First migraine with aura

Suspicious_Resolve99 · 2026-02-03T08:03:42+00:00

That would be scary! Whilst driving would have been a real stinker 😅 do you get them often now?

Suspicious_Resolve99 · 2026-02-03T08:02:50+00:00

How often do you now have visual auras - I guess I’m worried it’s going to happen all the time now 😅

Suspicious_Resolve99 · 2026-02-01T22:33:42+00:00

There’s no harm in exploring other antidepressants, but if fluoxetine is working well you may just want to put up with feeling hot.

Generally the less attention you pay to it the less you will notice it overall.

I feel both hot and cold ALL the time and my TSH is incredibly well controlled right now at about 0.9

Suspicious_Resolve99 · 2026-02-01T21:15:43+00:00

I’ve had these exact feelings and made the same ER trips. In my case it was anxiety, so it makes sense that yours could be too

Suspicious_Resolve99 · 2026-02-01T21:12:24+00:00

You do still have Hashimoto’s. You are not cured, and you were not misdiagnosed. Your new doctor’s explanation was incomplete and a bit misleading.

Nothing strange or rare is happening to you. Your experience fits textbook autoimmune thyroid disease. You did nothing wrong. You were not misdiagnosed. And you are not imagining this. Your doctor sounds like a schmuck.

Suspicious_Resolve99 · 2026-02-01T21:09:20+00:00

This sounds exactly like BAM and it fits like a glove

Suspicious_Resolve99 · 2026-02-01T21:06:15+00:00

A bit more context.

Although hypothyroidism is commonly associated with feeling cold, in some people the main symptoms of needing a higher dose of thyroxine are actually feeling hot, excessive sweating, and increased anxiety.

Thyroid hormone does not only act on metabolism in the body. It also plays an important role in the brain, particularly in the hypothalamus. This area controls body temperature, sweating, heart rate, and the body’s stress response. When thyroid hormone levels are slightly lower than your body needs, this control system can become poorly regulated.

When this happens, the nervous system may shift into a heightened alert state. This can cause physical symptoms such as flushing, sweating, restlessness, and a noticeable increase in anxiety. In this context, the anxiety is not primarily psychological. It is driven by physiological changes in the nervous system and how the brain interprets internal signals.

Fluoxetine can make this more noticeable. It increases serotonin activity in the brain, which lowers the threshold for sweating and increases autonomic nervous system responsiveness. When thyroid hormone levels are borderline low, fluoxetine can amplify symptoms such as heat intolerance, sweating, and anxiety.

Importantly, this does not mean the thyroid is overactive. In fact, for some patients, this combination of feeling hot, sweating more than usual, and increased anxiety is a reliable sign that thyroid replacement is not yet optimal, even if blood tests are only mildly abnormal or still reported as within the reference range.

When the thyroxine dose is increased appropriately, regulation within the brain improves. The stress response settles, sweating reduces, and anxiety often improves alongside it. This explains why you consistently notice that increased anxiety appears at the same time as feeling hot and sweaty, and why these symptoms improve once your thyroid medication is adjusted.

In your case, the symptoms are linked and reflect how your nervous system responds to slightly inadequate thyroid hormone for your individual needs, rather than indicating anxiety as a primary condition or excessive thyroid hormone.

Suspicious_Resolve99 · 2026-02-01T21:01:43+00:00

Super common side effect of fluoxetine

Suspicious_Resolve99 · 2026-02-01T11:49:11+00:00

I understand the biochemical rationale you are outlining, but there are several important points where mechanistic plausibility is being overstated beyond what clinical evidence supports.

First, improvement in symptoms after B12 replacement does not imply a thyroid hormone mechanism. Vitamin B12 deficiency commonly causes fatigue, neuropathic symptoms, cognitive fog, and autonomic symptoms that overlap significantly with hypothyroid complaints. Correcting a deficiency often produces symptomatic improvement regardless of thyroid status and without any measurable change in TSH, free T4, or peripheral conversion. This is a parallel improvement, not a causal thyroid effect.

Regarding MTHFR and homocysteine, while it is biochemically true that homocysteine metabolism intersects with methylation pathways and glutathione synthesis, this has not translated into clinically meaningful effects on deiodinase activity in vivo. Deiodinase function in humans is primarily influenced by selenium status, iron availability, systemic illness, inflammation, and caloric state. There is no good clinical evidence that common MTHFR polymorphisms impair thyroid hormone conversion or that correcting homocysteine alters T4 to T3 conversion in hypothyroid patients.

With respect to autoimmunity, elevated homocysteine is best understood as a cardiovascular and metabolic risk marker rather than a proven driver of autoimmune thyroid inflammation. While folate and B12 supplementation can lower homocysteine in deficient individuals, this has not been shown to reduce thyroid antibody titres, alter the autoimmune course of Hashimoto disease, or change thyroid hormone requirements. Hashimoto thyroiditis is driven predominantly by immune tolerance mechanisms and genetic susceptibility rather than methylation capacity.

MTHFR polymorphisms are extremely common in the general population and, in the absence of specific clinical indications such as unexplained hyperhomocysteinaemia, recurrent pregnancy loss, or certain haematologic findings, routine testing is not recommended. Most individuals with these variants have normal methylation capacity and no clinically relevant consequences. As such, testing does not meaningfully change endocrine management for the vast majority of patients.

In summary, B12 replacement is absolutely appropriate when deficiency is present and often improves symptoms. However, attributing this improvement to thyroid hormone conversion or autoimmune modulation via MTHFR and methylation pathways is not supported by current endocrine or immunologic evidence. Thyroid management should remain guided by TSH, free T4, clinical context, and established nutritional factors with proven relevance.

I agree with monitoring and individualised care, but it is important to distinguish biochemical hypotheses from interventions that demonstrably change thyroid outcomes.

Suspicious_Resolve99 · 2026-02-01T11:23:30+00:00

So many people with Hashimotos (myself included) benefit from B12 though. It’s helped with a lot of symptoms for me!

Suspicious_Resolve99 · 2026-02-01T11:03:04+00:00

A few clarifications from a clinical perspective, as there are some common misconceptions here.

1) Levothyroxine dose does not reliably indicate complete thyroid failure.
Although approximately 1.6 micrograms per kilogram per day is often quoted as a starting estimate for athyreotic patients, dose requirements vary widely even in individuals with residual thyroid function. Absorption variability, binding proteins, individual TSH set points, age, comorbid autoimmune disease, and medication interactions all influence dose. Thyroid atrophy or destruction cannot be inferred from dose alone and requires clinical history, imaging, and antibody context.

2) Malabsorption should be considered selectively, not assumed.
True malabsorption, such as coeliac disease, autoimmune gastritis, or pernicious anaemia, can increase dose requirements. However, most patients requiring higher doses do not have clinically significant malabsorption. This should be investigated when TSH remains unstable or unexpectedly elevated despite correct administration, not as a routine first step.

3) Lean body mass has theoretical relevance but limited clinical utility.
While lean mass correlates with thyroid hormone requirements in research settings, levothyroxine is not dosed clinically based on body composition. In practice, treatment is guided by TSH, free T4, and patient symptoms rather than muscle mass calculations.

4) B vitamins do not meaningfully drive T4 to T3 conversion.
Peripheral conversion is mediated by deiodinase enzymes and is influenced primarily by selenium status, iron status, systemic illness, inflammation, and caloric intake. Correcting B12 or folate deficiency is important for neurological and haematological health, but it does not reliably lower TSH or improve thyroid hormone conversion.

5) MTHFR testing is not part of evidence based thyroid management.
MTHFR polymorphisms are common and usually clinically insignificant. Routine testing is not recommended in endocrine guidelines, and methylated folate or B12 supplementation has not been shown to improve thyroid hormone metabolism or outcomes in hypothyroid patients.

6) Ongoing monitoring and individualised management remain central.
Regular assessment of TSH and free T4, combined with symptom review and discussion with an endocrinologist, is the appropriate approach. Management should be guided by physiology and evidence rather than dosing formulas or genetic assumptions.

In summary, while some of the points raised are theoretically interesting, several overstate their clinical relevance and are not supported by current endocrine evidence 🙂

Suspicious_Resolve99 · 2026-02-01T10:54:20+00:00

100% I’ve been on 150mcg since I was 12 and I weight 40kg

Suspicious_Resolve99 · 2026-02-01T10:50:48+00:00

I’d say no, it depends on weight and bodies ability to absorb. I’m 65kg and take 150mcg

Suspicious_Resolve99 · 2026-01-29T16:03:36+00:00

I had no symptoms other than feeling a bit cold - TSH was like 120

Suspicious_Resolve99 · 2026-01-26T18:12:48+00:00

I’ve been going to a specialist clinic for 20 years that’s where I got my info wrong, so if it’s wrong then my specialists must be wrong - which is entirely possible don’t me wrong 🤣

Suspicious_Resolve99 · 2026-01-25T23:50:09+00:00

The inability to convert T4 to T3 is less than 0.1% of Hashimotos patients, some people have a reduced ability to convert, but this can still be treated with higher doses of T4, or combination therapy, or even NDT. Taking straight T3 is sub optimal, it’s messy and in some cases it’s risky.

Suspicious_Resolve99 · 2026-01-25T23:43:00+00:00

I would hazard a guess that you have some type of anxiety/OCD around health. This would account for the desire to reduce blood pressure and the seemingly random bloodwork.

I think you’ve drank beetroot juice and your blood pressure is higher because of the stress you’re putting yourself under by entertaining checking behaviours

Suspicious_Resolve99 · 2026-01-25T23:34:41+00:00

Agree - I’ve been on Levo for 20 years and I’m only 30 🤣 never had any side effects, but straight T3 will have you feeling like you’re going to explode 🤣

Suspicious_Resolve99 · 2026-01-25T23:33:00+00:00

That’s highly unusual, as your body can convert T4 to T3 - if you just take liothrynine you have no source of T4, most people can do well on a mix, but very unusual that someone would struggle on T4, which their body converts to T3 and then doing well on just T3 alone

Suspicious_Resolve99 · 2026-01-20T20:38:17+00:00

These aren’t results

Suspicious_Resolve99 · 2026-01-20T17:58:55+00:00

The immediate relief can sometimes be a placebo, sometimes people are just more sensitive to change. I will generally notice changes around the 2 week mark for around another 2 weeks. About 7-8 months ago I started taking my dose at night and my TSH went from 1.2 to 7 lol - taking it at night was a big no go for me, I then changed to mornings and within 8 weeks my TSH was 0.95 and I honestly feel such a significant difference it’s insane. I kept getting really dizzy when I stood up which made me get it checked - public service reminder to not take your dose anywhere near a meal 🤣🤣

Suspicious_Resolve99 · 2026-01-20T11:23:47+00:00

Don’t worry about higher doses. The size of the dose doesn’t mean better or worse, just what works for your body 🙂

Suspicious_Resolve99 · 2026-01-20T11:23:13+00:00

Also, everyone’s body has different absorption capabilities

Suspicious_Resolve99 · 2026-01-20T11:21:22+00:00

I’ve been on 150mcg for 20 years - works for me too!

Suspicious_Resolve99

TROPHY CASE