@westinchilds's reverse T3 claims don't match the science

What did @westinchilds actually say?

The claim is that reverse T3 is an "anti-thyroid metabolite" your body overproduces under stress, and that it's the hidden reason levothyroxine fails so many patients. The three signs he lists, weight gain that won't budge, fatigue that sleep doesn't fix, and chronically cold extremities, supposedly point to elevated reverse T3. His fix is T3 and T2 therapy, not more levothyroxine, which he says makes things worse. He closes with the assertion that fixing this puts you "ahead of 95% of other thyroid patients." The 95% figure has no source. That matters, and we'll get to it.

Does the science back this up?

Partially, but the framing is significantly overstated. Reverse T3 (rT3) is real. It is produced when thyroxine (T4) is converted via deiodinase enzymes into an inactive metabolite rather than active T3. Under physiological stress, fasting, critical illness, or caloric restriction, this shift toward rT3 is documented (Bianco et al., 2019, Endocrine Reviews). Where the science gets messier is whether elevated rT3 in otherwise stable hypothyroid patients on levothyroxine is a meaningful driver of symptoms, rather than a marker of an underlying stressor.

• A 2019 study in the Journal of Clinical Endocrinology and Metabolism found no significant association between rT3 levels and quality-of-life scores in levothyroxine-treated patients (Peterson et al., 2016, J Clin Endocrinol Metab).
• The concept of rT3 "blocking" thyroid receptors competitively in humans is largely extrapolated from in vitro data and animal models, not robust human clinical trials.
• The idea that T2 (3,5-diiodothyronine) actively "flushes" rT3 is speculative. T2 research is almost entirely in rodents (Goglia, 2005, Physiology and Biochemistry).

What did they get wrong (or right)?

Credit where it's due: the core biochemistry of rT3 as a stress-response metabolite is accurate. The three symptoms he names, unexplained weight gain, non-restorative sleep, and cold intolerance, are legitimate hypothyroid complaints that often persist even on adequate levothyroxine therapy. That gap between TSH normalization and symptom resolution is real and under-studied.

What's wrong is the causal chain he builds on that foundation. Saying rT3's "sole purpose is to put the brake on your body and metabolism" is a dramatic oversimplification. rT3 appears to be more of a byproduct of regulated T4 clearance than a purposeful suppressor. More critically, framing levothyroxine as actively worsening the problem for most symptomatic patients is not supported by current evidence. Some patients genuinely do better on combination T4/T3 therapy (Idrees et al., 2020, Thyroid), but that is far from the majority, and it should be a physician-supervised decision based on full thyroid panels, not a rT3 reading alone. His endorsement of T2 therapy goes further than the evidence allows.

What should you actually know?

If your symptoms persist on levothyroxine and your TSH looks "normal," you are not imagining things, and you are not alone. Studies consistently show roughly 10-15% of levothyroxine-treated patients report persistent symptoms despite biochemical normalization (Saravanan et al., 2002, Clinical Endocrinology). That is a real problem worth investigating with a clinician, not a YouTube supplement protocol.

Getting an rT3 test is not unreasonable if your provider agrees, but interpret results carefully. High rT3 often signals something else is wrong, severe stress, caloric restriction, systemic illness, not necessarily that rT3 itself is the cause of your symptoms. Treating rT3 as the villain without addressing root causes is working backwards.

• Combination T3/T4 therapy is an option for some patients and is discussed in current ATA guidelines, but it carries risks including cardiac arrhythmia at higher T3 doses.
• T2 supplementation has no approved clinical use in humans. The research base is thin and almost entirely preclinical. Do not take it based on social media advice.
• Any changes to thyroid hormone therapy should involve a physician who can monitor TSH, free T3, free T4, and symptom burden together, not just an rT3 number.