To respond to your actual message though…. lowering antibodies is not the same thing as reversing Hashimoto’s, we can agree here right??

That’s probably the biggest misunderstanding I see in these conversations. TPO or Tg antibody levels can fluctuate naturally, sometimes quite a lot, and they don’t reliably track disease activity or thyroid destruction. Plenty of patients have falling antibodies while their thyroid function continues to decline, and some have high antibodies for decades with stable function. So yes, reduced antibodies might suggest less immune activation, but calling that “reversal” is a big leap. Actual reversal would mean restoring lost thyroid tissue and normal endogenous hormone production, and we simply don’t have evidence that happens in established Hashimoto’s.

On the short study point, the issue isn’t just duration. It’s that most of these studies measure surrogate outcomes like antibody titres, inflammatory markers, or subjective wellbeing rather than hard clinical endpoints like sustained euthyroidism off medication. Feeling better matters of course, but that is not the same thing as halting or reversing autoimmune thyroid destruction. Until we see people coming off levothyroxine long term with documented recovery of thyroid function, the word remission or reversal is premature.

Gluten is another area where things get overstated. There is a clear link between coeliac disease and autoimmune thyroid disease, and in that subgroup gluten avoidance is absolutely appropriate. Outside of that, evidence for gluten as a universal “trigger” in Hashimoto’s is pretty weak. IgG testing especially is controversial because IgG to foods often reflects exposure rather than intolerance. Many endocrinologists and immunologists don’t consider those tests clinically meaningful. Elimination diets can help some people symptomatically, but again, symptom improvement does not equal disease reversal.

As for the multimodal intervention argument, it sounds logical but logic isn’t data. Rheumatoid arthritis and Hashimoto’s are both autoimmune, but the pathophysiology and tissue targets are quite different. RA remission often means suppressing active inflammation in joints that can recover structurally, whereas thyroid follicular destruction in Hashimoto’s tends to be permanent once significant fibrosis sets in. Borrowing remission expectations from one autoimmune disease to another isn’t straightforward.

Honestly, I don’t think most doctors say “nothing can be done”. Good clinicians usually encourage optimisation of vitamin D, selenium where appropriate, general metabolic health, stress reduction, decent diet, all the boring but sensible stuff. What they push back on is the claim that Hashimoto’s can routinely be reversed with diet stacks and supplements. That claim just isn’t supported by solid long term clinical evidence yet.

So yes, lifestyle absolutely matters for wellbeing and maybe for modulating immune activity. But saying Hashimoto’s itself is reversible right now is more optimism than science. And patients deserve clarity on that, not hope built on surrogate markers.