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Thyroid11 February 2025 · 9 min read

Hashimoto’s: the autoimmune story behind your thyroid

Most hypothyroid patients get a prescription and a follow-up in six months. When Hashimoto’s is the cause, that is not enough.

Dr. Zaid Khan, founder and clinical lead at Rhiverse

Dr. Zaid Khan

Physician · Diabetologist · Metabolic Medicine

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Hypothyroidism is a description, not a diagnosis. It says the thyroid is underactive. It does not say why.

In India, as in most iodine-sufficient countries, the commonest reason is Hashimoto's thyroiditis — an autoimmune condition in which the immune system gradually attacks thyroid tissue. Distinguishing the two matters, because they need different care.

How Hashimoto's progresses

It is slow, and it is usually silent at the start.

The immune system produces antibodies against thyroid peroxidase (TPO) and thyroglobulin. Over years, inflammation damages the gland's capacity to produce hormone. The pituitary compensates by raising TSH, pushing the struggling thyroid to work harder.

For a long stretch, TSH is elevated while T4 remains normal — subclinical hypothyroidism. Many patients feel unwell during this phase and are told their thyroid is fine, because T4 is within range.

Eventually T4 falls and overt hypothyroidism appears: fatigue, cold intolerance, weight gain, dry skin, hair thinning, constipation, low mood, brain fog.

Some patients also experience transient thyrotoxic phases early on, as damaged follicles release stored hormone. This can be mistaken for Graves' disease.

What the tests should include

A TSH alone is not sufficient to characterise thyroid disease. A useful panel includes:

  • TSH — sensitive, but a lagging and sometimes misleading indicator
  • Free T4 — the circulating prohormone
  • Free T3 — the active hormone; conversion from T4 is where a subset of patients struggle
  • TPO antibodies — the marker that confirms autoimmunity
  • Thyroglobulin antibodies — adds sensitivity where TPO is negative
  • Thyroid ultrasound — where nodules or a heterogeneous gland are suspected

Positive antibodies with a normal TSH still mean something. It means the process has started, and it warrants monitoring rather than dismissal.

Why the treatment differs

Standard hypothyroid treatment is levothyroxine, and for many patients that is genuinely sufficient. Antibodies do not change the need for replacement.

What they change is everything around it.

The dose will move. In an autoimmune gland, remaining function declines over time. A dose that was right two years ago frequently is not right now. This needs periodic review, not a repeat prescription.

Other autoimmunity clusters. Hashimoto's travels with coeliac disease, Type 1 diabetes, pernicious anaemia and vitiligo more often than chance. Screening is reasonable, particularly for coeliac disease where symptoms overlap heavily.

Nutrient status affects function. Selenium, zinc, iron and vitamin D all participate in thyroid hormone production and conversion. Deficiency is common and correctable, and iron deficiency in particular is frequently missed in menstruating women with fatigue.

Conversion can be the problem. A minority of patients normalise TSH and T4 on levothyroxine but remain symptomatic with low free T3. Chronic stress, inflammation, low calorie intake and selenium deficiency all impair the conversion of T4 to T3. This is worth investigating rather than dismissing.

Metabolic health interacts. Insulin resistance and hypothyroidism worsen one another. Treating the thyroid while ignoring the metabolic picture leaves results on the table.

On dietary claims

Two things get overstated online.

Gluten elimination helps patients with coeliac disease or genuine sensitivity, and there is a plausible mechanism for the overlap. It is not established that everyone with Hashimoto's benefits, and unnecessary restriction has its own costs. Test first.

Iodine supplementation, meanwhile, can actively worsen autoimmune thyroid disease. High-dose iodine is not a general remedy here, and it should not be taken without a specific indication.

What good care looks like

Confirm whether it is autoimmune. Test the full panel, not TSH alone. Replace hormone properly and review the dose as the gland changes. Correct the nutrients that support conversion. Screen for the conditions that cluster with it. Treat the metabolic context around the gland.

Most patients feel considerably better than "in range but still tired" — but only if someone is looking past the single number.

Thyroid antibodies, full panels and metabolic assessment are part of our standard thyroid workup.

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Dr. Zaid Khan, founder and clinical lead at Rhiverse

Written by

Dr. Zaid Khan

MBBS · MD (Internal Medicine) · Metabolic Medicine Fellowship · CGM Certified · RSSDI Active Member

Trained in metabolic medicine across India and Singapore, with fifteen years treating obesity, diabetes, PCOS and thyroid disease at the root. Founded Rhiverse in Pune in 2020.

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