When influencers start diagnosing autoimmune disease as a ‘vitamin problem,’ we have a real problem.

When I saw this video, sent to me by my fiancée, it really highlighted something important: a lot of health misinformation is packaged so well that it feels convincing especially when it comes from charismatic voices. The problem is, calling something like Hashimoto’s a simple ‘vitamin issue’ ignores the real science and can lead people away from the care they truly need. My goal isn’t to attack anyone, but to help people become more discerning about where they get their health information, and to equip them with the knowledge to take control of their own health with clarity and confidence. I’m sharing the link here so you can see exactly what I’m referring to. After that, I’ll walk through the facts and explain what’s really going on.

https://www.instagram.com/reel/DLjIu7TtKmv/?igsh=NXh4dHdrenFiOGo1

The thyroid gland produces mostly T4 (thyroxine) and a much smaller amount of T3 (triiodothyronine). Rough ballpark: ~80–90% T4, ~10–20% T3. So the “20% T3, 80% T4” claim is somewhat misleading. The thyroid doesn’t make that much T3 directly—most circulating T3 is made peripherally, not in the thyroid gland.

T4 is a prohormone. It must be converted to T3, the active form, inside tissues like liver, kidney, muscle, and brain. This conversion is catalyzed by deiodinase enzymes (D1, D2, D3), which remove an iodine atom. This is not a methylation reaction. There’s no methyl group transfer involved. The key nutrient cofactors are selenium (for deiodinase activity), iron, zinc, and adequate caloric/redox balance.

Giving only T4 (levothyroxine) can be problematic in some individuals because if their deiodinase enzymes are impaired (due to stress, inflammation, nutrient deficiency, illness), they won’t convert enough T4 → T3, leaving them hypothyroid at the tissue level even if their TSH and T4 look “normal.”

Giving only T3 can overshoot and create spikes, since T3 has a short half-life.

That’s why some clinicians use a combination (like natural desiccated thyroid or compounded T4/T3).

There is a methylation link to thyroid in a different way: methylation pathways affect hormone receptor sensitivity and detoxification, but methylation is not the actual mechanism of T4 → T3 conversion. Saying “T4 is methylated to make T3” is simply inaccurate biochemistry.

To build on this a little more and simplify, Deiodinases = Traffic Lights

Think of T4 as the raw material and T3 as the active fuel. The deiodinase enzymes are like traffic lights deciding which lane the hormone goes down:

-D1: Green light in the liver and kidney—lets T4 move forward into T3 that fuels the whole body.

-D2: Local green light in the brain and muscle—makes sure those tissues get enough T3.

-D3: Red light—shunts T4 into reverse T3, a dead-end “dummy hormone.”

For the traffic lights to work, the city needs steady electricity. That “electricity” is your redox balance (glutathione, NADPH, selenium).

-If the grid is stable, lights work fine and T4 flows into T3.

-If the system is under a power surge (oxidative stress), the city cuts power to conserve energy D3 takes over and traffic is blocked.

When stress is high, cortisol shows up like police at an accident scene. They redirect traffic away from the main road (less T4 → T3) and push more cars onto the side streets (reverse T3). That’s the body protecting itself when it thinks resources are scarce.

Cytokines (like IL-6 and TNF-α) are like construction crews blocking lanes. They slow down the conversion process, close exits, and make more traffic pile up in the wrong places. That’s why chronic inflammation feels like metabolic gridlock.

You can’t run the traffic lights without wiring and parts:

-Selenium: The circuit boards.

-Iron & Zinc: The nuts and bolts holding the lights together.

-Iodine: The raw asphalt for the roads themselves.

If you’re low in these, the whole system flickers.

The liver is like the central freeway interchange most of the traffic passes through it. If the freeway is clogged from fatty liver or metabolic issues, traffic jams stop T4 from becoming T3. The gut acts like service roads: bacteria recycle hormones back into circulation. If gut flora are off, less T3 makes it back into traffic.

If the city doesn’t have enough fuel (calories), the government puts cars on rations. Traffic lights dim, fewer cars (T3) get through, and metabolism slows to conserve gas.

The city runs better on a predictable day-night cycle. If you’re up all night or working shifts, the schedule gets thrown off and the traffic system (especially D2) doesn’t operate smoothly.

T4 → T3 conversion isn’t a simple one-step chemical trick. It’s more like a whole city’s traffic system, with lights, power grids, cops, construction, highways, fuel rations, and schedules all working together. If one part of the system fails, traffic diverts into reverse T3 or slows down entirely.

That’s why Gary’s “it’s just methylation” explanation misses the real story and highlites the difference between compelling marketers and real cellular medicine and understanding things at a deeper level. The real levers are stress, redox health, inflammation, nutrients, and organ function.

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