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Risk of testing only TSH outweighs risk of pharmaceutical errors
The “risk” of a lower FT4 level during desiccated thyroid therapy, or synthetic combination T4-T3 therapy, would be completely eliminated by measuring FT4 levels during pregnancy.
Researchers also acknowledge that monitoring only TSH during combination therapy brings risk to pregnant women.
Summarizing the 2012 ATA and AACE Hypothyroidism guidelines by Garber et al, Foeller and silver write
“The authors propose that, in combination L-T4 + L-T3 therapy, excess T3 often acts to normalize TSH while lowering T4, thereby risking inadequate T4 availability to the fetus.”
Foeller and Silver, 2015
It is true that a higher T3: T4 level can “normalize TSH” while allowing T4 to fall too low during DTE or synthetic T3-T4 therapy.
However, Foeller & Silver’s wording “excess T3” is fallacious.
In T3-inclusive therapy, it certainly does not require “excess T3” — if by that, one means beyond reference — to normalize TSH when T4 is low.
Such a statement reveals ignorance of the range of patient response to DTE and the situations in which the pumped-up “exquisite sensitivity” of TSH becomes an overreaction.
In fact, the TSH may even be fully suppressed in some patients whose T4 and T3 levels do not exceed reference limits.
In addition, neither T3 nor T4 mildly over reference can be defined as “excess” in a pregnant woman, according to the research cited above.
Foeller and Silver go on to summarize ATA guidelines,
“They caution that if the provider monitors only TSH levels in his/her patient, maternal hypothyroxinemia may go undetected, placing the fetus at risk for delayed intellectual development because the fetus is dependent on maternal T4 as a primary substrate.”
Foeller and Silver, 2015
You see, the problem happens if the provider monitors only TSH levels.
A health problem does not happen because of any intrinsic flaw in DTE medication such as its supposedly “supraphysiological” T3 content. My calculator tells me that 100% levothyroxine and 0% liothyronine is an equally supraphysiological ratio of T4.
Desiccated thyroid medication has been saving women from adverse maternal and fetal health outcomes ever since it was first manufactured, and this medication can still do it when dosed properly to FT4 and FT3 and health outcomes.
The problem is the way we force a square peg, DTE, to fit into our TSH-constructed round hole. A safe, effective, and flexible medication is a mismatch for a broken, blind, narrow system.
It’s not the fault of DTE medication when FT4 levels fall low while a system trains doctors to look only at TSH. The contrary paradigm, which holds that thyroid hormones FT4 and FT3 should always veto the TSH in the context of thyroid therapy, is offensive to TSH-worshippers. It takes TSH off the pedestal.
This system has been designed to make its old pharmaceutical nemesis DTE therapy fail — at the cost of women and babies. Don’t play their cruel game.
Acella’s recall notice: Ethics, clarity, focus
Acella should not imitate thyroid guidelines’ sweeping, fearmongering statements about maternal risk due to “superpotent” DTE.
A single vague sentence in the recall notice plants the seed of fear without explaining the conditions under which such risk would apply.
“Pregnant women who take superpotent NP Thyroid may also experience negative maternal and fetal outcomes including miscarriage and/or impairment to fetal development.”
Acella, NP Thyroid Recall 2020
It almost sounds like a rabid anti-DTE proponent wrote this sentence hoping to scare patients and clinicians away from desiccated thyroid, the very product Acella is offering.
Blaming “superpotent NP Thyroid” simply does not make sense. The risk to maternal outcomes has little to do with a “superpotent” batch containing 1.035 bonus mcg of LT3. The risk is the fault of TSH-test worship.
In this particular recall statement, there is no call for this sentence at all. Just leave it at the risk of hypothyroid or hyperthyroid signs and symptoms in general.
Alternatively, dear Acella, you could have simply explained that risk only increases “if FT4 levels fall low as a result of an elevated T3:T4 ratio.”
Indeed, it would be helpful to nudge people to monitor FT4 and understand that any increased level of FT3 does not always “cause” FT4 to fall. Many patients only have one source of T4 — the tablet.
Conclusion: What we can do
The recall is an opportunity for us all to thank and respect Acella for their responsible behavior. It’s also an opportunity to learn about aspects of thyroid pharmaceuticals, our individualized response to them, and the hyper and hypo sides of pregnancy risk.
Levothyroxine, liothyronine, and desiccated thyroid preparations have experienced, and may continue to experience, manufacturing errors from time to time.
We have ways of dealing with this, in addition to strict quality control and issuing recalls when necessary.
Risks to human health can be minimized as doctors learn how to monitor and adjust the patient’s FT3 and FT4 levels, not just their TSH, to optimize thyroid therapy to the individual patient.
The simplest thing to do is to remove clinical ignorance, denounce anti-DTE pharmaceutical prejudice, and to fight against harmful policies that cancel FT4 and FT3 whenever TSH is normal.
1. Monitor FT3 and FT4 levels during thyroid therapy to ensure true euthyroidism is achieved, and that T4 sufficiency is maintained in pregnancy. This holds true for LT4 monotherapy as well as DTE therapy. However, it is more important for DTE therapy because the TSH can be falsely normal when hypothyroid and TSH can be falsely low when euthyroid. (Saberi and Utiger, 1973)
Shout it from the rooftops that TSH can be bribed by therapy to lie about one’s serum thyroid hormone status. Tell people that a LT3-bribed TSH will ignore a low FT4 level in DTE therapy, just as LT4-bribed TSH will ignore a low FT3 level in levothyroxine monotherapy. The former lie can harm a baby, and the latter can harm a hypothyroid person for the rest of their life.
2. Clinicians, learn not to fear “subclinical hyperthyroidism” (isolated low TSH with normal FT3 and FT4) as always harmful, because it does not necessarily mean “thyrotoxicosis.” Science teaches us that the TSH is biased lower in therapy, and as a result, a lower TSH is often necessary to achieve true euthyroidism even in LT4 monotherapy (Larisch et al, 2019; Hoearmann et al, 2020).
Of course, when TSH suddenly falls low at the same dose, take the opportunity to check for other causes:
- a) central hypothyroidism (which can appear during therapy),
- b) a relapse of Graves’ or the onset of Graves’ disease TSAb antibodies, which can cause fluctuations during therapy or
- c) hypersecreting nodules that could be inflating T3 far more than the medication can, thereby lowering TSH.
3. Help disseminate scientific knowledge about benign high T3/T4 and harmful low T4 in pregnancy. In our medical culture, lopsided fears of elevated T3 and T4 should become properly balanced with fear of Low T3 and Low T4. We must be vigilant to prevent thyroid hormone deficiency.
We can each do our part. Healthy DTE dosing is a partnership between patients, doctors, and pharmaceutical companies.
- Patients need to know enough to advocate for their health and the health of their unborn child when doctors are clueless about DTE distortion of TSH and laboratories are cancelling essential hormone tests.
- Clinicians who supervise DTE therapy should be responsible for learning how DTE doses are monitored and raised appropriately during pregnancy.
- Other thyroid hormone pharma manufacturers should follow Acella’s lead in quality control and transparency.
- Any DTE product information leaflet should recommend testing beyond TSH, given what Utiger learned and what all informed DTE patients and doctors already know about its bias.
Read Part 1:
References
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