To provide this, a specific feedback mechanism through the brain’s Hypothalamus and (anterior) Pituitary glands continuously control the rate of thyroid hormone secretion in proportion to metabolic needs of the body.

The Pituitary gland releases Thyroid-stimulating hormone (TSH) to stimulate the Thyroid gland to synthesise and release Thyroxine (T4) and Trii-odothyronine (T3) – the main thyroid hormones produced in the gland.

T4 is a ‘pro-hormone’ – simply put it has no receptor sites of its own and ‘exists’ to be converted in to T3 -the ‘active’ thyroid hormone. Greater than 80% of T3 is derived by what’s termed peripheral conversion; mainly within the liver.

Some physiological disturbances can corrupt this T4-T3 conversion, whereby a biologically-inactive compound is produced – Reverse T3 (rT3).

In healthy, minimally-stressed people rT3 is quickly purged from the body. However when rT3 levels become excessive, they inhibit and distort T4 – T3 conversion – thus producing further rT3 at the expense of T3.

The definition of Reverse T3  is: a measure of thyroid hormone conversion competency. In plain terms rT3 can be viewed as one of our body’s incredible protective mechanisms ‘to preserve itself for better times’ (Van Zanden: 2012). rT3 is de-activated T4 thyroid hormone – a thyroid hormone “blank”.

From a study of American chipmunks, rT3 is thought to ‘hibernate the body’; shutting it down to recover from physical trauma or serious illness, severe physiological or emotional stress, or where there is undesirable nutritional-metabolic-hormonal disturbance which threatens the body’s homeostasis or equilibrium. The largest single group of people with elevated rT3 levels are those lying in the ICU’s or HDU’s* of our nation’s hospitals..!

The usual reference range for rT3 was until recently 140-560pmol/L – although some laboratories have extended this out to 140-1200pmol/L.

Dr. John Lee – arguably Australia’s most progressive thyroid hormone researcher – is generally credited with setting-up this test in Australia at POW Hospital in Sydney. He suggests that if rT3 rises above 350-400pmol/L it will begin to interfere with further thyroid hormone (T4-T3) hepatic conversion and thyroid hormone transport throughout the body.

rT3 binds to – but does not activate – T3 intra-cell receptors (thyroid hormone receptors within the cell nuclei) – effectively blocking T3 interface, activation and thyroid receptor ‘expression’ .

Having rT3 levels less than 140pmol/L appears to have NO adverse effects on our body (Lee: 2007).

The common reasons for elevated rT3 are high Copper or Cortisol levels, toxic heavy metals – particularly Mercury, Lead and Cadmium; Hyperthyroidism (‘overactive’ thyroid function), nutritional starvation (such as Anorexia), or Selenium or Zinc deficiency. Intense, protracted emotional stress that results in increased Adrenal hormone output (high Cortisol/Adrenaline) is also thought to be a factor.

Inappropriate doses of the common thyroid medication (Thyroxine) as well as ‘natural’ thyroid supplements to treat hypothyroidism can also elevate rT3 to problem levels. 40% of oral Thyroxine is believed to ‘corrupt’ to rT3 (Lee: 2007) – so it’s imperative your treating health practitioner checks a patient’s baseline rT3 level – and then six monthly to monitor.

A characteristic of ‘Wilson’s (Thyroid) Syndrome’ is sufferers exhibit continually elevated rT3 levels because T4 is constantly being corrupted to rT3 in place of T3.

For practitioners unfamiliar with rT3 – testing the patient’s TSH is NOT an indicator of thyroid hormone conversion competency; ie: potential corruption of T3 active thyroid hormone to rT3. One must assess T4 and T3 levels and the ratio between them.

If T4 is at the higher end of its reference range (10-24pmol/L) but T3 is LOW range (<5.0pmol/L) – then rT3 ‘corruption’  is likely.

Patients will often present with symptoms of thyroid dysfunction : thinning scalp hair, lethargy, (sometimes) weight gain, ‘foggy’ thinking, mood disturbance etc. Those taking long-term thyroid medication will report ‘feeling little better’ for the taking of it.

Appropriate blood pathology testing should be done: full thyroid hormone panel – including rT3 and thyroid antibodies; Iron studies, urinary Iodine ‘spot screen’ and Zinc/Copper levels + ratios. An Adrenal Saliva Hormone Profile (SHP) is best to assess elevated Cortisol.

It’s crucial to test Vitamin D3 levels (as 25-OH Vitamin D) because Vitamin D is necessary to ‘push’  T3 onto the receptor site and dislodge rT3. To do this Vitamin D levels need to be greater than 100nmol/L (target 120-150) – Lee: 2010.

When a patient taking prescribed thyroid medication (Thyroxine) is found to have highly elevated rT3 levels, the treating Practitioner should make the judgment to alter the patient’s medication to Slow Release (SR) T3**. rT3 levels will then quickly fall away as T3 has NO substrates to be corrupted. INCREASING a patient’s Thyroxine medication (in this situation) will only further elevate rT3 levels….

Readers of this Post who take thyroid medication or feel conventional testing has thus far failed to reveal why they feel unwell, constantly tired, ‘stressed’ or have thinning scalp hair loss should NOT self-diagnose but consult their health practitioner for proper assessment + relevant testing – including Reverse T3.

*Intensive Care Unit/s and High Dependency Unit/s

**once other causes have been eliminated

Earlier this month a  mature-age professional woman consulted me for her illness + chemotherapy-induced diffuse hair loss. A brain tumour had been detected; she’d undergone a neurosurgical procedure to have it removed – followed by chemotherapy. Some months later her hair’s density still had not recovered to her satisfaction so she attended for a ‘free consultation’ with a commercial laser hair loss treatment company.

She advises me the Consultant gave her “total reassurance’ that an “intensive” course of laser therapy would be “totally safe” AND fully recover her scalp hair density. Their ‘treatment’ program was somewhere between $3000-5500 – less if she paid upfront.

Ironically it was the exorbitant treatment cost (you can purchase FIVE Dermaray PLA’s for that price) that likely saved her from further grief….

At the urging of her family she explored other treatment options – found my website – and decided to see me.

Laser therapy is ABSOLUTELY CONTRA-INDICATED in those with known malignancies, post neurosurgery generally- but especially following a tumour’s removal; ‘shunts’, cerebro-atherosclerosis, Glaucoma or surgical metal plates in the head.

Laser therapy (LLLT) is by definition bio-stimulating - it has the capacity to stimulate the faster-growing cells and tissue: hair, skin AND rapid-growth malignancies ….

Additionally this particular woman had a small surgical metal plate inserted in her skull at the time of her operation, so LLLT’s inappropriateness as a treatment consideration was doubly compounded.

In the years 2000-2004 I was a teaching consultant for Sweden’s leading LLLT manufacturer. I taught the clinical use of LLLT to Transplant + Plastic Surgeons, Dermatologists, MD’s and Cosmetologists in Europe and the USA. More recently I’ve had some association (as a Practitioner + Distributor) for the Australian-made Dermaray personal laser appliance.

I believe I have a sound understanding of the benefits, versatility and limitations of laser therapy as a treatment modality ….. I certainly know when it is NOT appropriate for use with particular clients – but then I don’t get paid a commission for ‘selling’ an LLLT treatment program to whoever walks in the door….

ANYONE considering seeking professional advice for hair loss – please….!!! do just that – seek professional advice from an experienced and QUALIFIED Practitioner. These so called “free” consultations from commission-hungry salesmen may end up costing you much more than money…..

And I could not believe how on point and helpful it is! I am a 48 YO woman and have had gradually thinning hair loss over the years, with greater/more visible loss on the crown, and this article makes it all make sense, as well as gives me hope for re-growth. So thank you first of all for writing it.

I had actually sort of accepted that my hair was going to be thin, so that is not what led me to looking on the internet for answers. It actually was the connection to low iron and adrenal/thyroid issues. Thanks to your article I have discovered that iron is needed for these organs (and other things) to function properly.

I have tested low ferritin in the past and have never taken iron supplements or done anything to raise the level. But recently, after going through an experience of great fatigue before and during my last period in August, noticing my face being pale day after day (not how I usually look), feeling fatigued and tired & not wanting to do things, I was always thinking it was my thyroid/adrenal glands, but now I realize it is must be my low iron (that I have never really addressed).

So in addition to discovering, through your article, that low iron affects these glands, I now have hope that if I correct the low iron, my hair will grow back in time, and will grow back with strands that are not so thin as they are now. This is also very exciting. I was not terribly excited to see you are located in Australia, as I live in New York City, but I decided to email you because I wanted to say thank you to Tony for the article (I hope you can forward my email to him) and because I wanted to know what I can do/where I should start in terms of figuring out the iron, etc. situation in my body.

I had a ferritin test in the past (2008) and the result was low as follows: 34 ng/mL — Reference Range of 10-232 ng/mL. I anxiously await your response and I strongly believe I was supposed to see Tony’s article. It is what I was looking for. Perhaps there are other things I could read that could help me in figuring out what to do next. As I highly suspect my blood ferritin level is still low, I was considering a hair mineral analysis test and would appreciate your feedback on this also. I truly am very thankful.
Thank you,

Mrs. G.P. (name withheld for privacy)

New York City NY.

(Her questions were replied to in a private email)

It’s now believed Vitamin D modifies THYROID receptors more appreciably than previously realised, meaning that Vitamin D supplementation could considerably alter thyroid blood test results – lower or higher. Of MOST concern are those people who do not require much Vitamin D; if given too much they can be pushed in to a HYPER-thyroid (over-active thyroid) state.

It’s therefore best to commence patients on no more than 5000IU/day – children 1/3-1/2 dose – and measure levels every six months (Lee:2010). Some patients may ultimately require 10,000-18,000IU/day in order to optimise thyroid functioning.

What requirements an individual needs ultimately depend on the interaction of their Triiodothyronine (T3), Vitamin D3 and Cortisol (CC) nuclear receptors – and the BALANCE between these three essential steroid hormones*. T3 receptors are considered to be one of the most important receptors in the body.

Ideally – all patients requiring high levels of Vitamin D to optimise/stabilise their thyroid function should have a Genetic Profile completed to assess for these SNP genetic mutations.

Health Practitioners should always do a baseline Vitamin D level at 1st encounter AND ascertain/advise patient against continuous self-medication (or any other supplement).

To be thyroid-adrenal hormone ‘sparing’ the ‘target’ level of Vitamin D was considered optimal between 150-200nmol/L …. that has been revised DOWN to a level around 120nmol/L (Van Zanden:2011).

*Vitamin D stored in its active form (in the liver) as Calcitonin is considered a steroid hormone (www.vitamindcouncil.org)

My continued gratitude to Dr. Philip Van Zanden (UNSW) and Dr. John Lee for their shared knowledge and support.

When a woman (of any age) is distressed over thinning or excessively shedding hair it may often be difficult to find the right answers for her. Here are some recent testimonials from women who have appreciated my approach to their respective problems:

HI Tony: