When TSH Goes Bananas: Iodine, TSH, and Thyroid Physiology Explained

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

If you’ve been dealing with fatigue, unexplained weight changes, or thinning hair, the thyroid is often part of the conversation. In our Adelaide clinic, one frequently overlooked factor is iodine status. However, when iodine supplementation begins, patients are often surprised to see a sharp rise in their TSH on follow-up testing.

At Elemental Health and Nutrition, we help patients interpret thyroid markers in context—so lab results support clinical decision-making rather than creating unnecessary alarm.

Quick Answer: Why can TSH rise after iodine supplementation?

Thyroid-stimulating hormone (TSH) is a pituitary-derived signalling hormone that regulates iodine uptake and thyroid hormone production. In individuals with iodine deficiency, introducing iodine may be associated with a temporary increase in TSH as the hypothalamic–pituitary–thyroid (HPT) axis adapts to restored iodine availability.

Importantly, this response does not automatically indicate hypothyroidism, particularly when Free T4 and Free T3 remain within reference ranges and symptoms such as fatigue are improving. Research shows iodine repletion can alter TSH dynamics during this adaptive phase, especially in previously deficient individuals (1–4).

Understanding the Iodine–TSH Relationship

Iodine is an essential micronutrient required for thyroid hormone synthesis:

• Thyroxine (T4) contains four iodine atoms
• Triiodothyronine (T3) contains three iodine atoms

While iodine availability directly affects hormone production, TSH is centrally regulated and may rise during periods of thyroid remodelling or altered iodine handling (1,2).

One key mechanism involves upregulation of the sodium–iodide symporter (NIS), the transport protein responsible for moving iodine into thyroid cells. Experimental and human studies indicate that increased TSH signalling can enhance NIS expression during iodine repletion, particularly following deficiency (3,4).

Clinical Observation (Non-Generalisable Data)

In our Adelaide clinical setting, we have observed that some individuals with low or low-normal Free T4 display biochemical patterns consistent with iodine insufficiency, even when baseline TSH falls within population reference ranges.

These observations are clinic-specific and not intended as population-level data. They are used to inform individualised assessment, not to infer prevalence or causation. Population studies confirm that iodine deficiency can exist despite apparently normal TSH values (5–7).

The Role of Cofactors in Iodine Utilisation

• Selenium – required for iodothyronine deiodinases that convert T4 to active T3 (8,9)
• Zinc – involved in thyroid hormone receptor binding and TSH regulation (10)
• Iron – essential for thyroid peroxidase activity (11)
• Physiological stress – elevated cortisol may be associated with reduced peripheral T4-to-T3 conversion (12,13)

Symptoms Commonly Associated With Iodine Deficiency

Iodine deficiency has been associated with impaired thyroid hormone production and metabolic slowing.

• Fatigue and cold intolerance
• Dry skin and hair thinning
• Cognitive slowing or “brain fog”
• Menstrual irregularities and reduced libido

Monitoring During Iodine Repletion

Following iodine introduction, TSH may remain elevated for several months in some individuals while thyroid signalling adapts. During this period, Free T4, Free T3, and symptom trends provide more meaningful clinical context than TSH alone (2,4,9).

Iodine supplementation is not appropriate for all individuals, particularly those with autoimmune thyroid disease, nodular thyroid conditions, or iodine sufficiency. Clinical supervision and appropriate testing are essential.

Key Insights

• TSH is a regulatory signal, not a thyroid hormone (1).
• Iodine repletion may be associated with transient TSH elevation in iodine-deficient individuals (2–4).
• Free T3 and Free T4 provide essential clinical context during thyroid adaptation (8,9).
• Cofactor sufficiency is critical for safe and effective iodine utilisation (8–11).

Take the Next Step

Thyroid markers are best interpreted in context, not isolation. If your thyroid results changed after starting iodine, a functional assessment of iodine status, thyroid hormones, and key cofactors can help distinguish adaptive changes from clinically significant dysfunction.

Book a consultation at Elemental Health and Nutrition to explore a personalised, evidence-informed approach to thyroid health in Adelaide.

References

1. Zimmermann MB. Iodine deficiency. Endocr Rev. 2009;30(4):376–408.
2. Leung AM, Braverman LE. Consequences of excess iodine. Nat Rev Endocrinol. 2014;10:136–142.
3. Wolff J, Chaikoff IL. Plasma inorganic iodide as a homeostatic regulator of thyroid function. J Biol Chem. 1948;174:555–564.
4. Eng PHK et al. Regulation of sodium-iodide symporter expression by iodide. Endocrinology. 1999;140(8):3404–3412.
5. Pearce EN et al. Iodine nutrition: thyroid disease and public health. Lancet Diabetes Endocrinol. 2013;1(2):152–162.
6. Andersson M et al. Iodine deficiency in Europe. Lancet. 2007;370:1856–1860.
7. Bath SC, Rayman MP. Iodine deficiency in the UK. Lancet. 2013;382:1154–1155.
8. Arthur JR, Beckett GJ. Thyroid function and selenium. Proc Nutr Soc. 1999;58:345–352.
9. Köhrle J. Selenium and thyroid hormone metabolism. Thyroid. 2005;15(8):841–853.
10. Baltaci AK et al. Zinc and thyroid function. Biol Trace Elem Res. 2017;179:1–9.
11. Beard JL et al. Iron deficiency and thyroid metabolism. Am J Clin Nutr. 1990;52:813–819.
12. Fekete C, Lechan RM. Central regulation of thyroid hormone levels. Endocr Rev. 2014;35(2):159–194.
13. McEwen BS. Stress and adaptation. Physiol Rev. 2007;87:873–904.
14. Zimmermann MB, Köhrle J. Iron, selenium and iodine interactions. Thyroid. 2002;12(10):867–878.
15. Laurberg P et al. Iodine intake and thyroid disorders. Best Pract Res Clin Endocrinol Metab. 2010;24:13–27.