Testing Your Thyroid Function - Everything you need to know!

14 July 2022

When it comes to the diagnosis and treatment of Hypothyroidism, standard laboratory blood tests, especially the analysis TSH levels, have very limited value. Many people have normal TSH levels, yet still experience clinical symptoms. TSH undergoes cyclical elevation and depression multiple times a year and is unreliable, as is fT4 and fT3, as both have such a short half-life. When TSH levels in the blood are used to determine the ‘ideal’ dose of thyroid medication, many patients still remain symptomatic!

A standard blood panel will not predict subclinical peripheral hypothyroidism, meaning that symptomatic patients are often denied treatment that would greatly improve their health and quality of life. By the time TSH is elevated over multiple consecutive points within a year, only then is a diagnosis of hypothyroidism accepted by medical convention. In fact, with the use of Thyroflex, subclinical hypothyroidism can be adequately detected in up to 98.7% of patients and this may precede a conventional biological disruption. Surprisingly, severe autoimmune attacks to the thyroid can also show normal TSH and normal to elevated T3 and T4 levels on a blood panel, further confusing the clinician that the patient is ‘hyper’, as opposed to ‘hypo’ thyroid. Patients can fluctuate from hyper to hypothyroidism and are then considered unstable.

This system of testing and treatment does not match the latest research guidelines for the past 10-15 years. Furthermore, this model fully neglects a systems biology approach. Addressing thyroid inflammation and prescribing biologics or disease modifying drugs is only a small part of the picture, whereas conventional medicine would be more effective by addressing lifestyle triggers and mediators, such as cross-reactive foods and pathogens, immune tolerance, dysglycaemia, chemicals and endocrine disruptors.diagnosis by at least 8-10 years!

Figure 1: Adapted from Datis Kharrazian: Seven problems associated with the conventional medical model of Hashimoto's 

Conventional management of hypothyroidism is poor (see diagram above).

Overt thyroid symptoms such as elevated TSH levels used to diagnose hypothyroidism, treated with T4 therapy, are retested annually. This is a very linear, reductionistic and flawed approach on how to treat and manage hypothyroidism, yet this is the accepted standard in conventional medicine. Furthermore, Anti-TPO and Anti-TG antibodies can be elevated, but are often not measured due to not being covered by Medicare. These autoantibodies that are elevated, may be present for years, causing silent or asymptomatic autoimmunity. By the time the patient has symptoms, there is a whole web of interrelated systems.

Unfortunately, many doctors are not comfortable with diagnosing hypothyroidism based on a patient’s clinical symptoms, especially when their blood tests fall within the normal range. They require more objective evidence that a symptomatic individual is actually hypothyroid before offering treatment.

Thyroflex is a little known and under-utilised method of testing that can be used to make a diagnosis of hypothyroidism, as well as for determining the optimal dose of thyroid medication for symptomatic patients. 

The Thyroflex test, developed by Dr. Daryl Turner, is able to determine a person’s thyroid status based on the measurement of conduction velocity through a tendon reflex.

What could the speed of nerve conduction possibly have to do with Hypothyroidism?

The connection was made late in the 19th century, when doctors studying patients with hypothyroidism observed that clinically hypothyroid patients had very slow or absent tendon reflexes. A tendon reflex is a movement of a muscle caused by the stimulation of a nerve that controls the muscle and causes it to move involuntarily. The speed at which this reaction occurs is an indicator of cellular function. The lower the speed of conduction, the lower the cellular energy and function.

Cellular function is ultimately controlled by T3, the most biologically active thyroid hormone. Low levels of T3 in the cells result in diminished cellular function, which ultimately causes people to suffer with the clinical symptoms of hypothyroidism. Since blood tests cannot measure the level of intracellular T3, one way to objectively test cellular function is by measuring the speed at which a nerve impulse is conducted through nerve and muscle cells. A slow rate of nerve conduction demonstrates low cellular function and confirms a diagnosis of hypothyroidism.

As mentioned, Thyroflex can also be used to establish the optimal dose of thyroid medication for symptomatic individuals. Using the Thyroflex, a clinician can immediately see if the patient’s dose of thyroid medication is adequate by the velocity of their nerve conduction. When slow nerve conduction is found with Thyroflex testing, an increase in the dose of thyroid medication is needed if the patient is symptomatic, irrespective of blood test results. This is especially true when a patient is taking Natural Dessicated Thyroid (NDT), since clinicians unfamiliar with it are often confused by blood test results when patients are taking NDT.

There is an excellent correlation between Thyroflex results and clinical symptoms!

As compared to Thyroflex results, there is a poor correlation between TSH levels in the blood and patients’ symptoms, since approximately 40% of patients on thyroid medication have TSH levels in the ideal range but still experience symptoms!

The Thyroflex records the rate and calibre of the reflex response of the forearm extensor tendon in the arm to identify your resting metabolic rate, brain neurotransmission and synaptic reflex latency, all of which can be affected by low thyroid function, autoimmune hypothyroidism or chronic progressive hashimoto's encephalopathy.

Blood tests alone DO NOT provide a functional quantitative assessment on how these conditions impact muscle metabolism, neuromuscular latency and brain neurotransmitter storage, release and re-uptake.

Figure 2: Adapted from Datis Kharrazian

The above diagram illustrates how Hashimoto's or uncontrolled autoimmune hypothyroidism can lead to serious neurological consequences including but not limited to:

  • The inability to learn new movement or novel activities
  • Brain degeneration, possible leading to Alzheimers 
  • Impaired neurotransmitter function at the brain and spinal cord level, impacting mood, attention, sleep, cognition, memory, brain and muscle endurance capacity and an inability to relax.
  • Nerve entrapments masquerading as muscle and joint dysfunctions
  • Balance, coordination and gait abnormalities 

Many conventional doctors will routinely suggest the regular consumption of iodine to promote thyroid health but under the influence of thyroid glandular destruction, regular ingestion of iodine can promote further oxidative stress and destruction to thyroid follicular cells leading to reduce ability to synthesise thyroid hormones! Whilst there may appear to be a rationale for the use of iodine supplementation, it can cause thyroperoxidase (TPO) to be elevated, in turn causing hyperthyroid symptoms, anxiety OR supposed improvement, but will eventually progress to thyroid gland destruction. 

How can a functional  medicine approach assist?

Blood lab biomarkers still form part of the evaluation but is certainly not the only objective test to rely on. It is imperative to identify cross-reactive foods that will require elimination with the use of lab testing, removal of iodine, supplementation with a range of evidence-based support products such as selenium, Vitamin D, glutathione, myo-inositol, nigella sativa and desiccated porcine glandular extract.

So in summary, the symptoms of hyperthyroidism are the result of inadequate levels of T3 in the cells of the body. Low levels of T3 cannot be detected by the levels of thyroid hormones in the blood. In the hypothyroid state, low T3 levels within the cell cause the cells of the body to produce inadequate amounts of energy, which results in the symptoms experienced by hypothyroid individuals. Slow nerve impulse speed, as measured by Thyroflex testing, demonstrates low cellular function, which correlates with clinical symptoms. 

Diagnosing and treating hypothyroidism according to patients’ clinical symptoms is very effective, however if the clinician requires objective proof of the existence of hypothyroidism prior to treating symptomatic patients with normal blood test results, Thyroflex testing can be used to confirm the clinical diagnosis. Furthermore, if a patient is being treated with thyroid medication and remains symptomatic, Thyroflex testing can immediately determine if an increase in dosage is needed to relieve the patient’s symptoms.

Ultimately,  Thyroflex is more sensitive than blood tests in determining the optimal dosage of thyroid medication.

How is the Thyroflex test performed?

  • First, a detailed questionnaire is completed prior to the test.
  • The client is connected to the Thyroflex program by placing a sensor above the middle knuckle of the Left hand.
  • A point above the brachioradialis tendon is identified, where the nerve will be stimulated.
  • When stimulated, the nerve will make the middle finger move involuntarily.
  • The time interval between the stimulation of the tendon and the involuntary movement of the middle finger is measured by the Thyroflex program.
  • The average speed of conduction is calculated, indicating the level of intracellular thyroid function.
  • A normal test result, in which the average rate of nerve conduction is in the green zone, indicates ideal thyroid function.

Figure 3: Example of a Thyroflex test report

If an abnormal test result is obtained, a reasonably priced, direct online consultation with an accredited US physician is recommended who can also administer an Australian recognised prescription for thyroid medication.

This is far more cost effective, efficient, thorough and more investigative than a standard conventional model!

To make an appointment for Thyroflex testing or for a comprehensive consult with Dr. Yazbek, click here.

References:

  1. Razvi S, Bhana S, Mrabeti S. Challenges in Interpreting Thyroid Stimulating Hormone Results in the Diagnosis of Thyroid Dysfunction. J Thyroid Res. 2019 Sep 22;2019:4106816. doi: 10.1155/2019/4106816. PMID: 31662841; PMCID: PMC6778876.
  2. Ma WT, Chang C, Gershwin ME, Lian ZX. Development of autoantibodies precedes clinical manifestations of autoimmune diseases: A comprehensive review. J Autoimmun. 2017 Sep;83:95-112. doi: 10.1016/j.jaut.2017.07.003. Epub 2017 Jul 21. PMID: 28739356.
  3. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014 Apr;94(2):355-82. doi: 10.1152/physrev.00030.2013. PMID: 24692351; PMCID: PMC4044302.
Testing Your Thyroid Function - Everything you need to know!
Testing Your Thyroid Function - Everything you need to know!
Testing Your Thyroid Function - Everything you need to know!
Testing Your Thyroid Function - Everything you need to know!