Thyroid Disorders

THE FOLLOWING DISCUSSION MAY BE AT TIMES TECHNICAL, PURPOSELY, SO YOU CAN GIVE THE INFORMATION TO YOUR HEALTH PROVIDERS WHO MAY BE UNFAMILIAR WITH THE TERM ‘FUNCTIONAL MEDICINE’ AND ITS ROLE IN MEDICAL MANAGEMENT IN ENDOCRINE DISORDERS ESPECIALLY HYPOTHYROIDISM.

What is in this page

This page discusses the option of non-conventional thyroid treatment – dessicated thyroid extract (DTE), T3 and other nutritional therapies as potentially successful management for many cases where conventional standard of care (SOC) L-thyroxine fails to provide full recovery of health. Also known as armor, natural thyroid, whole thyroid extract (WTE), desiccated thyroid (DTE), compounded t4+t3 and t3 alone.

Standard of care treatment (SOC) with L–thyroxine is generally successful, cost effective, absorbs well usually, has long half-life so no sudden changes with altering or missing doses.   

Is failure to respond to standard meds common

• 27 Million: The number of Americans estimated to suffer from Thyroid Disease
• 13 Million: The number of Americans estimated to suffer from Thyroid Disease…but remain undiagnosed.
• 14 Million: Estimated number of Americans affected by Hashimoto’s Thyroiditis (Autoimmune Thyroiditis / Hypothyroidism).
• Women are 5 to 8 times more likely to suffer from Hypothyroidism than men.
• 25%: Approximate number of women that will develop permanent hypothyroidism.

Can doctors only prescribe standard thyroid medications

As doctors, we are required to follow ‘best practice’ guidelines. But what exactly are these? They may apply to the majority but not every single case. Human individuality, genetics, epigenetics and other factors come into play thus complicating interpretation and treatment strategies. Especially in the endocrine (hormone) systems.
So when the patient who is on L-thyroxine, with in-range TSH, says ‘why do I still not feel well’ and after we exclude other differential diagnoses – what then, antidepressants?  That seems to be the present pathway in many cases.

Or should we ask –

• Is the Thyroxine dose really the right dose for her, despite the ‘TSH’ saying it is?
• Is the TSH the only determinant for our judgement – does every patient respond the same to a given hormone dose and brand?
• Should we be more guided by our patients reporting of health – in other words what do we value most – the clinical presentation of the patient or one lab reference range result? Preferably we assess everything.
• Is the synthetic T4 – largely a pro-hormone, actually working? Is it being absorbed?
• Is it converting to T3? Is there selenium, iron, zinc or progesterone deficiency? Or other hormone dysfunctions including adrenal insufficiency. Drug interactions. Xeno-chemical receptor disruption (emerging to be a modern day environmental catastrophe).
• Increasing research shows our almost total fixation on TSH could be flawed – at least for some of our patients.
• Is low or suppressed TSH reason for concern when the patient finally feels normal? Only certain cases of suppressed TSH are associated with increased risks, such as true Graves thyrotoxicosis and toxic nodular goitre. Low or even suppressed TSH is not the same as thyrotoxicosis – which is a specific clinical diagnosis backed up with biochemical evidence. Low TSH in a healthy symptom-free patient is not thyrotoxicosis. Nevertheless, research is still mixed depending on other variables. Some say suppressed TSH itself may cause some increased bone loss, others say not. Whatever the case, it would be extremely unlikely to be clinically relevant and certainly not a common finding. [This needs more clarification].

There is a wealth of literature condemning the blind adherence to TSH in the face of a clearly symptomatic thyroid patient – and even questioning the relevance of T4 and T3 ‘normal ranges’ for that matter – in view of the high complexity of hormones in the human.

• It is understandable that mainstream clinicians refute these TSH concerns – it has been enshrined for many decades. Change is slow. Endocrine societies are conservative by nature – it protects from radical ideas but also dismisses the concept of personalised medicine. It awaits robust clinical studies to prove the claim. Laudable of course. But what of the suffering? Do they just have to wait? It is time that endocrinologists work WITH functional medical doctors and their patients rather than AGAINST them.
• Can patients on ‘alternative options’ become thyrotoxic? Of course, like many other guideline-based medical treatments, when instigating a new treatment to find optimum dosing, temporary overtreatment can happen. Patients can self-treat, alter their medications and forget to take them just like standard thyroid medications.

FOR THE TECHS AMONGST YOU

What now

Is there a solution

Internationally, the problem is well recognised, but still not so much by mainstream medicine where TSH is THE reference point and predominant guide. There has been some relaxation by reducing the lower limit for TSH to 3 (some groups even say it should be 2). UPDATE – local Path Lab RR is now 0.3-5.0.

Depending on the patient herself and other possible factors selenium for T3 conversion etc. – a consistently good solution has been the prescribing of the combined gland extract which contains T4, T3, T2, and T1. This has been in existence for decades and now strictly standardised like other pharmaceuticals. But why not just increase the dose of the standard L-Thyroxin medication? Yes, that is an option in some cases. Some patients just need levels up in the top reference range to feel well, finally.

WTE used to be THE treatment for hypothyroidism, but got superseded by synthetic patented T4 brands which were more consistent in quality though not always, especially as products are manufactured all over the world and standards are not guaranteed. Fortunately in NZ our Pharmac endeavours to source quality product.