Cancer scientists point finger at T4 & RT3 hormones

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Responses to this research

Despite the hope and the caution, the medical community prefers to do something very different than therapeutically or preventively reduce T4 concentrations.

1. Cancer therapy chooses a more lucrative pathway

Research articles are being published about ways to block the integrin αvβ3 receptor that T4 and Reverse T3 activate to make cancer cells grow. They want to develop an additional blocking drug that can be marketed to cancer patients. In a similar way, arthritis patients who are prescribed Diclofenac are routinely also prescribed a protein-pump inhibitor (PPI) to mitigate the gastrointestinal damage that can be done by the drug.

However, LT3 therapies are available today, and integrin αvβ3 receptor blockers are not yet available and on the market. When they are available, they will likely be expensive.

Excluding the inflated cost of LT3 in the UK, what is the average cost of LT3 therapy in Germany, France, Canada, US, Thailand, Mexico and Turkey compared to surgeries and chemotherapy and a potentially shorter lifespan?

The degree of human suffering involved in a cancer therapy is something to ponder. When cancer therapies are offered to people without damaged or removed thyroid glands, why would people rather engage in surgeries and chemotherapy than alter their thyroid hormone concentrations by replacing T4 with LT3 hormone, when there is rarely any human suffering involved in the latter therapy if you have a doctor that knows how to render you truly euthyroid on LT3?

2. Thyroid therapy retrenches its paradigm

Thyroid therapy leaders are also largely ignoring or diminishing this research, not because of profit. Levothyroxine is cheap and there is no further drug development necessary. It is because of a staunch attitude of conservatism.

First of all, a conservative stance of medical isolationism or departmentalization points to the fact that people who suffer cancer do not necessarily have a thyroid gland productivity problem. They have a healthy thyroid, pituitary and hypothalamus. Those people are not supposed to take thyroid medication because they have a thyroid hormone supply. It’s considered not indicated, non-physiological and potentially harmful just because they have functioning equipment.

However, this stance does not take into account the dysfunctional and pathological response to normal T4 thyroid hormone in Cancer.

Of course thyroid hormone derangement can occur and cause widespread health problems even while a thyroid gland and HPT axis is healthy.

There is no law of medicine that says one must protect the healthy HPT axis when altering it can extend someone’s life or prevent harm.

Clearly, this prohibition of thyroid hormone therapies to people with non-thyroidal illnesses is a defensive, territorial, imaginary barrier created by departmentalizing the human body organ by organ and disease by disease, ignoring the derangements that occur when thyroid hormones interact with cancer cells. Cancer does not respect the political boundaries we erect between medical departments. Both thyroid hormones cross all barriers in the body.

Secondly, a major barrier is conservatism within thyroid therapy, a defense of therapy policy decisions made in the 1970s and 1980s.

It is still acceptable to raise T4 concentrations to suppress or lower TSH secretion in high-risk thyroid cancer patients. This is based on the understanding that some cancer types and pathways of cancer development are “TSH-dependent” because of TSH’s direct effects on thyroid cells (Fiore & Vitti, 2012).

It may indeed be true that “patients take advantage of TSH suppressive treatment with LT4 with a decreased disease progression, recurrence rates, and cancer-related mortality” (Fiore & Vitti, 2012).

But could decreases in cancer be even greater with the use of T3-dominant therapies that also suppress TSH?

If both TSH and T4 are implicated in cancer, T3 therapy is effective at suppressing TSH while also lowering T4, achieving both goals at once in thyroid cancer patients.

In contrast, the status quo is not very attractive. Given the research done by Hercbergs and Davis, there is reason to believe LT4 monotherapy is the more risky means of achieving TSH suppression. Science has long known that today’s standard thyroid therapy modality raises T4 concentrations significantly above the population mean while reducing T3 concentrations below the mean, even while both hormones usually stay within reference range (Midgley et al, 2015).

Today, given the dose-dependent effect of T4 at this receptor throughout the normal FT4 reference range, endocrinologists should be concerned about cancer risk being higher in hypothyroid patients being treated with T4 monotherapy compared to people treated with T4-lowering T3-dominant replacement therapies.

What else would hold endocrinologists back from offering T3 monotherapy to hypothyroid patients on therapy who have no cancer yet, but risk of cancer?

LT3-induced “euthyroid hypothyroxinemia” is directly opposite to the kind of monotherapy currently promoted by thyroid therapy guideline-writers. The tradition since the 1980s is to prefer the use of synthetic T4 monotherapy and to defend it at all costs while casting fear and disapproval on therapies involving the dosing of T3 hormone, which can reduce T4 concentrations.

This choice to stand with tradition at all costs is just another chimaera standing in the way of medical progress and harm reduction.

Why must we perpetuate a warfare between two or three bioidentical thyroid hormone pharmaceuticals when none of them are intrinsically harmful except when underdosed or overdosed or when its use worsens another illness such as Cancer?

This old thyroid pharmaceutical war might have served industry or medical interests in the 1970s and 1980s, but whose interests does it serve in 2020? Drugs like Humira now make far more profit than Synthroid does for Abbvie, if you look at their financial reports. Many generic brands of Levothyroxine have arisen to compete since 2000.

On the medical evidence front, the belief that T4 monotherapy is superior to all other forms of thyroid therapy was never derived from any double-blind studies comparing long-term health outcomes between levothyroxine alone and the wide range of T3-dominant therapy alternatives that were in common use. No such studies were done in the 1970s or 1980s, only polemical studies that attacked other bioidentical hormones for having different biochemical profiles. The superficial bickering continues to act as a smokescreen for the lack of core evidence of LT4 superiority. Look in the thyroid clinical guidelines and you will find no such comparative health outcome studies cited.

The very first double-blind controlled comparative study of desiccated thyroid and LT4 occurred in 2013 by Hoang and colleagues, and it proved neither therapy was superior to the other in terms of short term outcomes and biochemistry, not long term health outcomes.

Even more importantly for our most vulnerable patients, no evidence proves LT4 superiority over desiccated thyroid or T3 monotherapy at critical junctures in life and death, such as the ability to recover from a critical nonthyroidal illness like a stroke, heart attack, or kidney failure without a thyroid gland. Instead, treated thyroid patients have been excluded from almost all studies of nonthyroidal illness.

Likewise, no one has proven the superiority of LT4 monotherapy over T3-based therapies within chronic illnesses like type 1 diabetes, adrenal insufficiency, heart failure, or liver failure, or cancer.

An entire field’s reluctance to perform this essential comparative research on health outcomes in extremely vulnerable patients is proof of its reluctance to risk a favorite therapy from being proven inferior in certain dire circumstances.

Resources for effective and safe euthyroid hypothyroxinemia

Fortunately, there is knowledge within the field of thyroid science and clinical practice to guide effective and safe “euthyroid hypothyroxinemia” as proposed by Hercbergs.

T3 monotherapy has long been used in six to eight weeks of preparation for radioiodine (RAI) ablation of thyroid fragments after thyroidectomy for thyroid cancer patients. At least since the late 1970s (see Busnardo et al, 1980, 1983) and even today (see Celi et al, 2010, 2011 and Yavuz et al, 2013), it has been viewed as more compassionate to use T3 monotherapy in this circumstance. This is because using the more quickly-dissipating T3 hormone significantly reduces the duration of hypothyroidism when thyroid medication is withdrawn to raise TSH prior to RAI therapy. (See some of Busnardo’s, Celi’s & Yavuz’s graphs and findings discussed our article on Free T3 peaks and valleys.)

One may also follow confident consensus of those who have mastered T3 monotherapy in the past, such as those who gave guidance on dosage equivalency to LT4 (Selenkow & Rose, 1976; Refetoff, 1975; Chopra et al, 1973; Green, 1968) – see their equivalency tables showing T3 monotherapy dose here.

And finally, even today, a global community of thyroid patients is maintained long term on T3 monotherapy; they flourish as leaders provide online communities and books to support their safe titration of LT3 (Robinson, 2018). This community of patients may be consulted and studied at any time if approached with respect by honest, unbiased researchers.

  • Tania S. Smith

References: on Page 3

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Categories: Cancers, T4 hormone

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