If you truly care to help, optimize my Free T3. Listen to the research.

My-thyroid-is-deadOur image makes strong claims that Free T3, not TSH, needs to become the main target in thyroid therapy.

It is based on three scientific articles in 2015, 2016, and 2018 by a team of four thyroid researchers. I summarize and quote them here.

(1) “My free T3 is at risk”

This research reveals the human body prioritizes the protection of FT3 levels. The healthy body does so by stimulating the thyroid gland to keep bloodstream FT3 levels steady.

However, in T4 monotherapy, Free T3 levels become destabilized.

Therefore, the standard thyroid therapy is unable to regulate FT3 levels like a healthy thyroid gland can.

TSH levels are not capable of judging FT3 status in treated patients. Thyroid patients can have Free T3 and TSH both simultaneously below range on LT4 therapy. In some patients, the higher the T4 dose climbs, the lower the FT3 becomes. This paradox is absolutely impossible outside of thyroid therapy. It does not fit the model of the HPT axis outside of therapy.

(2) “I don’t convert T4 well”

Thyroid patients vary widely in their ability to convert T4.

Free T3 levels are more likely to be lower if you have very little to no thyroid gland tissue.

Poor converters of T4 hormone have a significantly lower Free T3:T4 ratio. The higher their FT4 is, the lower their FT3 is.

Everyone on T4 therapy has a lower ratio than healthy patients who are not on therapy.

Therefore, T4 therapy does not function effectively as a thyroid gland replacement, and T4 therapy can cause serious thyroid hormone imbalances leading to chronic FT3 deficits in poor converters.

(3) “Normalizing my TSH won’t help.”

This research discovered that “an LT4 (Levothyroxine) dose sufficient to maintain TSH within its reference range could not raise FT3 adequately in the majority of treated patients.”

Maintaining TSH in range simply can’t raise FT3 enough for most people on T4 therapy. They found that the majority of LT4-treated patients have “FT3 concentrations in the lower range.”

Thyroid patients’ suffering from hypothyroid symptoms is strongly associated with lower Free T3 levels, but weakly associated with Free T4 or TSH levels.

Hypothyroid symptoms increased significantly below a Free T3 level of 5.0. (reference 3.1 – 6.8 pmol/L).

At the other end of the FT3 reference range, hyperthyroid symptoms on LT4 only occurred with Free T3 levels over 7.5 pmol/L.

Also, as many as 1/3 of their post-thyroidectomy patients had FT3 levels below reference range, despite a T4 dose that suppressed their TSH.

The scientists therefore recommend testing Free T3 and targeting Free T3 levels in therapy:

A LONG QUOTATION [with paraphrases]:

  • LMDH = Larisch, Midgley, Dietrich, and Hoermann
  • TPC = [Paraphrases by Thyroid Patients’ Campaign researcher]

LMDH: “Owing to the altered interactions of the three functional parameters in therapy, decision-making criteria must be revised significantly.”

TPC: [Because TSH, FT4 and FT3 interact differently in thyroid therapy, we can’t continue to use old medical decision-making criteria based primarily on TSH, and occasionally FT4.]

LMDH: “A compromise must be sought that simultaneously promotes attaining relief of hypothyroid complaints and avoidance of hyperthyroid symptoms.”

TPC: [The goal of thyroid therapy should be to alleviate relief of symptoms of hypothyroidism and hyperthyroidism, not merely to normalize TSH levels.]

LMDH: “From present data, TSH and FT4 concentrations appropriate for clinical euthyroidism differ considerably in therapy from their respective euthyroid ranges, thereby compromising their diagnostic aim in invariably defining true euthyroidism.”

TPC: [in other words, TSH and FT4 reference ranges can’t define thyroid hormone balance under the conditions of therapy. The normal reference ranges that apply outside of therapy are unable to diagnose a person’s true status on thyroid therapy. ]

LMDH: “Since FT3 seems to be less affected in this regard, optimum therapy may be best approached by maintaining adequate FT3 levels and, if required for symptom relief, elevating FT3 above the median, though remaining within its euthyroid reference range of healthy controls.”

TPC: [Adequate FT3 always remains the body’s target whether you are on therapy or not. The importance of FT3 is maintained. Suffering is associated with lower Free T3.

TPC: Adequate FT3 should be defined as the median, or average, for healthy controls, which is around 5.2 pmol/L or just above mid reference range, and if necessary to relieve symptoms, patients should be able to access FT3 levels that are above the statistical average of 5.2. ]

LMDH: “While the altered biochemical equilibria have been well documented this study adds further clinical significance to the previous biochemical findings by demonstrating their close association with patient complaints.

TPC: [This alteration in thyroid hormone relationships is not news. Thyroid researchers have known about it for a long time but have failed to study its clinical significance. Our study demonstrates further that Free T3 levels are indeed clinically significant to thyroid patients.]

LMDH: “The highly individual boundaries that indicate the ‘optimum homeostatic compromise’ have to be defined more exactly for a given population and a particular assay by further study, but it becomes increasingly clear that the lower reference limit of TSH may be an unphysiological arbitrary cut-off for diagnosis of LT4-treated patients.”

TPC: [We need more study on Free T3 and TSH levels that are optimal in thyroid therapy because it is highly individualized. Different populations of patients and different lab test technologies will make the targets variable. One thing is clear: the low boundary of TSH has to be re-thought for thyroid therapy. The low TSH cutoff may not be a boundary that makes biological sense in thyroid therapy.]

OUR CONCLUSIONS

Normalizing TSH in therapy neither helps our bodies normalize Free T3 levels nor helps us get rid of hypothyroid symptoms.

Hypothyroid symptoms associated with lower-than-average T3 persists far below the TSH reference range.

We have to stop judging thyroid patients’ therapy by the TSH and FT4 reference ranges.

The true target of thyroid therapy should be the FT3 median level found in healthy people, and FT3 should be even higher when necessary for an individual’s symptom relief.

REFERENCES

1. Hoermann, R., Midgley, J. E. M., Larisch, R., & Dietrich, J. W. (2016). Relational Stability in the Expression of Normality, Variation, and Control of Thyroid Function. Frontiers in Endocrinology, 7. https://doi.org/10.3389/fendo.2016.00142

2. Midgley, J. E. M., Larisch, R., Dietrich, J. W., & Hoermann, R. (2015). Variation in the biochemical response to l-thyroxine therapy and relationship with peripheral thyroid hormone conversion efficiency. Endocrine Connections, 4(4), 196–205. https://doi.org/10.1530/EC-15-0056

3. 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, 126(09), 546–552. https://doi.org/10.1055/s-0043-125064

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