My body composition before and during thyroid therapy

This post is a brief outline of my physical “Thyroid Therapy Transformation,” a glimpse into my personal life and how symptoms and body composition changed in response to changes in thyroid therapy and diet.

You can see my favorite colors are pinks and blues. And it also shows many hairstyle transformations, ha ha!

This post will be supplemented later with more detail on my laboratory results in the latter phases of therapy.

The main points are that

  1. Thyroid therapy changes might not change your body as much as many people assume they will.
  2. Diet changes can make a huge difference in some people in spite of significant thyroid therapy struggles.
  3. Even if you lose weight while on thyroid therapy, your health may be in danger if your FT3 is chronically low.

I enjoyed getting thinner. But ultimately, health matters more than body shape, and sufficient FT3 is necessary for health.

2001 photo. Pre-diagnosis, before therapy

Pre-diagnosis I was living with severe hypothyroidism, with fatigue and brain fog. I was diagnosed in 2003 by my TSH alone.

I’m not a Hashimoto’s patient. No goiter (no thyroid swelling) despite a TSH of >150 at diagnosis was an early sign that my hypothyroidism was either Blocking Hypothyroidism or Atrophic Thryoiditis (thyroid gland atrophy), but most doctors don’t know this.

Atrophic thyroiditis is an autoimmune thyroid disease caused by TBAb antibody (TSH receptor-blocking antibody) and other autoimmune factors, not by the TPO antibody found in Hashimoto’s. I’ve always had normal TPOAb over 4 lab tests since I was first tested in 2016.

My form of hypothyroidism is different and more rare than Hashimoto’s.

2005, 2011 photos. During LT4 thyroid therapy

As you can see, my body composition didn’t change much from before to during Synthroid (LT4) monotherapy. I just got more and more overweight.

My TSH may have been normalized, but nothing changed in the body composition department.

I chose T-shirt images to show the weight gain in my arms. Around my neck were “rings” — skin creases that were caused by fat.

I didn’t have any hair loss, ever. I’ve always had a very thick head of curly hair. Dryish skin, yes. Cold intolerance.

I was diagnosed with sleep apnea within a year after LT4 therapy began. My husband witnessed this as loud snoring and a sudden stop in breathing, then gasping for air. I refused CPAP therapy and just tried to sleep on my side instead of my back, which helped.

Mentally, I struggled with slow cognition — for example, finding myself rewriting the same paragraph for an hour, not being able to complete the mental process.

Emotionally, I would find that even missing 1 Synthroid dose would cause uncontrollable crying 3 days later for no reason, with no precipitating event in my life other than the missed dose. I was likely often on the edge of hypothyroidism in my dosage.

The year 2011 was my heaviest, at around 186 lbs and size 16+ petite (image with the hat on).

I am 5 feet 2 inches tall (157.48 cm), and my healthier weight in 2017 was around 115 lbs (52 kg). I have rather thick and heavy bones.

You can see that my body shows weight gain from fat, but not the shapes you see in the “myxedema” (non-pitting edema) caused by TSH-receptor overstimulation in Hashimoto’s or Graves’ disease.

Throughout my LT4 therapy, I had high total / LDL cholesterol, probably because my FT3 was low-normal, despite my top-of-range FT4 (total cholesterol has an inverse relationship to T3).

2014 photo. LT4 therapy plus Gluten free LCHF diet

Finally, my mental and physical health changed with a major diet change toward Low Carb High Fat (LCHF) and Gluten-free starting in July 2012.

I made this transition even while I was on TSH-normalized Synthroid monotherapy and likely still had a low-normal FT3 and mildly high FT4. Although I have no data but TSH for some tests (they didn’t test my FT3 and FT4 due to TSH-reflex testing policies), an abnormally low FT3:FT4 ratio of 0.135-0.15 pmol/L later revealed itself as a continuous sign of poor metabolism at various FT4 levels.

My excess body fat melted off mostly over 12 months and my new shape was achieved by Summer 2013 and maintained thereafter, alongside the new “way of eating.” I generally followed websites like Mark’s Daily Apple (Mark Sisson’s modified paleo or “primal” way of eating) and Diet Doctor (Dr. Eenfelt from Sweden) for tips.

My diet was NOT a strict ketogenic diet with less than 50g of carbs per day.

This is important. Some people with hypothyroidism find that ketosis destabilizes the enzymes that convert our thyroid hormones: lowers FT3 levels, affects adrenal health, and can cause a decline in health.

To be cautious, I even purchased a breathalyzer that could measure ketones in breath. I was rarely in ketosis. I was borderline.

My diet took a lot of effort to change shopping habits and cooking, but it was so delicious and fulfilling! I did not cut calories at all. I ate to satiety a lot of vegetables and high-quality fats and meats.

My husband also enjoyed the food. In fact, he had always struggled with chronic headaches ever since I knew him. A major motivator for me, showing that our diet was healthy for both of us was seeing him go from “80% life is a headache” to “80% of life is headache free.” Losing the gluten was the biggest benefit for his health, but he also lost his little pot belly on the LCHF.

I did not add any extra physical activity at all. My life is rather sedentary. I’m a research professor, so I spend most of my time in front of a computer when I’m not teaching or walking around campus. I have “ankylosing spondylitis” (though it’s been largely in remission since 2003). It’s a type of autoimmune arthritis, which in my case (unlike others), often gets worse with exercise, so I can’t do vigorous cardio without consequences.

At that point, in the picture, I thought I could live well on Synthroid for the rest of my life. Woohoo!

I was wrong.

A healthy diet and weight loss are not enough to defend health.

During thyroid therapy, T3 sufficiency is more fundamental to health.

Thyroid lab test challenges began before this photo, in Fall 2013. It started with a dose decrease because my TSH had fallen mildly low. Of course the doctor told me she was worried for my bones and heart. But she didn’t understand how to interpret my FT3 in the context of my TSH and FT4.

Because I had such a low FT3/FT4 ratio, a tiny decrease brought both hormones lower, and the FT3/T3 fell below range. Starting from a TSH that mildly low, I suddenly had a TSH of 18.08 at the next blood test, even though my FT4 had only dropped a little and was still in the upper half of range! (very abnormal.) From that point forward, my TSH had no logical or stable relationship to my FT4 or FT3 levels (as you’ll see in a future post). I later learned I have a completely atrophied thyroid gland (adult onset “atrophic thyroiditis”), so I now theorize the unreliable TSH was due to the known influence of TSH-receptor antibodies on the pituitary’s TSH ultrashort feedback loop.

Despite my low FT3, I fortunately did not have any other major illnesses interfering with thyroid hormone metabolism. My RT3 was found to be normal at 18 (ref 8-25), and this RT3 is to be expected with a FT4 around the same position in its range.

Jan-March 2016: my Low-T3 Health crisis

After almost 3 years of chronic low T3 (2013-2016) in which I think only my healthy diet sustained me, I had a health crisis in Jan-March 2016 that drove me to the emergency 3 times in 3 months.

Over late 2015, I started gradually feeling more and more hypothyroid. By January I was having trouble walking. So I asked for a dose increase, and it was almost logical to request it because my TSH was high at the time, though my FT4 was very high-normal.

Body-jolting random chest pains were triggered by a brief dose increase to 137 mcg. I was so disappointed. I wanted this dose increase to work but it backfired. Of course, I stopped after a few days and went back to my former dose of 125, but the symptoms didn’t go away after a few days. Then I called the 811 health line for advice. They said go to emergency, so I did.

They ran tests, but didn’t know what else to do but refer me to a heart clinic.

The pain was located not in the heart, but on the left side of my chest in one of the various branches leading away from the aorta, most often the subclavian artery, sometimes the renal, splenic or iliac artery. It was not triggered by exercise, stress, certain foods, or movements. Following a vascular spasm would often be a numb or tingling left arm if it was the subclavian artery. An attack would routinely wake me up once or twice a night while sleeping. The randomness was the most distressing part. And still being hypothyroid with low T3, I wasn’t able to stand for long without holding something for support. I could not walk very fast or very far without taking a lot of rests.

I had to read scientific literature to figure it out myself. In retrospect, from what I know now, it seems like I had acquired a mysterious adverse cardiovascular problem, possibly due to endothelial dysfunction in blood vessels, because T3 signaling is essential to regulating the health of the endothelial layer and vascular smooth muscle.

I didn’t know what else to do other than see my prescribing doctor again and again and go to emergency when I felt I had no other choice. This was a horrible time of seeing various doctors, asking for tests, and them believing nothing was wrong with me, while I lived in pain and fear and could barely perform my job. Somedays I could not drive myself home from work and had to ask my husband to take the C-train to campus, find our car in the parking lot, and pick me up at my office building.

During these months my low FT3 fell between 2.9 and 3.4 (3.5-6.5), along with failing health.

This was clearly an illness that affected my thyroid hormone metabolism, because my previous RT3 was 18 ng/dL. This mysterious health issue drove up my RT3 to 33 (range 8-25) on a blood draw showing FT4 was 22 (10-25).

The final time I went to emergency was after I woke up at night in excruciating pain, and it was, unfortunately, Easter Sunday! Nobody wants to ask her husband to drive her to Emergency and sit in waiting rooms for 5 hours starting at 5 am on Easter Sunday! I was in tears at the prospect of yet another humiliating ordeal at the hospital being dismissed as someone imagining her symptoms. But at least I’d be in the right place if I was going to have a heart attack. And fortunately, the emergency waiting room was rather empty.

By the end, I had seen many doctors and specialists, and some privately-paid healthcare practitioners. I had had many tests that cost the healthcare system a lot of money, including even a CT scan showing no problems.

One of the most useful tests I had was a thyroid gland ultrasound, which revealed that my thyroid had shriveled to a flattened, fibrosed, irregularly-shaped collection of cells 0.5mL in volume — one-tenth of a teaspoon. Normal volume for women is about 11 mL. That later drove me to study and write about my special thyroid condition of atrophic thyroiditis. Hashimoto’s can’t shrink your thyroid. TPO antibodies are not capable of this. The medical literature eventually helped me understand how TSH-receptor-blocking antibodies are the only known molecules that can act as an inverse agonist at the TSH receptor and completely silence TSH-receptor signaling.

The only other major lab test anomalies were low FT3 and high cholesterol, and some mixed plaque in my carotid artery bulb.

Fortunately, I found a compassionate doctor who was willing to dose me on T3, but only after my conventional cardio tests came back showing no major dysfunctions in my cardio plumbing or electrical system.

A careful transition to LT3 monotherapy (Cytomel) helped me recover my health. I used Paul Robinson’s T3 books to help me make the switch safely.

2017. T3 monotherapy since Apr 2016

No, I was NOT motivated to lose more weight by transitioning to T3 mono (liothyronine, L-T3, Pfizer’s Cytomel).

I didn’t need to lose more weight anyway. I had been happy with my body composition since 2013.

When I sought T3 therapy, I was seeking health by removing a well-documented chronic T3 deficiency.

I would not have bothered to try T3 had it not been for my excruciating day and night suffering. LT4 dosing once a day is convenient and it had worked for me for 13 years.

But the more I read in the medical literature about low T3 and its associated risks, the more I realized I was walking on thin ice even though I had a healthy diet.

It’s sad that doctors were so fearful of giving me T3 when it was so logical. If the FT3 level is chronically low, make sure that the FT4 isn’t too high, then add T3.

And it worked to improve my health. My day and night random vascular “spasms” significantly decreased on my first dose of 5mcg of T3, and eventually went away completely as I lowered FT4 and increased FT3 levels every 2 weeks.

I have no adverse effects from T3 dosing. My heart seems to appreciate it. My liver likes it — my high cholesterol fell low, and then normalized. And my adrenals must be capable of keeping up with the fact that “thyroid hormones increase tissue demands for adrenocortical hormones,” as mentioned in my Cytomel product monograph. (No, I haven’t been interested in measuring saliva cortisol. I don’t see why I need to. My morning blood cortisol is fine.)

After 1 year of stabilizing in good health on T3 only, I tried to reintegrate T4 hormone via desiccated thyroid (NDT). I had been gradually cutting back on T3 and replacing it with doses of NDT on a schedule developed in consultation with my physician. Then, after I went symptomatically hypothyroid, I had a lab test showing FT3, FT4 and TSH all just below range (yet more evidence of my unreliable TSH). My pharmacist and doctor both agreed, increase my dose. First, I increased my T3 dosing by a cautious amount. I felt better. I waited a week to stabilize before making the next change. That’s when I increased the NDT dose from 30 mg (19 mcg T4 + 4.5 mcg T3) to 60 mg (38 mcg T4 + 9 mcg T3).

One week later, while calmly watching TV one night, the same body-jolting cardio symptoms I had had with T4 mono occurred. Not again! I contacted my thyroid doctor immediately.

I seem to have acquired an unexplained cardiovascular intolerance to T4 dosing. An adverse effect occurred somewhere between 19 and 38 mcg per day, a dose that is way lower than my former maintenance dose of 118-125 mcg/day of LT4 monotherapy. Given the lab data, there was no way this symptom was triggered by an LT4 overdose this time. And it can’t be blamed on LT3 dosing because these were the exact same terrifying symptoms I had lived with for 3 months day and night before beginning T3. And it’s not the fillers or excipients in the tablets, because ERFA Canada’s desiccated thyroid has very different fillers than Synthroid.

So, I went back to LT3 monotherapy. My vascular spasm symptoms gradually subsided over 2 weeks.

All the while, I continued my LCHF Gluten-free diet.

2017 to December 2021

In 2018, I wanted to see if my LT3 monotherapy, my LCHF diet, and my supplements were harming me in any way, so I did some thorough patient-paid testing through a functional medicine clinic. Nothing showed up as being a problem.

Since 2019, I’ve reintegrated more carbohydrates (potatoes, chocolate, some gluten-free treats).

I’ve also gained the “COV1D 15”, the extra 15 pounds or so of padding that comes from less walking around and a little too many indulgences.

That means you can still GAIN weight while on T3 monotherapy!

I still have sleep apnea symptoms when I sleep on my back.

In the past 2 years, I developed complete arm & leg hair loss, which is not troublesome at all, since I don’t need to shave legs in summer! All head and trunk hair is normal. It’s not easy to find out why it happened — it could well be autoimmune / genetic, since my mom has the same arm/leg hair loss and she is mildly undertreated with a normal TSH on NDT therapy.


Some people might have been hoping to read a story saying “I started dosing T3 and I lost weight,” but NO, that’s not what this story is about.

In summary,

  • I struggled with weight before diagnosis of severe hypothyroidism.
  • My weight gradually got worse over 10 years on standard LT4 monotherapy.
  • By strategically changing my diet to paleo/primal low-carb high-fat, I lost all that weight while remaining on LT4 monotherapy.
  • I maintained my weight loss even after my physician dropped my dose and it induced chronic low T3 hormone levels.
  • Then I ran into some serious mysterious cardiovascular health problems that could not be explained by anything but my low T3, as nothing else showed up in tests.
  • I started T3 to resolve my T3 deficiency and recover my health. It worked.
  • I maintained my weight loss during and after my transition to T3 monotherapy. No, I did not get even thinner, because I was not overdosed.
  • I tried to reintegrate T4 hormone into my therapy, but I seem to have developed a mysterious cardiovascular intolerance to T4 dosing.
  • Then I relaxed my strict eating habits and gained some weight back during COVID.
  • Today I’m healthy and happy despite a little more padding around my middle.

I now understand the value of early warning signs in lab tests, and I know that standard LT4 thyroid therapy has a lot more risks from low FT3 and high-normal FT4 than most doctors understand.

You may be able to lose weight without optimal T3 levels like I did, but I can’t imagine doing it without significantly lowering carbohydrates and sugars because you need optimized T3 to metabolize those before they get stored as fat.

Please, do not try T3 just because you want to lose weight. Having optimal T3 helps, but it isn’t enough.

Above all, never be tempted to overdose. Thyroid hormone overdose may cause weight loss in a bad way. “Thyrotoxicosis” from any cause leads to muscle loss, muscle weakness, and bone density loss. It increases appetite and makes food go through your body too quickly. It does not give you good energy. Instead, it causes an overactive sympathetic nervous system, fatigue, and tremors. This is a powerful hormone that needs to be kept in the “Goldilocks zone.”

LT3-inclusive therapy is a better health choice for a poor converter like me with a dismally low FT3/FT4 ratio of 0.15 pmol/L. However, I do not wish to promote my path of LT3 monotherapy because it is unnecessary for most poor converters and can be very challenging to manage with multiple doses per day. My body changes its rate of T3 metabolism several times per year, and T3 losses seem to be higher in winter. I must adjust dosing based on heart rate data, body temperature data, and measuring FT3 levels 12 hours post-dose, to prevent hypo or hyper between regular lab tests and doctor visits.

Someday, if another health crisis arrives, I may try a 2nd time to crawl back to a T4-T3 combo, but currently, I’m healthy and stable, so my approach is, “if it ain’t broke, don’t fix it.”

To read more of what I’ve already posted publicly about my thyroid therapy journey, read “Case study: What my life is like in the T3-monotherapy wheelchair

22 thoughts on “My body composition before and during thyroid therapy

  1. We will continue to be lost until we have an actual way to quickly test FT3 and FT4 levels with a finger prick, much like testing blood sugar with a glucometer. Until then we are left guessing on a daily basis.

    1. I would also like to see a similar thing so we can monitor ourselves on T3 dosing, between blood tests at the lab. However, the concentrations of FT3 and FT4 are so tiny that they would likely not be measurable by a handheld device we can purchase. It’s hard enough to measure them accurately in an immunoassay. A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal. My lab’s FT3 range is 3.5 to 6.5 pmol/L, and FT4 is 10 to 25 pmol/L.

      1 pmol/L = 0.000000001 mmol/L
      1 mmol/L = 1,000,000,000 mmol/L

      The amount of blood sugar in blood is more than 1 billion times the amount of Free T3 or Free T4.

      Maybe Total hormones could be measured, since the range for TT3 is 0.9 to 2.8 nanomoles per liter (nmol/L) and for TT4 is 58 – 140 nmol/L.
      1 nmol/L = 0.000001 mmol/L
      1 mmol/L = 1,000,000 nmol/L

      The amount of blood sugar in blood is still more than 1 million times the amount of Total T3 or Total T4.

      I know, it sucks. There’s more chance of measuring them at home in urine where concentrations are higher, but there’s two drawbacks to that: 1) you’d have to make a ratio of Urinary T3 to something else like Urinary Creatinine to rule out the influence of dehydration. 2) And then you’d have to realize that kidney health is a major influence on urinary thyroid hormones, due to higher rates of T3-bound albumin and TBG lost in urine during proteinuria / nephrotic syndrome.

  2. My thyroid was atrophied already 30 years ago. I was told I had Hashimoto’s. And maybe I do because I have TGab antibodies (which lead to confusion as well, since the last doctor did only test for TPO and figured that I did not even have Hashimotos, just hypothyroidism). I envy you your T3 (not really….I’m glad you managed to get it). I’ve been trying to persuade many a doctor to at least try it and have now completely given up. It is too stressful to be disparaged continuously. It does often not end with just one reprimand but carries into each following appointment where the doctor now has to prove whose in charge. I’m sure it is also reflected in my record or the next doctor is somehow warned about my “attitude” and continues the same approach towards me without me even having mentioned anything “contrary”.

    I so do love the information you make available. It makes me even more desperate or sad, or anxious, though, because I know that I’m totally powerless no matter what I know and no matter what research, in other words what much doctor quoted evidence based proof, I could present. I hope it will be better for my daughter who finally got diagnosed (after being on a truckload of psych meds for a number of years). Maybe the new research in thyroid issues will soon be more known to doctors so she does not have to suffer as much. Right now, though, I see that she is on the same path as me, which makes me very sad for her.

    1. Thanks for your comment, Elke. Yes “it is too stressful to be disparaged continuously.” The medical ignorance, arrogance and bullying is despicable. I’ve seen and experienced it myself in appointments where “the doctor now has to prove whose in charge.” I also had disparaging letters written on my record during my Low T3 health crisis. Like you, I was powerless in the medical office and the emergency room. They didn’t care that I brought with me research articles that cautioned about mortality rates in people with Low T3. They were impervious to science and evidence. Medical ignorance and arrogance is harming many people.

    2. Dear Elke, I want to ask you a question and I hope that Tania will forgive me for doing this on her blog.
      Why don’t you want to try using T3 without a doctor’s prescription?
      Buy online Turkish T3 – Tiromel, a very weak and mild acting drug. This is what you need to get started. It is sold in Turkish pharmacies without a prescription. It is very cheap 0.3-0.5 dollars one pack of 100 tablets of 25 mcg in Turkish pharmacies. Online pharmacies will be around $ 1. 2-3 weeks take 1/8 tablet (3mkg) per day, then 2-3 weeks 1/4 tablet. Then, based on the test results, slowly lower the T4 and add the T3. Once your body has adapted to T3, you can add another dose of Tiromel at a different time, as well as switch to stronger T3 medications. I use the German drug T3 Thybon, it is very high quality, but strong and tough. I buy it online too.
      Take responsibility for your health into your own hands.

      In our country (Russia), there is no T3 in pharmacies since 2012 and doctors do not prescribe it. But we have a support group for patients with thyroid problems, which already has 37,000 patients, and this is how we all create combination therapy ourselves.
      If the legislation of your country does not allow you to buy online even the OTC drug Tiromel, then I very much ask you to excuse me for this post.

      1. Thank you for your concern, Vera. I have looked at different options to order T3 from several sources (even from my cousin outside Canada who is a pharmacist). My assumption is that it is not legal for these to be shipped to Canada because companies I looked into don’t. There is the option of getting a PO Box in the States. I’ve looked at that. My concern is that with all the problems I already have with physicians, even if I could pull it off, if something goes wrong (impure drug, any health concern, even outside from thyroid, any medical anything) there will be hell to pay. I really would prefer to have this monitored by a knowledgeable physician. The very last option is to leave friends, family and home behind and move to where such a physician can be found. In the meantime I take responsibility for my health in other ways (despite the hostility from doctors). It is a learning journey on which I am often accompanied by well meaning people who want to support me with their knowledge and experience. I very much appreciate all those who look out for me. So my thanks also go to you. I’m happy to hear that you found your way.

      2. Vera, we have to do what we can to survive, taking both the responsibility and the risk into our own hands when our healthcare system or economy fail to support our thyroid hormone health. I have a post in this blog about the economics of T3 pharma in which I mention the Turkish and Mexican brands. The only thing I don’t want on my website is mention of or links to underground, unregulated sellers of pharma, because they may be adulterated and spiked with other substances and could be unsafe.

    1. Dear Glensbo, thanks for pointing out that article on obesity and thyroid hormones. This article is fertile for analysis and critique.

      An important thing to notice is that the study excluded anyone with a thyroid diagnosis and anyone on thyroid hormone therapy. Their thyroid glands were healthy. Therefore, their FT3:FT4 ratio was going to be higher per unit of TSH than anyone on LT4 monotherapy who has little to no thyroid gland function.

      In fact, their T4-T3 metabolism was abnormally high for their TSH level of 2.0

      These were THEIR population means:
      FT4 mean 10.3 (pmol/l, reference range 7.7-16)
      FT3 mean 5.4 (pmol/l, reference range 3.1-5.8),
      TSH mean 2.0 (reference range 0.4-4.5)

      In contrast with their obesity with low-normal FT4, I was overweight with a high FT4. And then, with very little change in FT4, I lost weight because of a change in eating habits. Then I retained my thinner body composition despite a flip from TSH 0.07 to 18.08 that stayed high. I also remained thin despite a FT3 that fell low and stayed low, while eating to satiety and eating a lot more fat. I think it’s very interesting to see the contrast. My results just don’t make much sense in light of this study, and it’s partly because I’m one of the patient types they excluded both due to my thyroid status and diet status.

      1. Thanks for your thorough analysis of the study. I thought more in what defines obesity in euthyroid vs hypothyroid persons? Fat vs water and the effect on leptin? It could be interesting to see a similar study on hypothyroid persons. This could give us some objective measures on hormone deficits?

  3. Dear Tanya, thanks for the article!
    I am delighted with your transformation – every year you became younger and younger and now you look just wonderful.

  4. Hello,

    I sincerely thank you for creating this website and sharing your story along with a wealth of information. I am petite 5’1, live with untreated sleep apnea because I couldn’t tolerate cpap and have had an ultrasound that showed atrophy thyroiditis and have been struggling with hypothyroidism over 20 years. The last two years I have had my free t3 fall below range. I have been on combo therapy Synthroid and Cytomel and havent been able to increase my Cytomel over a single dose of 5mcg without experiencing chest pain, tachycardia, sweating and insomnia.

    Can you please share with me if you’re on CPAP now and if so when did you begin? I’m in Ontario and on ODSP because I’m barely functioning because of my mild sleep apnea coupled with unresolved hypothyroidism symptoms.

    Please do a post on your journey from switching to t3 monotherapy only and share your results. Also please share the timing of your doses and how you incorporate food and supplements. I would be so grateful.

    Thank you

    1. Dear Idil, Thanks for letting me know that yet another person has a connection between atrophic thyroiditis, sleep apnea and low FT3. Doctors and scientists should look into this constellation of disorders.

      Sorry to hear that you’re unable to increase over 5 mcg at once. I’m thinking about an insufficient cortisol response to T3 from adrenals. Do your symptoms occur during the FT3 peak, 3 hours post dose? Or <1 hour before peak? or 8-24 hours later before your next dose? It may help to understand whether it is caused by the fast speed of T3 absorption, or the peak post dose, or the FT3 valley between doses.

      I am still not on CPAP, but I'm thinking of asking for a sleep study for potential "REM Sleep Behavior Disorder" (see ). One night I physically kicked my husband out of bed and he actually landed on the floor and yelled out as he did. It happened while I was dreaming that I was kicking through a wall trying to escape from a cow running at me! By talking with him, it came to light that not only do I snore, but I talk and I flail and jerk around wildly in my sleep. This kick occurred while I was on compounded T3 hormone, some of which were later found to be very sub-potent when I composed my entire day’s dosage from that bottle of capsules. (I was angry and switched back to Cytomel, which is more expensive). It’s possible that insufficient T3 is related to REM sleep disorder, and maybe even to sleep apnea, through neurology.

      In addition to taking multiple 5 mcg T3s throughout the day to build up a higher average FT3 level, you might want to obtain your T3 from desiccated thyroid extract ( NDT / DTE ) because many patients report the T3 obtained from that pharmaceutical is slower-release or more gentle. This may be because is bound to thyroglobulin, a protein. I knew an individual who dosed both T3 and NDT and they verified the different effect by taking the two at separate times with almost the same amount of T3 hormone from each. The ratio of T4:T3 is 4.2 to 1 in DTE, but a 30 mg or 1/2 grain only includes 4.5 mcg of T3 that you can combine with T4 to reduce the mcg of T3 dosed per day. Have you seen my series on circadian FT3 rhythm? It ends with a Q&A post about adjusting doses to roughly imitate a natural rhythm.

      Given that tissue T3 raises demand for cortisol, I recommend asking your doctors for a thorough check of cortisol and ACTH-stimulated adrenal function, plus an early morning measurement of renin and aldosterone with blood drawn 3 hours after a dose of T3 (within the FT3 peak). I noticed in one of my colleagues with the same intolerance to higher synthetic T3 a mismatch appeared between very high renin and low or normal aldosterone. According to the literature, this “insufficient aldosterone response” to renin may appear not only in some patients with severe illness, but also in early autoimmune adrenal failure, and it may show that your mineralocorticoid secretion response is flagging in part of your adrenal glands even if your cortisol is normal or high. Or you may have mast cell activation — prostaglandins can also elevate renin.

      Best wishes, Tania

  5. Hi,

    I literally burst into tears upon seeing that you responded and I am beyond grateful to God that you took time to reply. Thank you. In the past when I tried to introduce a second dose of 5 mcg I would experience symptoms of tachycardia and palpitations an hour later and it would continue until the next day. If I stuck to just my morning dose of 56 mcg of Synthroid and 5 mcg of Cytomel it would also produce symptoms of tachycardia and palpitations about an hour later as well but by lunch time the tachycardia/ palpitations would have subsided.

    I am about 105 pounds and my doctor wants to try ndt and t4 but I have been very hesitant. The last 2 years have been extremely difficult to deal with whenever I make little changes to my thyroid meds. She wants to be conservative and start with 1/2 a 30mg of Erfa along with 25 mcg of synthroid. I did some reading and I think that might cause me to become under medicated. Would you mind giving me some suggestions? I was think of trying 30 mg of erfa along with 25 mcg of synthroid in the morning and another 25 mcg of synthroid at night. Also does cytomel require to be taken away from food and supplements?

    As for sleep, poor you and your husband. If you cant tolerate cpap, have you ever looked into mandibular advancement devices or Aveotsd? My nose is congested 24 hours and more so at night so I havent had luck with the tongue stabilizing device. Can you share with me whether you were diagnosed with mild, moderate or severe apnea when you learnt about your sleep apnea? I havent had the opportunity to meet anyone else with hypothyroidism and sleep apnea and communicating with you has been a God send. By the way a new product has just been approved by health Canada for mild sleep apnea called exciteosa and I’m trying to learn more about it. Hope you get the sleep study done for REM sleep behavior disorder.

    I figured as much that it could be my adrenals that are causing me to be intolerant to a second dose so thank you for bringing that up. I’m using ashwagandha to help me at the moment. I will ask for those tests that you mentioned but I might not be able to make sense out of them. I’m barely understanding reading through your posts because of my brain fog.

    1. Hi Idil, instead of replying to this additional reply, please consider joining our Facebook group for more discussion (click on Groups in our main menu), since that’s where we provide non-medical peer advice discussion. — Wow, I’ve never heard about tachy & palps lasting for so long after such a small 5mcg trigger. Very sensitive. I really do suspect something else in your body is interacting with T3 pharma action if it comes that quickly before the peak. I would even suspect an excipient or filler in the Cytomel, perhaps. I understand hesitation re: switching to ERFA, but it may be worth a try if it helps you in the long term with a gentler T3 effect. Every 60 mcg = 38 mcg T4 + 9 mcg T3, but estimate a bit lower to creep up safely to an optimal dose. Like all other pharma, each tablet is permitted to vary 90-110% of the stated dose, so you might really get more like 37+9.7 per 60. My “pharmaceutical equivalency” posts collected scientific research to support a roughly 3:1 pharma potency, meaning every 5 mcg of LT3 is “equivalent to” 15 mcg of LT4. But this estimate is for people who absorb T4 well and convert T4 to T3 at the average rate. Your body will likely absorb any thyroid pharma brand differently. We metabolize at different rates when levels / ratios of T3 and T4 change. A person with less T4 in circulation may need more T3 to compensate. So be ready to adjust. So sorry to hear about the brain fog; I sympathize.

  6. Hello. I wanted to als why your doctor needed “conventional tests came back showing no major dysfunctions in my cardio plumbing or electrical system”. What did those test involve?

    1. Hi David, thanks for your curiosity, and sorry for the delay in reply. The answer is Xray, ECG, chest ultrasound focusing on heart and aorta, exercise stress testing, and 48-hour holter monitor. A finding of mixed plaque in my carotid artery bulb finally led to a CT scan of chest that was of moderate image quality.

    1. Dear Jordan, Dr. Christianson’s page is an enormous mixed bag of things that are true and wise plus now and then things that are scientifically incorrect and overgeneralizations. My response is to the current version I’ve publicly archived here

      I agree with Dr. Christianson that it’s wrongheaded to do T3 monotherapy to clear RT3 from blood. Of course RT3 is not a toxin, and people need to hear that. Sure, go to town debunking silly Wilson-esque ideas. It’s good to discourage naive and gullible people from trying T3 monotherapy for the wrong or superficial reasons, and to discourage thyroid hormone overdose. But Dr. C’s is an outsider’s view of T3 monotherapy. He reveals no experience managing a person who truly needs T3 monotherapy and does well on it. To him, it’s always dangerous.

      How much does Dr. C understand about health risk and thyroid hormones? His page reveals a lot of thyroid ignorance. He can’t properly distinguish thyroglobulin from tyrosine in the thyroid hormone molecule. He incorrectly compares (Total) RT3 to Free T3 instead of comparing RT3 with Total T3. He doesn’t seem to know there are 3 types of T2 hormone. He doesn’t know that D3 enzyme prefers to take apart T3 into T2 and is upregulated by T3, in the brain and everywhere. He incorrectly says that T3 dosing in non-thyroidal illness has always been unsuccessful.

      More importantly, can Dr. C distinguish TSH receptors from T3 receptors? Apparently not. This makes him think circulating TSH is more essential than it truly is. There are not “two types” of TSH receptors, alpha and beta as he claims, but rather two subunits of one TSH receptor. This alpha / beta made him confuse TSH receptors on the surface of the cell with the T3 receptors in the nucleus called TRa1, TRb1 and TRb2. No, the TSH hormone does not enter those T3 receptors in the nucleus. Wires crossed! Next, he should learn about the constitutive signaling of the empty TSH receptor. Yes, TSH receptors can signal on their own even when TSH is absent from blood.

      So, Dr. C, just because on average, most people are thyrotoxic and at higher health risk with low TSH, everyone is thyrotoxic and at risk? No. Learn about the many things that can interfere with TSH secretion without causing thyrotoxicosis. Next, learn that people on TSH-suppressive LT4 therapy without a thyroid are not always thyrotoxic or at risk of osteoporosis because their FT3:FT4 ratio is often very low. Next, look in the science to see if people with treated central hypothyroidism — pituitary failure — suffer health risk from their inability to secrete any TSH. They don’t suffer risk.

      So, Dr C, TSH receptors exist beyond the thyroid, and therefore a certain level of TSH in blood is essential to fill those receptors? No, one has to first understand how the non-thyroidal TSH Receptors function when they are empty vs. filled. By the same naive argument, since all women have uteruses, fetus-receptors, they should always be filling them with fetuses, and there is no other healthy function of reproductive equipment without the fetus involved.

      So, Dr. C, whenever FT3 is above reference range, it’s always thryotoxic, even to the person with low or undetectable FT4? How can that be always true? Let’s do the metabolic math. How much extra T3 in blood is biologically necessary to replace the lack of T4 in blood that would have converted to T3 in cells? Next, how much T3 is lost within cells by quickly being converted to 3,3-T2 and 3,5-T2 during the post-dose T3 peak before it gets to receptors? Finally, learn how T3 metabolism and clearance changes in the absence of normal T4. Having an isolated FT3 is very different from people with Graves’ disease where FT4 is also high-normal or high.

      1. Thank you so much for your thoughtful and thorough response. Yes, I agree. I have tried adding T4 due to my doctor who is afraid of T3 monotherapy and a suppressed tsh. I felt extremely fatigued and sick. It took me two and half weeks to recover from that. Thankfully, I recently found an excellent doctor, after a year of searching, who is confident about T3 monotherapy. I am sorry for those who are in the midst of fear and discouragement because they cannot find a doctor who has knowledge about the thyroid. Thank you again!

  7. I appreciate your situation and what you’ve been able to find works for you. However, would you consider your situation a very specific and or rare case? It seems like mono T3 is what I would consider a last resort treatment and probably specific to a small amount of cases. I even believe Paul Robinson agrees it’s not the first or second way to go. I really like this website as it is science based blog posts (rare). But sometimes I feel the content is geared toward people who are needing T3 in one way or another (no thyroid, RAI, or complete destruction from Hashimotos). I feel like the majority of people, who may do OK on the right dose of T4 only, are a bit left out of the posts on here. I’m of the opinion that each form of therapy (T4 only, T4 and T3, NDT, and T3 only) has it’s own unique ways of interpreting labs and symptoms. T3 only has the most extreme labs from my understanding. I actually (shocking as it may sound) think TSH isn’t so bad for people on T4 only (assuming they also get FT4 and FT3 to ensure there isn’t a high FT4 and low FT3 situation). What I’d like to see (And maybe there are some from a long time ago) is discussions about different forms of T4 medicine, lifestyle changes that have science behind them (dairy, gluten, exercise, sleep, stress reduction, etc). Often the online groups are low on science and high on assumptions. Some of those maybe OK but I believe many are providing bad advice. Scary actually some of the groups and advice. Anyways, that’s a long way of saying I really like the site, but would like to see some more general topics that may cover more folks who don’t have a very specific situation. Some help for us T4 only folks.

  8. Thank you for this incredibly helpful blog. I’m petite at 5’1 and have always been lean due to the fact that I ate low carb and less calories than the average person, of course this was all unintentional, growing up with a tiny mother who eats like a bird and never paid attention to what I ate as an adolescent. I wouldn’t be surprised if any of this led to my thyroid dysfunction. Recently I decided to up my calories quite significantly and eat at least 130 g carbs per day. Quickly I gained 20 lbs. Needless to point out, I’m quite uncomfortable at this weight and I’ve noticed my blood glucose is higher. I’ve had to increase my thyroid hormone as well. I’m intrigued to try out this high fat low carb because I’ve noticed I tend to exceed the fat amount while struggling to eat more carbs and I’ve gained a fat tire around my stomach. Extremely insightful and helpful!

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