Biochemical bigotry: Enforcing normalized thyroid lab results

Valentine’s day is a good day to attempt to promote kindness and tolerance toward people suffering from a rather invisible health condition. Thyroid disease.

What better day than today to identify and attempt to remove a medical attitude that is a barrier to effective thyroid therapy … “biochemical bigotry”?

Most doctors take for granted that the target of thyroid therapy is to normalize levels of TSH, the Thyroid Stimulating Hormone, secreted from the pituitary gland.

Since the 1980s, as thyroid lab tests were being developed refined, doctors have understood that normalizing the TSH will likely normalize the two major thyroid hormones, Free T4 and Free T3, within their reference ranges as well.

For as many decades, the medical system has taught doctors and patients that therapeutic thyroid biochemistry ought to be judged by exactly the same standards as normo-thyroid people’s biochemistry.

This belief system is paved with charitable motives to restore health, but a presumption that imitating the biochemistry of the healthy population can remove disease can be deceptive and seductive.

In medical terms, the normalization of TSH and Free T4 is called a “surrogate endpoint.” This surrogate endpoint of biochemical normalization has often replaced the ultimate clinical endpoints of euthyroid health outcomes.

Health outcomes of therapy ought to include evidence such as the removal of inexplicable depression and anxiety, debilitating fatigue, cognitive dysfunction, hair loss, tremor, or atrial fibrillation. These outcomes are not always achieved anywhere within the normal reference ranges for TSH or thyroid hormones.

This widespread presumption that thyroid hormone normalization is synonymous with full restoration of thyroid hormone health sows the seeds of “biochemical bigotry.”

I choose to use the hot-button word of “bigotry” because the discrimination that thyroid patients often experience is real. It is often rendered invisible because the drive to normalize is so pervasive and taken for granted in many areas of medicine.

Nobody, especially a doctor with sincere compassion and ethical integrity, wants to admit they might be guilty of bigotry toward a class of patients or individual patients.

However, it sometimes takes an analogy with political and social injustice and suffering to bring medical discrimination against thyroid patients into the light so that it can start to be removed.

In this post, I’ll define the concept of biochemical bigotry and its pervasiveness within thyroid health care. I’ll talk about both rare and common ways in which the thyroid hormone economy can become abnormal. We may need to accommodate the individual’s health condition by viewing euthyroid thyroid biochemistry differently. In this context, it becomes clearer how rigid, normalization-based thyroid therapy guidelines and attitudes can promote biochemical bigotry, and how illogical, unjust, and harmful this bigotry can be to the health of thyroid patients.

To prevent us from wallowing in inactive despair, I will end by pointing to the light at the end of the tunnel and calling us to action.

Biochemical bigotry?

The word “bigotry” is defined by Google’s dictionary as

“intolerance toward those who hold different opinions from oneself. Example: “the difficulties of combating prejudice and bigotry.”

With a slightly different angle, the Cambridge dictionary says bigotry is

“the fact of having and expressing strong, unreasonable beliefs and disliking other people who have different beliefs or a different way of life: religious/racial bigotry.”

Biochemical bigotry in thyroid therapy is a rigid and intolerant belief about normal thyroid hormone biochemistry being the only acceptable standard and target for thyroid therapy.

Biochemical bigotry refuses therapeutic accommodations because they look abnormal and different from a population of people that has all their thyroid hormone equipment working.

Biochemical bigotry dismisses the special needs of the thyroid-disabled individual.

The biochemical bigot takes descriptive statistics in the healthy population and applies them as if they are also Nature’s prescriptions for the disabled.

Biochemical bigotry refuses to allow concentrations of TSH, T4 and T3 to fall outside their reference ranges even if it is for the benefit of the individual’s health. Their belief system can’t compute the possibility that health may coexist with abnormal thyroid biochemistry.

Biochemical bigotry, rather than long-term proof of health outcomes, was a driving force in persuading doctors to move their patients away from the former gold standard therapy of desiccated thyroid and toward TSH-normalized levothyroxine monotherapy in the 1970s.

Today, biochemical bigotry is often a justification for thyroid pharmaceutical prejudice, the practice of debasing or forbidding the use of some bioidentical thyroid hormone preparations in favor of others. A fully equipped health care system needs all three subclasses of thyroid hormone agents (LT3, LT4 and desiccated thyroid) to remain accessible as therapeutic tools.

However, there are often healthy exceptions to norms when we lose a vital part of our body or suffer from a disorder. We may need a prosthesis, or a wheelchair, or a pharmaceutical, or some other accommodations in life.

All therapeutic accommodations can be abnormal and artificial.

Unfortunately, an accommodation like a wheelchair makes the disability more evident. Whoever sees the visible accommodation has a choice to either respect the person’s uniqueness and accommodate it, or to devalue the person’s divergence from normalcy and refuse to accommodate.

Doctors are taught that normalizing biochemistry eliminates both hypothyroidism and thyrotoxicosis. However, what it sometimes does is render unresolved tissue hypothyroidism invisible.

This is likely the main reason why an enlightened nation like Canada has not yet acknowledged thyroid disease as a chronic disease. They think we’ve been fixed. We’ve been biochemically normalized. Our thyroid disease and its normalizing therapy can’t possibly be making our other chronic diseases worse. Unexamined assumptions are dangerous.

Some accommodations are already permissible.

Some of the rarer disorders in thyroid disease already get biochemical accommodations once thyroid experts diagnose them.

Thyroid experts know that certain genetic conditions like Resistance to Thyroid Hormone (RTH) exist, in which thyroid hormone receptor beta (THRB), or less commonly, alpha (THRA) is less sensitive to thyroid hormone. This condition will require a person to have higher than normal levels of circulating thyroid hormone. The degree to which T4 and/or T3 need to be maintained above reference range depends on the person. Diagnosis of RTH, however, is difficult and requires a doctor to know what biochemical patterns to look for within and outside of therapy.

Central hypothyroidism gets an accommodation. TSH is allowed to be suppressed because it can’t be trusted. But like RTH, you need to be lucky enough to have a doctor diagnose you by testing TSH and FT4 and knowing what to look for.

Lesser known thyroid conditions: no accommodations yet

Other rare thyroid disorders are more difficult to see and accommodate, such as

Read more about the third type of Autoimmune Thyroid Disease at https://thyroidpatients.ca/2018/12/27/the-third-type-of-autoimmune-thyroid-disease-atrophic-thyroiditis/

Thyroid disability requires biochemical adaptation

The thyroid hormone system is immensely adaptible, as long as you have a healthy thyroid gland, hypothalamus, and pituitary to help you adapt.

When one or more of these are lost, you can’t adapt well, and you need to rely on hormone dosing as the adaptive variable.

After thyroid or central gland failure, when a person loses normal HPT axis function and goes on thyroid hormone therapy, the physiology of thyroid hormone economy changes. The TSH-T3 disjoint often begins to appear, a pattern often found in LT4 monotherapy in which the TSH no longer represents normal euthyroid TSH-T4-T3 relationships.

A damaged, removed or shrivelled thyroid gland can no longer function as a thyroid hormone converting organ as blood flows through it. In addition, the metabolism shifts to respond to the type and amount of hormone you are dosing.

When you rely on thyroid hormone dosing, you are then more vulnerable to the health or dysfunction of your thyroid hormone metabolism and the health of other organs that now carry more of the burden of T4-T3 conversion.

Are your deiodinases genetically handicapped? It is after thyroid failure that you will see whether or not your deiodinases can help you maintain high enough Free T3 levels if all you are permitted to dose is T4 hormone.

Can your thyroid hormone economy be more vulnerable to distortions from concurrent diseases such as heart, liver or kidney disease? Yes, because liver and kidney influence thyroid hormone conversion rate, and a disease or shock to these organs or the cardiovascular system can significantly increase one’s thyroid hormone inactivation rate by strengthening Deiodinase type 3 (which converts T4 to RT3 as well as T3 to T2).

With a genetically handicapped or imbalanced thyroid hormone metabolism, you really must carefully optimize thyroid hormone levels to the individual and not hold too tightly to reference range boundaries as if they are prescriptive laws or limits. Once you already have thyroid disease, using thyroid therapy to cross a statistical reference boundary does not always cause or worsen thyroid disease or other diseases. It might actually improve some things.

In the context of thyroid disease and therapy, thyroid hormone and TSH reference ranges have a very different function. They become landmarks. They are useful for understanding relative changes over time in relationship to a stable standard. External landmarks are helpful when your built-in hormone compass can’t be trusted anymore.

You will need permission to move beyond the boundaries if or when your disability requires the accommodation.

Accommodation within reference range

Fine tuning hormone levels to the individual (optimizing therapy) is very important when you don’t have TSH autopilot doing the fine tuning for you within the reference range.

Even once thyroid hormone levels are within reference range, small accommodations can make a huge difference for health. In full thyroid health, the FT3 reference range of an individual is extremely narrow, and its level within the population range is not predictable. What happens in thyroid disease? Does that range become narrower for some people and wider for others? Perhaps those with concurrent disability to regulate cortisol will not have as much tolerance for fluctuation.

Finding optimal levels

It is disheartening to some thyroid patients to hear the message that there is no universal “optimal” Free T3 and Free T4 that applies to all thyroid patients on a particular therapy. Standardized targets can be deceptively comforting to both doctors and patients.

There are only common principles, such as a high-normal TSH and/or a low-normal FT3 often confirming tissue hypothyroidism while on therapy.

Some poor converters of T4 hormone who suffer from very low FT3: FT4 ratios on LT4 monotherapy can have their low conversion rate diagnosed by programs like the SPINA-Thyr app. These patients may benefit greatly from the reduction of the Free T4 they aren’t efficiently converting, and an elevation of Free T3 to the upper part of reference or even mildly above reference to compensate for their lower FT4.

(Learn more about the imprecision of statistical norms — their poor fit to individual norms even outside of thyroid therapy. )

Many patients who completely lack thyroid function suffer no harm by lowering or suppressing TSH in therapy if their FT4 and FT3 are monitored to prevent excess in either, just as a person with a suppressed TSH due to central hypothyroidism is not necessarily harmed by TSH’s absence.

On the other hand, many people who still rely on some thyroid gland function will benefit from some degree of TSH stimulation of that gland fragment to supply enough T3 hormone that their medical system may not be willing to provide as a pharmaceutical.

Beyond those generalizations, individuals’ unique genetics and concurrent health conditions will always create puzzling exceptions in which lower thyroid hormones do not induce symptoms of hypothyroidism. Sometimes a healthy state is achieved by natural backup systems, at least until the compensatory mechanisms fail.

If you try to target levels and ratios that work for other thyroid patients or target the statistical averages found in normo-thyroid health, you may discover once you get there that their optimal is not your optimal.

This is why we need freedom and support from peers, from science, and expert thyroidologists to help us discover where our individual optimal thyroid hormone levels and ratios fall.

The fallacies underlying biochemical bigotry

Once you consider all the adaptations that could be needed in thyroid disease and dosing, you can see how punitive, unhealthy and discriminatory it is to forbid biochemical accommodations and force statistical biochemical normalcy on all thyroid patients.

Yet this is often what thyroid therapy guidelines have done. Forbid therapeutic accommodation beyond, and fine tuning within, normal biochemistry.

To medical people taught to respond only when biochemistry is out of range, the biochemically abnormal is too often presumed to be unhealthy.

It is an essentially naive and “ableist” belief that making a thyroid-disabled person’s TSH, T4 and T3 biochemistry fit anywhere in the broad statistical reference ranges will remove the state of hypothyroidism from their tissues.

This approach to laboratory test normalization is a fallacious fantasy of “undoing disease” by medically inducing conformity to the norms of able-bodied persons. 

The biochemical bigot presumes that health risk always exists outside these statistical norms while safety always exists within them, regardless of major alterations in a person’s physiology that may prevent them from benefiting from this supposedly perfectly normal biochemistry.

It is like the Humpty Dumpty nursery rhyme and cartoon, in which the egg-man falls off the wall and shatters, and the king’s men try to put his shell together again, but fail to do so.

Allowing Mr. Humpty Dumpty to get a prosthetic shell that is misshapen or lopsided would not be permitted by the simpleminded king’s men in the tale.

They believe his health must be achieved by forcing him to conform to the classic egg shape on the superficial outside even if his insides are now distorted as well as the outsides after the injury.

The injustice of biochemical bigotry

Thyroid patients lack choice and agency to request accommodations, and this is an ethical failure of the rigidly controlled thyroid therapy system.

Sometimes increased health risk coexists with benefits beyond the reference ranges. Risk-benefit consultations with the patient are common in therapies in other diseases, but in thyroid therapy they tend to be denied. We can’t even sign an informed consent form to obtain our optimal, out-of-reach thyroid levels — the door is slammed shut and we’re considered an obstacle to our own therapy.

(Read our rebuttal of a recent American Thyroid Association article that blames thyroid patients for being barriers to their own therapy when requesting reasonable accommodations for their disability. )

In thyroid therapy, decisions are more often paternalistically made on our behalf by administrators and leading endocrinologists at a system-wide level.

For instance, patients diagnosed with risky types of thyroid cancer are usually permitted to have their TSH suppressed because there is evidence that TSH can trigger thyroid cancer regrowth. This entails risk, because low TSH may sometimes be a sign of T4 overdose that may also increase risk of cancer proliferation or osteoporosis, and yet there is still no evidence that low TSH alone causes osteoporosis. Such major risk-benefit decisions ought to involve the thyroid patient’s informed consent, but they often do not.

We often can’t give consent for our therapy because only one therapy may be forced on us based on where we live and the policies and doctors’ attitudes in that region.

Being permitted only the use of the LT4 pharmaceutical severely limits the tools available to achieve individualized therapeutic accommodations in our biochemistry.

Diabetes type 1 patients are often given the tools to micromanage their own dosing of fast-release and slow-release insulin and other medications on a daily basis, but thyroid patients are kept on a strict leash and budget. We don’t get implanted T3 monitors and we aren’t trusted to read our symptoms.

We often can’t request tests because administrators forbid them, or doctors refuse to order them, or Free T3 tests are cancelled by people who know nothing about our unique disabilities and presume we don’t need such tests.

Image source: BC Guidelines, British Columbia, Canada

Admittedly, some symptoms of hypothyroidism can mimic those of thyrotoxicosis, and thyroid patients can experience a concurrent mix of hypo and thyrotoxic symptoms at the same time. How can we confirm that we’re adjusting our biochemical levels in the right direction if we can’t test Free T3 and T4 when TSH is within reference to see whether we have hindered our T4-T3 conversion, enhanced it, or replaced it enough with T3 dosing?

Why are policies cancelling access to the most relevant evidence?

When the thyroid patient is not permitted to optimize hormone ratios and levels within reference range, it is usually because doctors think it is too trivial and unnecessary because normo-thyroid people can have huge sine waves in their circadian rhythms of TSH and Free T4. They forget how precise the individual healthy thyroid economy is in fine tuning the most powerful hormone, Free T3, within individualized healthy peaks and valleys on a daily basis.

The tools necessary for the customization of the therapy to the patient are stolen from us by guidelines that promote and justify biochemical bigotry.

Where is the evidence of health outcomes?

The replacement of health outcomes with biochemical normalcy is a recipe for deeper chronic illness among those who already have thyroid disease as a chronic illness.

Such policies can make thyroid patients more vulnerable to other illnesses that won’t be acknowledged as thyroid-hormone caused illness whenever the TSH, Free T3 and Free T4 are normalized. When our biochemistry looks normal, our status of thyroid disability and illness will be denied when we suffer. Dose adjustments and pharmaceutical alternatives are often denied once we are trapped within these reference ranges.

A system set up merely to normalize biochemistry is not set up to detect its own failure to achieve health outcomes.

(Learn about the “Organ System Manifestations of hypothyroidism & thyrotoxicosis” chapters that have been removed from the endocrinology textbook “Werner & Ingbar’s The Thyroid” https://thyroidpatients.ca/2019/10/02/the-loss-of-thyroid-clinical-knowledge/ )

Where is the evidence in health outcomes that the statistical norms of the normo-thyroid population always provide the prescription and limitation for each and every thyroid patient’s health?

Why should the individual’s “Organ system manifestations” of hypothyroidism or thyrotoxicosis within reference range, or their disappearance outside of range, not be admitted as powerful clinical evidence that can trump the normative statistics of an entirely different population?

I’ve described the thyroid patient’s dystopia. Our worst nightmare is a system of biochemical oppression that serves the system’s own selfish ends, not the goals of health.

Change is possible

There is hope. Consider the ways in which the beliefs and behaviors called up by the word “bigotry” have changed in various parts of the world.

Social change happens. Political change happens. History teaches inspiring lessons about the struggle for change.

Medical change can also happen.

We just have to engage in a public advocacy dialogue outside the power dynamics of the doctor’s office. We can help each other realize how unjust and unscientific are certain standardized, rigid ways of viewing thyroid therapy targets and limits.

We must not allow entire medical systems to enact this harmful programme of biochemical normalization and standardization at all costs.

We must all do our best to rescue fellow thyroid patients who are trapped and suffering from biochemical bigotry, people who may be too brain-fogged and disabled by systemic normo-thyroidism to advocate for themselves.

Every thyroid patient’s life is precious. Our biochemical fingerprint is unique. There are many ways to achieve euthyroid status, just as there are many ways to fail to achieve it.

There is a good reason to celebrate, but no room for complacency, when a thyroid patient achieves their optimal thyroid hormone levels and ratios.

We could be optimal today and then acquire a concurrent health condition that renders our once “perfect” and “optimal” thyroid hormone levels inadequate and in need of adjustment once more.

Will our thyroid therapy system allow us to make the adaptive changes our unique, disabled bodies truly need or will they say “no, your thyroid levels are fine” or “we must reduce your dose because TSH is below reference”?

This is why thyroid patients’ self-advocacy and public advocacy for one another as a group is necessary. Our disease is invisible, so we will always tend to be judged by hormone concentrations and their faceless statistics.

We can be trapped by our disease and our therapy unless we continually remind each other that adaptation and accommodation for a thyroid disability requires flexibility, compassion, and respect for individuals’ euthyroid biochemical diversity.

With sincere hope and encouragement for the work we each do to improve thyroid therapy locally and globally,

Tania S. Smith



Categories: Reference ranges, Therapy paradigms

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