July 25, 20254 min read

Navigating Low T3 on a Carnivore Diet: Autoimmune Disease and Multiple Sclerosis

By Yannick Wolfe

My T3 on a carnivore diet is 1.5, TSH is normal, and T4 is 19. I can't quit keto as the carnivore diet keeps my autoimmunity (progressive multiple sclerosis) in full remission. Is T3 supplementation the only option?

Your current thyroid profile, with normal TSH, elevated Free T4, and low Free T3, reflects the well-documented metabolic adaptation to a zero-carbohydrate diet. I see this all the time, and it's one of the reasons why I do not recommend the carnivore diet long-term, even though it is part of the early scorch protocol. Everything you currently know about the benefits is what I want to see from someone in the first three months, but then I want you to transition to dry fasting and end it by reintroducing carbohydrates.

Your thyroid is producing T4 in sufficient quantities with minimal TSH stimulation, which confirms that your gland itself remains responsive and intact. Your issue lies in peripheral conversion.

When carbohydrate intake is absent, the body suppresses the diiodinase activity required to convert T4 into T3 within peripheral tissues. This suppression occurs because insulin, which rises in response to carbohydrate and amino acid availability, acts not only to regulate glucose uptake but also to signal energy abundance to the central nervous system. Consequently, when insulin remains chronically low, the body interprets this as a state of internal resource scarcity and shifts into a state of conservation, even if daily caloric intake is sufficient. One of the primary ways it does this is by limiting T3 production and action, thereby reducing metabolic rate and preserving energy for only the essential physiological functions required to keep you alive as an organism in the here and now.

How a zero-carb diet suppresses peripheral T3 production Long-term carnivore or ketogenic diet keeps insulin chronically low. Low insulin signals resource scarcity to the brain. The body responds by suppressing diiodinase enzyme activity, which cuts peripheral T4-to-T3 conversion, leaving blood T4 high, blood T3 low, and TSH deceptively normal. WHY CARNIVORE LOWERS T3 Zero carbs, chronically low insulin, suppressed conversion Long-term Carnivore / zero-carb diet no glucose, no carbs Chronically Low Insulin no energy signal brain reads: scarcity SUPPRESSED Diiodinase enzyme that converts T4 into active T3 body throttles it to conserve RESULT Low Free T3 T4 elevated or high TSH: normal euthyroid sick pattern What you see on labs TSH Normal thyroid gland intact Free T4 High / Normal-High gland producing fine Free T3 Low (e.g. 1.5) conversion blocked at tissue level The gland is healthy. The conversion step is suppressed by the metabolic state, not by thyroid disease.
💡When you eat a ketogenic diet, like a carnivore diet (the ultimate keto diet), your body increases growth hormone and autophagy + ketosis. This is a powerful combination for addressing inflammation, energy problems, etc. But this is best done as a form of medication, a temporary state. This state gives us a boost of healing and prepares the body to dry fast with minimal complications. However, if it persists for too long, you begin to encounter complications arising from being in a 'resource scarcity state of conservation'. We don't want that because it comes with its own set of problems, like peripheral thyroid T3 conversion errors, opportunistic infections like parasites and fungi, worse insulin resistance, and an increase in heart attacks and liver complications.

Supplementing with exogenous T3 may increase your serum Free T3, but this is unlikely to produce meaningful symptomatic improvement. T3 is not primarily an endocrine hormone in the classical sense. It is produced and acts locally within tissues through autocrine and paracrine mechanisms. This means that raising its concentration in the blood does not guarantee increased intracellular action if the underlying suppressive environment remains unchanged, which it will if you continue to exclude carbohydrate from your diet.

Why levothyroxine (T4) fails to relieve symptoms Levothyroxine delivers T4, an inert storage hormone. T4 must convert to active T3 before cells can use it. Three mechanisms break that conversion step: reverse T3 diversion, the DIO2 gene variant, and selenoprotein P blockade by autoantibodies. WHY THE PILL FALLS SHORT T4 is inert. Conversion is where it breaks. Levothyroxine T4 inert, storage form CONVERSION STEP T4 → active T3 happens at the cell level panels cannot see this step LITTLE ACTIVE T3 cells stay under-fueled still hypothyroid at cell level 3 things break here ↓ 1. Reverse T3 diversion T4 routed to a dead-end decoy instead of active T3 more T4 feeds the wrong path triggered by chronic illness or stress 2. DIO2 gene variant DIO2 enzyme performs most T4 → T3 conversion Thr92Ala variant: enzyme works poorly tissues T3-deficient, labs look fine 3. Selenoprotein blockade selenoprotein P carries selenium needed for conversion autoantibodies block it (Heim 2023) found in ME/CFS patients Each break point leaves cells T3-deficient. Adding more T4 does not fix any of them. Functional marker: body temperature below ~98.6°F on waking signals cells are still under-fueled. TSH alone cannot detect any of the three failure modes above.
💡There are some schools of thought that it is enough to supplement T3 while staying a low-carb ketogenic diet. I think this may work for some people, but overall, you need to bring carbohydrates back into the diet to truly start reversing the underlying condition. Why it may work for some people? It will slow down the diiodinase enzyme flip, thereby slowing down the peripheral t3 conversion issues. However it will speed up bone turnover and other high metabolic issues that will get paired with worse nutrient absorption intracellulary (you need insulin for good absorption) and you see this with the inability to hold unto salt by carnivore dieters.

The only way to reverse this state is to identify a form of carbohydrate that you can tolerate without exacerbating your autoimmune condition. That will involve targeted experimentation with specific starches, fruits, and juices, alongside working to address the immunological drivers of your food reactivity so that broader dietary flexibility becomes possible over time.

Keep in mind it takes around 30 days for your thyroid hormone levels to return to baseline after a 40 day water fast, assuming that you are refeeding in a carbohydrate focused diet - notice tT3 levels stable after a water fast, but we dont know if intracellularly they are working - we'd need to do a temperature test, energy test, ldl-c check, etc.
Compare to dry fasting where the T3 levels significantly fall. With great power come greater side effects.

It is easier said than done, I know, but there is no other way around this, unfortunately. Attempting to pharmacologically bypass this adaptive state while maintaining the dietary condition that induces it is unlikely to result in a sustainable or physiologically coherent solution and may actually be harmful to your health in the long run.

💡For many people even normal T3 levels may indicate a peripheral conversion issue. The easiest way to monitor is to do the oral temperature test and assess from there. Sometimes it gets even more complicated when thyroid tests are all normal, temperature is normal, yet the chronic illness sufferer still has all the symptoms of low t3 levels. This could still be a case for T3 therapy, but often requires addressing secondary issues like the opportunistic infections that no doubt have taken root throughout the body. (Ofc there's also: high LDL-c levels, low SHBG, high estrogen/cortisol/prolactin, low testosterone, all of which can point to hypothyroidism effects).

Be sure to check out the Dry Fasting Club's members section, which features in-depth interviews and videos, as well as protocols and questionnaires that assess your dry fasting readiness levels.

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