Is Your Thyroid Holding You Back? Understanding Hidden Causes of Thyroid Symptoms

Author: Rohan Smith | Functional Medicine Practitioner | Adelaide, SA

Quick Answer

Ongoing fatigue, brain fog, weight changes, or low mood can occur even when standard thyroid tests appear “normal.” This is because thyroid function depends not only on thyroid-stimulating hormone (TSH), but also on hormone conversion, nutrient availability, stress physiology, and hormone-binding dynamics. A broader assessment may help explain persistent symptoms when basic testing is inconclusive (1–3).

The Core Concept: Why “Normal” Thyroid Tests Can Miss Dysfunction

The thyroid is a regulatory gland that influences metabolic rate, energy production, temperature regulation, and neurological function. While TSH is commonly used as a screening tool, it reflects pituitary signalling rather than thyroid hormone activity at the tissue level (2,4). For an overview of thyroid physiology and common patterns of dysfunction, see our thyroid health resource.

For thyroid hormones to exert their effects, they must be produced, converted, transported, and utilised efficiently. Disruption at any of these stages may contribute to symptoms, even when TSH remains within laboratory reference ranges (3,5).

Deeper Drivers of Thyroid Dysfunction

Iodine Status and Thyroid Hormone Production

Iodine is required for the synthesis of thyroxine (T4) and triiodothyronine (T3). Inadequate iodine intake may impair hormone production, while excessive intake may worsen thyroid dysfunction in susceptible individuals (6,7).

Impaired Conversion of T4 to Active T3

Most active T3 is produced outside the thyroid through enzymatic conversion in the liver, gut, and peripheral tissues. Factors such as nutrient deficiencies, inflammation, liver impairment, and gastrointestinal dysfunction may reduce conversion efficiency (8–10). The role of the gut in hormone metabolism is explored further in our gut microbiome overview.

Key Nutrient Deficiencies

Several micronutrients play essential roles in thyroid hormone synthesis and metabolism:

• Selenium supports deiodinase enzymes and helps protect thyroid tissue from oxidative stress (11).
• Zinc contributes to thyroid hormone production and receptor activity (12).
• Iron is required for thyroid peroxidase activity and hormone synthesis (13).

Stress Physiology and Reverse T3

Chronic physiological stress may alter thyroid hormone metabolism, increasing conversion of T4 into reverse T3 (rT3). Reverse T3 is an inactive metabolite that can competitively inhibit T3 action at the receptor level (14–16). This overlap between stress physiology and fatigue patterns is discussed further in our chronic fatigue resource.

Oestrogen and Thyroid Hormone Availability

Elevated oestrogen levels may increase thyroid-binding globulin (TBG), reducing the proportion of free, biologically active thyroid hormones available to tissues (17,18). Hormone interactions and their systemic effects are also addressed in our mental health and hormones overview.

Assessment: When to Look Beyond TSH

A more comprehensive thyroid evaluation may be considered when symptoms persist despite normal screening results. Depending on the clinical picture, this may include:

• Free T3 and free T4
• Reverse T3
• Thyroid antibodies (TPO and Tg)
• Relevant nutrient markers (iron studies, selenium, zinc)

Management Considerations (Clinician-Guided)

Addressing thyroid dysfunction typically requires an individualised approach. Nutrient repletion, stress regulation, gut and liver support, and hormone balance strategies are best guided by clinical assessment and laboratory findings rather than applied universally (6,11,14).

Key Insights

• Thyroid-related symptoms can occur despite “normal” screening results.
• Hormone conversion, nutrient status, stress physiology, and binding proteins all influence thyroid activity.
• A broader assessment may help clarify unexplained or persistent symptoms.

Next Steps

If thyroid-related symptoms persist despite standard testing, a broader functional assessment may help identify contributing factors and guide a more targeted management strategy. Learn more about our clinical approach at Elemental Health and Nutrition.

References

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3. Escobar-Morreale HF et al. Thyroid hormone replacement therapy: limitations of TSH. J Clin Endocrinol Metab. 2005.
4. Spencer CA et al. Clinical utility of TSH measurement. Thyroid. 2007.
5. Bianco AC et al. Thyroid hormone metabolism and action. Endocr Rev. 2019.
6. Zimmermann MB. Iodine deficiency and thyroid disorders. Endocr Rev. 2009.
7. Leung AM et al. Iodine intake and autoimmune thyroid disease. Thyroid. 2012.
8. Peeters RP et al. Thyroid hormone metabolism. Endocr Rev. 2003.
9. Virili C et al. Gut microbiota and thyroid hormone metabolism. Thyroid. 2018.
10. Chiovato L et al. Peripheral thyroid hormone metabolism. Best Pract Res Clin Endocrinol Metab. 2019.
11. Ventura M et al. Selenium and thyroid disease. Eur Thyroid J. 2017.
12. Bonofiglio D et al. Zinc and thyroid function. Biol Trace Elem Res. 2013.
13. Beard JL et al. Iron deficiency and thyroid metabolism. Am J Clin Nutr. 1990.
14. Fliers E et al. Stress, illness, and thyroid hormone metabolism. Endocr Rev. 2014.
15. De Groot LJ. Non-thyroidal illness syndrome. Endotext. 2015.
16. Peeters RP. Reverse T3 and thyroid hormone economy. Best Pract Res Clin Endocrinol Metab. 2017.
17. Arafah BM. Estrogen effects on thyroid hormone binding. Ann Intern Med. 2001.
18. Glinoer D. Thyroid regulation in women. Thyroid. 2001.