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
- Thyroid therapy changes might not change your body as much as many people assume they will.
- Diet changes can make a huge difference in some people in spite of significant thyroid therapy struggles.
- 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.
- 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”