Thyroid T3 secretion compensates for peripheral T4-T3 conversion

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How does TSH affect T3 secretion and conversion rate?

This study’s data shows that TSH is by no means a proxy for T3 secretion and conversion rate, even in the healthy.

You can see it in this table — now re-sorted by FT3 in pg/ml, which they measured before the 8 days of iodine dosing and injection of the radioiodine-tagged T4 and T3.

As you can see, there is no pattern in relationship to this middle FT3 column that ranges from 2.6 to 5.7.

The T3 secretion/conversion ratio in the final two columns used to show that smooth gradation from dark to light colors.

Now when you re-sort by the TSH column, the TSH does not correlate with T3 secretion or T3 conversion ratios at all.

The lack of a pattern is metabolically significant.

Why doesn’t TSH fully regulate the T3 portion of thyroid metabolism? Because our T3 supply doesn’t all depend on TSH.

  • Deiodinase enzymes D1, D2, and D3 in tissues throughout our bodies are in control of peripheral thyroid hormone conversion.
  • Deiodinase type 2 (D2) can be upregulated by TSH, but it will still function when TSH is suppressed.
  • Deiodinase enzymes D2 and D1 in the hypothalamus and pituitary control TSH secretion locally by negative feedback. The T4-T3 conversion rate in these central organs is different from the conversion rate in other organs.
  • Powerful feed-forward mechanisms can signal TSH to take a leading role in shifting metabolic rate higher or lower, such as during adaptation to cold, or recovery from nonthyroidal illness (NTIS).

Central regulation of TSH is just as complex as thyroid metabolism; it is not just a passive hormone regulated by thyroid hormone feedback.

Instead of trying to understand the complex systems that regulate Free T3 levels, the old paradigm of thyroid therapy decided to focus on TSH and ignore Free T3 altogether.

The body never ignores FT3.

It’s foolish to ignore what we don’t understand.

Even though T3 is not the most abundant hormone, it is the most important and powerful thyroid hormone. In health, it is so important that Free T3 blood levels are individually customized.

T3 is not singlehandedly regulated by the TSH level, but by the complex metabolic dance between thyroidal secretion and peripheral conversion seen in the graphs above this one.

This individual variation in FT3 levels accords with the phenomenon observed since Anderson and team published an article in 2002 showing that each individual has an unique “optimal” level and ratio for FT3 and FT4 thyroid hormones in blood, and their individual ranges are much narrower than the population-wide reference range.

A later study by Ankrah-Tetteh in 2008 in ten healthy people discovered how carefully each individual’s body regulated their FT3 supply.


Ankrah-Tetteh found that each individual’s TSH and FT3 pair was unique and tightly controlled.

The image from Ankrah-Tetteh below shows individualized FT3 levels in relationship to TSH.

You can see by the varying sizes and heights of the rectangles of data that in each of these 10 patients,

  • the TSH levels are generally flatter and in the lower half of the reference range. They don’t seem to relate to the FT3 levels in a consistently inverse way as one may expect.
  • The TSH was not inversely related to FT3 as one would expect, but rather mildly positively related to FT3 in some patients.
  • the Free T3 levels are highly varied in different positions across the full reference range for the population.
  • Each individual does not wander far from their TSH and FT3 anchor points over time, and each stays within a narrow range.

Based on mathematical calculations, the “index of individuality” (IOI) for FT3 was 0.38.

This is low, and the result is statistically significant in an interesting way. According to Petersen et al, 1999,

  • Any low IOI below 0.6 makes the width of the population reference range significantly wider than the range of variation for each individual.
  • Such a low IOI means that individuals’ levels are not tightly clustered around an average, but vary significantly from each other within the population.
  • A low IOI also makes the FT3 level in health very dependable, with not much change expected from one test result to the next. The FT3 level is just as dependable as FT4 in health, since the IOI for FT4 was 0.41.

In contrast to FT3, the IOI for the TSH in Ankrah-Tetteh’s study was significantly higher, at 0.68, according to their calculations. This is because TSH lab results in the population were more tightly clustered around a mean of 1.58 mU/L, which is consistent with the average TSH in larger populations.

Therefore, Pilo’s data are consistent with the modern research on TSH and thyroid hormone level differences between individuals.

All Pilo’s study could not do was measure change over time, data which studies like Ankrah-Tetteh et al’s and Andersen et al’s now provide.

Human variation within a wider population range is the principle of thyroid hormone economy.

Optimal FT3 thyroid hormone levels and FT3:FT4 ratios are highly individualized.

A FT3 level anywhere within the population reference range is not precise enough for the health of the individual.

Unfortunately, basic flaws of Pilo’s study prevent us from understanding how TSH influenced T3 secretion, T4-T3 conversion, and overall thyroid hormone supply:

  • No reference ranges were given for TSH, FT3 or FT4, so we cannot see how levels varied across the reference range.
  • Nobody in Pilo’s study had a TSH level outside the narrow range of 1-2 mU/L, so it was impossible to see how TSH variation could affect the results.
    • We now know that higher TSH levels seen in untreated hypothyroidism can push a failing thyroid to secrete and convert relatively more T3 than T4 (Citterio et al, 2017; Hoermann et al, 2020).
  • Pilo’s study could not account for huge circadian rhythms seen in TSH, and their article did not specify the time of day at which baseline TSH was measured.

How do sex and age influence these rates?

Next, let’s look at a fundamental feature of Pilo’s data–their unbalanced selection of 14 young, old, male, and female participants.

In a study of only 14 people, it’s difficult to come to conclusions about how sex may or may not be a variable in secretion and conversion rates of T4 and T3.

However, we can notice the bias in selection of participants:

  • the smaller number of women (5) were generally older (43-59, average 49.4)
  • the larger number of men (9) were generally younger (19-65, average 35.7).

Does the sex bias in participants bias the calculated averages in Pilo’s study?

Let’s take a look.

The table below is sorted primarily by sex and secondarily by age.

The younger women had more T3 coming from their thyroid gland, and the oldest woman had the least thyroidal T3 secretion rate among all subjects in the study.

Hmm, why did the older women have the lowest T3 secretion rates?

Among women, the secretion/conversion ratio was 16% / 84%,

  • but if you remove one outlier, the youngest 43-year-old patient #2 with a high T3 secretion of 36.2%, the ratio would be 11% / 89%.

Among men, the secretion/conversion ratio was 24.1% / 75.9%,

  • but if you remove the highest outlier, the 31-year old male patient #3 with a high T3 secretion of 42%, the ratio would be 21.8% / 78.2%

This next table was sorted by Age, allowing Sex to fall where it may:

There is clearly an age pattern in the secretion/conversion ratio. The older participants between 44 and 59 years of age had less T3 coming from their thyroids, according to Pilo’s team’s estimates.

Exceptions existed in a few men, such as the 36-year-old male and the 20-year-old male who had significantly lower T3 secretion ratios than the rest of their cohort, and I’ve already explained why these anomalies exist.

Surprisingly, the oldest patient in the cohort, a 65-year-old male, had quite a robust thyroidal T3 secretion of 24.9%.

What are the implications of this imbalanced group?

Older women represent the majority of patients with thyroid disease.
They are the people whose thyroid therapy is being influenced by misrepresentations of Pilo’s findings.

The younger men’s data compensated for the older women’s data, making the study’s averages less applicable to older women.

Middle-aged women’s health problems during thyroid therapy can too easily be blamed on stress, diet, exercise, and sex hormones.

One can only wonder how different the “average” 20/80% ratio estimate would have been with improvements in sampling and interpretation:

  • a larger sample size,
  • a balance of both sexes,
  • a balance of ages, and
  • the choice to specify age- and sex- specific ranges of thyroidal secretion and conversion.

What about health factors?

Finally, let’s ponder how health factors may have influenced the wide human diversity seen in Pilo’s estimates.

Pilo’s article gave no information about how they screened their 14 patients for health factors.

Many factors could lower T3 secretion, such as:

  • Mild central hypothyroidism. TSH secretion rate may be too low in people with genetic handicaps in pituitary TSH signalling, permanent damage to the central glands, and even degenerative diseases such as “empty sella” and autoimmune pituitary disease. Central hypothyroidism varies in severity from person to person and will hinder both T4 and T3 secretion.
  • An undiagnosed nonthyroidal illness. Measuring Reverse T3 would have revealed whether any of these people were having even a mild case of “Low T3 syndrome” in which the TSH is normal but T3 drops while RT3 rises above the healthy mean.
  • Iodine excess. Perhaps some patients with lower body weight had a more extreme reaction to the drops of Lugol’s iodine that all patients were forced to take during the 8 days of the study.
  • Substances that limit T4-T3 conversion.
  • DIO1 and DIO2 genetic handicaps that changed peripheral conversion rate.

Unfortunately, this study showed only biochemistry, not health outcomes.

It did not measure biomarkers that are sensitive to circulating T3 thyroid hormone and are commonly used to verify tissue euthyroid status, such as

  • heart rate,
  • body temperature,
  • cholesterol,
  • ankle reflex,
  • creatine kinase,
  • liver health,
  • bone metabolism biomarkers,
  • kidney health,
  • mental health, or
  • cardiovascular health.

(Ito et al, 2017; Meier et al, 2003)


1. Respect T3 flexibility and diversity.

Spread awareness of Berberich et al’s 2018 update on Pilo’s study, which acknowledges the wide flexibility of thyroid homeostasis.

“the HPT axis is a much more dynamic system than has been previously thought. In particular, the interrelationships between FT3FT4, and TSH are less constantly fixed, rather conditional and contextually adaptive.”

(Berberich et al, 2018)

2. change the mantra.

State the wide range!

3. Study how to optimize each thyroid patient’s FT3 and FT4

This study by Pilo is not focused on thyroid therapy.

It’s about the “normal, healthy” TSH- and thyroid-gland-driven thyroid hormone economy.

In thyroid therapy, each patient has unique thyroid gland disabilities.

Each patient has unique thyroid metabolism handicaps.

Only recently have researchers begun to study how to optimize FT3 levels during thyroid therapy to achieve tangible health outcomes:

  • Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2019). Individualised requirements for optimum treatment of hypothyroidism: Complex needs, limited options. Drugs in Context, 8, 1–18.
  • Ito, M., Miyauchi, A., Hisakado, M., Yoshioka, W., Kudo, T., Nishihara, E., Kihara, M., Ito, Y., Miya, A., Fukata, S., Nishikawa, M., & Nakamura, H. (2019). Thyroid function related symptoms during levothyroxine monotherapy in athyreotic patients. Endocrine Journal, 66(11).
  • Ito, M., Kawasaki, M., Danno, H., Kohsaka, K., Nakamura, T., Hisakado, M., Yoshioka, W., Kasahara, T., Kudo, T., Nishihara, E., Fukata, S., Nishikawa, M., Nakamura, H., & Miyauchi, A. (2019). Serum Thyroid Hormone Balance in Levothyroxine Monotherapy-Treated Patients with Atrophic Thyroid After Radioiodine Treatment for Graves’ Disease. Thyroid: Official Journal of the American Thyroid Association.
  • Larisch, R., Midgley, J. E. M., Dietrich, J. W., & Hoermann, R. (2018). Symptomatic Relief is Related to Serum Free Triiodothyronine Concentrations during Follow-up in Levothyroxine-Treated Patients with Differentiated Thyroid Cancer. Experimental and Clinical Endocrinology & Diabetes: Official Journal, German Society of Endocrinology [and] German Diabetes Association, 126(9), 546–552.

If we really want to respect natural human diversity, flexibility and adaptation in thyroid hormone economy, we have to give doctors the tools to optimize Free T3 to the individual using FT3 and FT4 evidence.

We don’t need to do fancy genetic studies to identify why some people do not fare well on TSH-normalized therapy using LT4 alone or fixed ratios of T3-T4 combination therapy that supply limited T3.

All we need to understand is that some individuals require more T3 than others, and that our T3 needs can change over time as our bodies and metabolic demands change throughout life.

Let’s respect that the individualized thyroid hormone economy may require a wide diversity of thyroid therapy approaches, just as each person’s T3 secretion and T4-T3 conversion rate adapts to challenges like iodine supply, childhood, pregnancy, cold climates, and nonthyroidal illness.


Click to view reference list:

Andersen, S., Pedersen, K. M., Bruun, N. H., & Laurberg, P. (2002). Narrow Individual Variations in Serum T4 and T3 in Normal Subjects: A Clue to the Understanding of Subclinical Thyroid Disease. The Journal of Clinical Endocrinology & Metabolism, 87(3), 1068–1072.

Ankrah-Tetteh, T., Wijeratne, S., & Swaminathan, R. (2008). Intraindividual variation in serum thyroid hormones, parathyroid hormone and insulin-like growth factor-1. Annals of Clinical Biochemistry, 45(Pt 2), 167–169.

Berberich, J., Dietrich, J. W., Hoermann, R., & Müller, M. A. (2018). Mathematical Modeling of the Pituitary–Thyroid Feedback Loop: Role of a TSH-T3-Shunt and Sensitivity Analysis. Frontiers in Endocrinology, 9.

Citterio, C. E., Veluswamy, B., Morgan, S. J., Galton, V. A., Banga, J. P., Atkins, S., Morishita, Y., Neumann, S., Latif, R., Gershengorn, M. C., Smith, T. J., & Arvan, P. (2017). De novo triiodothyronine formation from thyrocytes activated by thyroid-stimulating hormone. The Journal of Biological Chemistry, 292(37), 15434–15444.

Escobar-Morreale, H. F., Del Rey, F. E., Obregón, M. J., & de Escobar, G. M. (1996). Only the combined treatment with thyroxine and triiodothyronine ensures euthyroidism in all tissues of the thyroidectomized rat. Endocrinology, 137(6), 2490–2502.

Galton, V. A., Schneider, M. J., Clark, A. S., & St. Germain, D. L. (2009). Life without Thyroxine to 3,5,3′-Triiodothyronine Conversion: Studies in Mice Devoid of the 5′-Deiodinases. Endocrinology, 150(6), 2957–2963.

Gullo, D., Latina, A., Frasca, F., Squatrito, S., Belfiore, A., & Vigneri, R. (2017). Seasonal variations in TSH serum levels in athyreotic patients under L-thyroxine replacement monotherapy. Clinical Endocrinology, 87(2), 207–215.

Hoermann, R., Pekker, M. J., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2020). Triiodothyronine secretion in early thyroid failure: The adaptive response of central feedforward control. European Journal of Clinical Investigation, 50(2), e13192.

Ito, M., Miyauchi, A., Hisakado, M., Yoshioka, W., Ide, A., Kudo, T., Nishihara, E., Kihara, M., Ito, Y., Kobayashi, K., Miya, A., Fukata, S., Nishikawa, M., Nakamura, H., & Amino, N. (2017). Biochemical Markers Reflecting Thyroid Function in Athyreotic Patients on Levothyroxine Monotherapy. Thyroid, 27(4), 484–490.

Jeon, M. J., Lee, S. H., Lee, J. J., Han, M. K., Kim, H.-K., Kim, W. G., Kim, T. Y., Kim, W. B., Shong, Y. K., & Ryu, J.-S. (2019). Comparison of Thyroid Hormones in Euthyroid Athyreotic Patients Treated with Levothyroxine and Euthyroid Healthy Subjects. International Journal of Thyroidology, 12(1), 28.

Jonklaas, J., Bianco, A. C., Bauer, A. J., Burman, K. D., Cappola, A. R., Celi, F. S., Cooper, D. S., Kim, B. W., Peeters, R. P., Rosenthal, M. S., & Sawka, A. M. (2014). Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid, 24(12), 1670–1751.

Marsili, A., Zavacki, A. M., Harney, J. W., & Larsen, P. R. (2011). Physiological role and regulation of iodothyronine deiodinases: A 2011 update. Journal of Endocrinological Investigation, 34(5), 395–407.

Meier, C., Trittibach, P., Guglielmetti, M., Staub, J.-J., & Müller, B. (2003). Serum thyroid stimulating hormone in assessment of severity of tissue hypothyroidism in patients with overt primary thyroid failure: Cross sectional survey. BMJ, 326(7384), 311–312.

Petersen, P. H., Fraser, C. G., Sandberg, S., & Goldschmidt, H. (1999). The Index of Individuality Is Often a Misinterpreted Quantity Characteristic. Clinical Chemistry and Laboratory Medicine (CCLM), 37(6), 655–661.

Pilo, A., Iervasi, G., Vitek, F., Ferdeghini, M., Cazzuola, F., & Bianchi, R. (1990). Thyroidal and peripheral production of 3,5,3’-triiodothyronine in humans by multicompartmental analysis. The American Journal of Physiology, 258(4 Pt 1), E715-726.

Rendell, M., & Salmon, D. (1985). “Chemical hyperthyroidism”: The significance of elevated serum thyroxine levels in L-thyroxine treated individuals. Clinical Endocrinology, 22(6), 693.

Wiersinga, W. M., Duntas, L., Fadeyev, V., & Nygaard, B. (2012). 2012 ETA Guidelines: The Use of L-T4 + L-T3 in the Treatment of Hypothyroidism. European Thyroid Journal, 1(2).

21 thoughts on “Thyroid T3 secretion compensates for peripheral T4-T3 conversion

  1. I have this in my blood test. All the symptons of low thyroid whit above range TSH but my Free T3 is also high on the range. No Hashimoto and my thyroid gland is perfect in the ultrasoud.

    1. Dear Lucas, if your TSH is above range and your FT3 is high within range, it makes sense that you have a healthy thyroid gland pushing T3 higher. Your case looks like one of two things that come immediately to mind:

      1) the higher T3 seen in obese patients with “metabolic syndrome,” and

      2) people with Resistance to Thyroid Hormone often have the paradox of higher TSH along with higher T3 and T4.

      In your case I would suspect #1 before #2. Metabolic syndrome is MUCH more common. “Resistance to Thyroid Hormone” requires a genetic mutation.

      I wish I could link to articles on our blog on these two topics, but I haven’t had time to cover them yet, so all I can do is refer you to literature.

      Here is a reference for you on higher T3 + TSH in metabolic syndrome:

      Kim, H. J., Bae, J. C., Park, H. K., Byun, D. W., Suh, K., Yoo, M. H., Kim, J. H., Min, Y. K., Kim, S. W., & Chung, J. H. (2016). Triiodothyronine Levels Are Independently Associated with Metabolic Syndrome in Euthyroid Middle-Aged Subjects. Endocrinology and Metabolism (Seoul, Korea), 31(2), 311–319.

      1. Do you have a name of an Endocrinologist in Ottawa OnT that is not afraid to test a patient that is not just the routine blood tests that always comes back as normal. I would sincerely appreciate this. Thank you

      2. Hi Suzanne, normally we don’t give public recommendations. We welcome you to our online Facebook group to ask other patients. See our “Groups” tab in the main menu above

  2. Based on the article, it would seem that the “everyone needs their FT3 in the upper part of the range” is incorrect. It seems like everyone is unique and finding that correct FT3 would be more of a trial and error thing since the majority of us do not know our pre-hypothyroidism FT3 levels.

    1. Yes you are correct. In a state of thyroid gland health FT3 may be optimal in the lower half of reference in one individual, and in the upper half of range for another.

      Yes, trial and error is our only path to finding optimal levels.

      However, even if we did have a record of pre-hypothyroid levels, targeting them would not necessarily optimize our hormone replacement.

      After thyroid gland removal or severe autoimmune thyroid destruction, FT3 levels usually need to be in the middle to upper half of reference range on LT4 monotherapy, according to the recent research. Thyroid gland tissue loss means loss of deiodinases expressed mostly in the thyroid gland, as well as loss of flexible secretion.

      The healthy thyroid gland responds to nightly rise in TSH by elevating FT3 significantly at night. The elevated fT3 disappears by normal lab testing time, but it is significant to the organs and tissues that received this nightly infusion.

      This is a secret T3 dose given only to the thyroid healthy.

      In thyroidless people on LT4 mono, the FT3 does not rise over 24 hours but is flatlined. (See the post on FT3 peaks and valleys, the graphs by Saravanan)

      With the loss of the gland providing metabolic flexibility and loss of nightly T3 rise, the same FT3, FT4 and TSH measured in August at 1pm does not mean the same thing it once did in the body with the healthy thyroid gland.

      Hormone levels must be more than normalized because the loss goes deeper than a snapshot of biochemistry. We need to be compensated for a loss of vital metabolic equipment.

      1. Hello Ms, and thanks for your question. It’s not a “should.” Yes, it may work well for some people to imitate natural FT3 circadian rhythm by dosing T3 at bedtime or by waking up to take a T3 dose during sleeping hours. If you read Paul Robinson’s three books on thyroid hormone therapy, he would say night-time T3, or T3 dosing before rising from bed (which he calls the circadian dose), works well for many people, often establishing a better response to dosing that occurs during daytime hours.

        I would echo that from my personal experience: after learning about the FT3 rhythm in healthy people, I switched to taking my largest dose of T3 at bedtime. I wear a heart rate tracker on my wrist. After that large dose, my heart responds with no rise in heart rate at all (my lowest heart rate occurs while sleeping, just like in most people), and I sleep soundly. My body wakes me up naturally about 5-6 hours later to take a booster small T3 dose. I go back to sleep very easily after that booster and sleep for another two or three hours. If I have trouble sleeping, occasionally due to troubling thoughts or dreams, I tend to sleep more soundly after a small booster dose takes effect.

        However, nighttime dosing is not necessarily needed in many people dosing less than 15 mcg of T3 or 120 mg of desiccated thyroid per day. They can do just fine with 2 doses spread out during daytime hours. Generally the more T3 one doses and the less T4 is available to convert to T3 in cells, the better it is to spread out one’s T3 doses across the 24 hour period, and to induce a daily rhythm rather than spreading it out evenly.

        See our 3 posts on the FT3 circadian rhythm to understand what this rhythm looks like in people with healthy thyroids, and how a strong rhythm supports health and longevity. There’s also a Q&A post on inducing a FT3 rhythm while dosing T3 or desiccated thyroid.

  3. Do thyroid supplements like Thyroid Pro, Thyroid Gold, Thyroid Glandular work ? Do they contain active FT4 and FT3, FT1, FT2. Whether iodine, selenium , iron and zinc helps in hypothyroidism ? How Gluten in wheat, casein in A1 milk affects Hashimoto’s or Graves’ disease?

    1. I have heard from people taking ThyroGold bovine desiccated thyroid. It works. In general, bovine has a different ratio of T4 to T3 than porcine, with much less T3 per unit of T4. Kologlu et al, in 1966 did a study and found the contents were “active bovine T4 21.3%, T3 4.3%” which means a ratio of 5:1 approximately.

      Each brand of thyroid “glandular” may have a different potency. Before you trust them, you may want to do research to discover whether their ingredients are regulated by third party agencies (governments) to stay within 90-110% of their stated dose of T4 and T3 in mcg per pill.

      The contents of thyroid supplements also depend on what is permitted within your country. In Canada, these hormones are prescription only, so products sold over the counter officially cannot contain thyroid hormones (levo)thyroxine (T4) or liothyronine (T3) even if they have the word “thyroid” on the label.

      As for iodine, selenium, iron and zinc, they each support the thyroid gland’s hormone production in a different way. See this 2020 review of these nutrients by Khan et al

      Gluten and casein have effects on the autoimmune response. See this article by Vojdani, 2014 — scroll down to the section heading “5.2. The Role of Milk and Wheat Components in Autoimmune Diseases”

  4. I went on Levothyroxine two years after my partial thyroidectomy. My TSH was 5. I’ve had no appetite since the surgery so I know from personal experience you lose that extra T3 secreted from the thyroid gland. On T4 only I have never regained my appetite and still suffer blood sugar issues, hoarse voice, cold etc, despite having a TSH between 1-2, T4 levels 82-113% in range and T3 levels 39-70%. My FT levels look ‘normal’ but at a cellular level I’m not okay. Levo has severely affected my body’s rate of conversion. Adding T3 to my Levo doesn’t quite work as I thought it would, simply ‘topping’ it up. Only it seems to put the breaks on conversion when I start adding T3.I’ve tried lowering Levo to 75, 88, an increasing to 100, now trying 94. I don’t see how I will ever get the amount of T3 I need with any significant amount of T4 in the mix, but I am dreadfully afraid to lower the T4 because I develope anxiety, Insomnia, and myxedema very quickly.

    1. Dear Janiece, thanks for your comment. It is always enlightening to see examples of patients’ therapy experience over time. Yes, it is a struggle for many of us, and complex patients often need to mix and match thyroid pharmaceuticals and even different brands or compounded versions, to find out what works for our bodies. Sometimes one organ or system will dislike the FT4 level or the FT3 level while the rest of your body tolerates a wider range of FT4-FT3 levels and ratios.

      If you haven’t already tried it, you might want to try combining desiccated thyroid (NDT / DTE) with synthetic T4 or T3 to adjust its ratio. The body responds differently to thyroid hormone absorption via GI tract when it is coming in bound to porcine thyroglobulin protein, not just as a sodium salt. Synthetic vs. porcine sources of T3 appear to change the post-dose peak FT3 profile and its subsequent trigger of D3 and D1 enzymes in our cells, which can alter T3’s rate of metabolism into three types of T2 as well as affect T4’s metabolic pathway.

      More studies are needed on the comparative pharmacology of DTE and LT4 / LT3 medications, but scientists fearing for their own careers shy away from the analysis of desiccated thyroid pharmaceuticals because of the pharmaceutical prejudices among their peers. It’s so silly to be prejudiced against a porcine source, since heparin is a respected porcine-derived blood thinner used for decades in hospitals – Tania S. Smith

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