms in patients with severe illness or starvation (‘sick euthyroid’).
Some nutritional interventions.
Multiple micronutrients are critical in supporting healthy function of the thyroid gland, via impacts on thyroid hormone synthesis, conversion and metabolism. Many of these nutrients may also offer complementary benefts due to their role in immune function, detoxifcation and oxidative stress – processes which can impact thyroid gland activity
Iodine is essential for thyroid hormone synthesis and is well known for its role in thyroid function. In Australia, the recommended daily allowance (RDA) is 150 µg/day, increasing to 250 µg/day during pregnancy and lactation. Deficiency may lead to low T4 levels, hence adequate intake should be ensured to maintain healthy thyroid function. Iodine has been considered a ‘double-edged sword’ as excessive intake can be detrimental to thyroid function. Worldwide, increased thyroid antibodies and autoimmune hypothyroidism have been reported following mandatory iodization of salt, in iodine-replete areas and following excess iodine consumption.
Zinc is well known for its critical role in neurotransmitter synthesis, and preliminary evidence suggests that zinc may play a role in thyroid function by influencing aspects of peripheral thyroid hormone conversion.30 In addition, zinc appears to be involved in the formation and mechanism of action of thyrotropin-releasing hormone (TRH) and T3 binding to its nuclear receptor.
A deficiency of vitamin D has been linked to a number of autoimmune conditions, including autoimmune thyroid disease. Several studies have shown that low vitamin D status is correlated with the presence of both Hashimoto’s thyroiditis and Grave’s disease, as well as TPO antibodies.
Unravelling the web that contributes to underlying your thyroid challenges is best done with the support of a practitioner.