Vitamins, Minerals + your Thyroid

Upon completing my Trichology studies, I decided to specialise in female hair loss issues. I’d discovered early – contrary to general opinion – female hair loss is quite complex in what both influences and impels it. Moreover, there seemed to be few within the industry who truly understood these apparent complexities.

Although males can (and do) experience different forms of alopecia, overwhelmingly the most commonly seen hair loss issue in males is male androgenic alopecia – aka male ‘pattern’ balding. When a male has the genetics to exhibit this, it’s as much a natural part of post-pubertal secondary sex characteristics as facial whiskers, deepening voice, muscle bulk, and body hair.

By contrast thinning scalp hair in women is usually an indication of internal deficiency or dysfunction; a collapsing of body homeostasis to the point where hair growth can no longer be supported.

Iron, Vitamin D, Iodine and Zinc (not always in that in that order) are considered the most important nutrients for optimal metabolic functioning. By virtue of a woman’s ‘femaleness’ she is more ‘at risk’ to be deficient in these nutrients than are males.

As a NON-essential skin appendage (in nutrient-metabolic-hormonal terms) hair is often the first tissue to have these supports withdrawn when body levels are becoming depleted. Hair shedding or a gradual thinning of scalp hair density or the activation of an autoimmune condition is often the initial symptom of internal disturbance or deficiency.

From menarche (1) to menopause it’s reasonable to assert most menstruating females will have some degree of iron deficiency at times in their life. Very few functions of the body are activated without sufficient iron.

Iron storage (termed ferritin) is considered the true indicator of iron status – with an accepted reference range of 20-300 ug/L. To aspire to a ‘target’ level about mid-range – i.e.: 120-150 ug/L (2) – could not be considered unrealistic given the importance of iron in body system functioning (Lee: 2007).

The significance of reaching and maintaining this target level was the research of Dr. John Lee – Australia’s most prolific thyroid researcher. Insufficient iron restricts cell mitochondria production from which Adenosine Triphosphate (ATP) – ‘cellular energy’ is created. Our metabolic activity and Phase II liver detoxification pathways are ATP dependent.

When assessing one’s iron status, an iron studies panel (including Hemoglobin) should be requested. Careful assessment of iron studies (following the ‘Rushton Protocol’ – Rushton et al) can reveal:

  1. Depleted or acceptable iron stores but insufficient iron ‘availability’
  2. ‘Inadequate Protein Availability’ due to insufficient protein consumption or – more commonly – the body is under-producing pancreatic enzymes to break- down dietary protein, fats, or carbohydrates.  This quite common condition is termed ‘Exocrine Pancreatic Insufficiency’.
  3. ‘Inflammatory process’ indicated by elevated Ferritin. A low Transferrin or elevated TIBC will confirm this representation is not iron overload.
  4. ‘Haemochromatosis’ or iron overload – thought to be an inherited condition that is more prevalent in females: https://hairlossclinic.com.au/haemochromatosis-what-it-is-and-how-it-affects-the-hair/

In terms of metabolic importance, Iodine is deemed the next most essential (trace) nutrient after iron. Simply put: Iodine deficiency = compromised thyroid hormone production (Baratosy: 2005). There is also a studied correlation between Iodine deficiency and reduced IQ in children, and breast disease in women: https://hairlossclinic.com.au/iodine-what-it-is-why-it-is-so-important-for-women/

A random 1st morning urine Iodine is generally a convenient marker for an individual’s Iodine status, but not particularly useful to track supplementation. However a baseline reading should be obtained where poor thyroid function is suspected.

In 2008 Professor Creswell Eastman from the Australian Council of Control (Iodine Deficiency Disorders) – urged food manufacturers to again add Iodine to their products (3). His statement arose from a national study which found almost half of all Australian children of primary school age revealed Iodine deficiency.

Whilst population Iodine levels around the world vary significantly, the work of noted Sydney Cancer researcher – Dr. Joachim Fleurer – found it best to keep Iodine levels as close to but UNDER 300 ug/L (target: >120 ug/L for adequate Iodine pools) to maximise breast disease protection BUT minimise risk of benign goitre (neck swelling).

Iodine levels consistently >300 ug/L are associated with increased potential risk of Iodine-induced hyperthyroidism and autoimmune thyroiditis (Graves’ Disease): Palms Ref: 501017835.

The research of noted medical researchers around the world (Drs. David Brownstein, John Lee, David Zhava found long-term Iodine deficiency increased a woman’s potential risk of breast disease by 25%.

The NHMRC recommends Iodine supplementation of 150 mcg/day to ensure women who are pregnant, breastfeeding or considering pregnancy have adequate Iodine status. Prominent researchers (Chan et al) suggest 300-600 mcg/day for deficiency – up to 900 mcg/day for 1st Trimester pregnant women if they are found to be significantly deficient.

NHMRC guidelines also recommend kelp (seaweed) supplements OR kelp-based products should NOT be taken by pregnant women as they may contain varying (non-standardised) levels of Iodine AND be contaminated with heavy metals such as Mercury.

Iodine supplementation must be taken daily (rather than every other day) as Iodine has a very short ‘half-life’ and if not supplemented daily is ineffective in repleting Iodine pools (stores) – Chan: 2014.

As a keynote speaker at the 2014 PCCA conference, Dr. John Lee advocates practitioners should seek to “optimise” Iodine pools (Iodine stores) in patients – not just “normalise” them. To this end he advises supplementing for at least 12 months – with periodic re-testing (via Iodine excretion testing) to optimise Iodine pools.

NOTE to above: There has been growing concern among progressive health professionals with patients self-medicating (or being provided) Iodine supplementation without first measuring Iodine levels to assess Iodine status.

Whilst Iodine is a crucial trace element nutrient for metabolic functioning, it can be potentially quite harmful because it may exacerbate autoimmune disease (thyroiditis) AND potentially increase risk of thyroid cancer when supplementation is not required. For optimal Iodine synthesis and thyroid hormone conversion, it must be combined with Selenium, Zinc, and the amino acid Tyrosine (Van Zanden: 2014).

Practitioner’s Note: A urine ‘spot screen’ for Iodine is generally accurate enough to obtain a baseline for your patient. To obtain ‘corrected’ (more accurate) Iodine level use this formula: Iodine (expressed as u/g or mcg) divided by Creatinine level (expressed as mmol/L) multiplied by 8.85 = CORRECTED IODINE’ level

Research confirms Vitamin D (4) is one of the three most important nutrients to health. Vitamin D is essential for the active absorption, utilization and regulation of Calcium and Phosphorus within the body; it’s also vital for optimal thyroid functioning. Vitamin D is obviously ‘seasonal;’ the reason people are often deficient at winter’s end.

According to 2007 published guidelines for Vitamin D: <75 nmol-51 nmol/L is deemed insufficient, potentially compromising calcium retention, whilst levels less than 50 nmol/L is judged deficient.

The revised 2016 reference range is 50 – 375 nmol/L; levels must be >100 nmol/L for optimal metabolic functioning and are thyroid/adrenal hormone ‘sparing at upper ranges, i.e.: 150-200 nmol/L (Lee: 2011).

When Vitamin D is optimised at 200 nmol/L, it will ‘auto-adjust’ ionised Calcium to its ideal level of 1.25-1.26 mmol/L (Van Zanden: 2016)

A 2009 study found women with Vitamin D levels greater than 85 nmol/L had a 50% LOWER RISK of being diagnosed with breast cancer than those women with levels less than 60 nmol/L (Rejnmark:2009).

Vitamin D deficiency has an adverse effect on hair growth due to its influence on thyroid-adrenal function. There are Vitamin D receptors in the scalp; Vitamin D is essential for hair follicle maturation. To positively influence any thyroid corruption or autoimmune issues – or assist stable blood sugar levels – Vitamin D should be maintained at or above 120 nmol/L.

A Vitamin D deficiency can also initiate an autoimmune reaction in pre-disposed people as deficiency disorientates the immune system, attacking susceptible tissues such as the skin or thyroid gland.

For reader’s information: progressive medical researchers (5) speculate that just annually testing (and then) maintaining a woman’s Vitamin D and Iodine at respective target levels (i.e.: minimum 120), the rate of breast disease/malignancy could be decreased by as much as 25%. They also propose the body requires less demand for Thyroid and Cortisol hormone with optimized Iodine and Vitamin D levels – allowing the body to function more efficiently.

Supplementing Vitamin D when taking thyroid medication must be strictly monitored to prevent adverse interference of thyroid function by Vitamin D; the addition of Vitamin D in those taking prescribed thyroid medication is “less flexible” (Van Zanden: 2014): https://hairlossclinic.com.au/hypervitaminosis-d-the-complications-of-excess-vitamin-d-supplementation/

Zinc is required for more than three hundred enzymatic actions within the body. Its main contributions to thyroid homeostasis are:

  • The synthesis of Thyrotropin Releasing Hormone (TRH) – produced by the Hypothalamus to stimulate production of Thyroid Stimulating Hormone (TSH) – also known as Thyrotrophin. It’s important to note that TSH is a brain (trophic) hormone NOT a thyroid hormone – a common misconception.
  • A crucial catalyst in the binding and activation of the active thyroid hormone Triiodothyronine (T3) to receptors on the cell nucleus.
  • Zinc deficiency contributes to poor thyroid hormone conversion and diminishes healthy genetic expression of thyroid hormone.

A refractory zinc deficiency may result from inadequate protein availability (Baratosy: 2006). The amino acid Tyrosine is derived from protein, and a foundation nutrient to thyroid hormone production.

There is also a synergistic relationship between Zinc and stomach acid (HCL). The gut requires sufficient HCL production to absorb Zinc, whilst good Zinc levels are necessary for HCL production (Chan: 2011).

Symptoms of zinc deficiency is dry, fragile/brittle hair with an accompanying greasy/oily/scaling scalp. Other deficiency signs include poor wound healing, ‘white spotting’ on fingernails, lethargy, easy bruising, and dry, scaly facial acne if the Zinc deficiency becomes severe. Zinc toxicity may occur at levels of 40-50 umol/L.

Reviewing Copper (Cu) levels is particularly crucial. Low copper inhibits thyroid gland hormone production, whilst elevated copper obstructs cell receptor interaction with thyroid hormone.

A deficiency of copper hinders the deployment of iron by the red blood cells, resulting in an accumulation of iron within the organs of the body. Because this stored iron cannot be utilised whilst the copper deficiency persists, symptoms of iron deficiency may present – despite an actual iron sufficiency (Watts: 1995).

A refractory low-range or copper deficiency (with a concomitant Zinc dominance) is often seen with Vitamin D deficiency (low Copper and Vitamin D tend to go together).

Deficiencies of BOTH Copper and Zinc usually indicates malabsorption. Zinc and copper directly compete for absorption at the gut interface, so if Copper is elevated, Zinc tends to be low or deficient (and vice versa).

An elevated copper level (6) and Sex Hormone Binding Globulin (SHBG) is regularly seen in females being prescribed synthetic oestrogen found in contraceptives and hormone replacement therapy. Oestrogen preservation results in increasing copper retention – and vice versa – ultimately leading to zinc and other nutrient depletion, and oestrogen dominance. Copper may also be elevated in Cortisol insufficiency (Rebic: 2010)

Once copper is in excess and too dominant in relation to zinc, it can exert what Baratosy (2005) describes as an ‘anti-nutrient’ or toxic heavy metal influence more so than lead or mercury. Elevated copper levels restrict the absorption and utilisation of zinc (particularly), iron, magnesium, Vitamins B3, 5, 6, B12, Vitamins E and certain trace elements. It degrades Vitamin C whilst causing Cortisol, Insulin and Vitamin A to rise.

Thyroid function is significantly compromised due to a corrupting of the thyroid hormone conversion process REVERSE T3 (rT3) – a deactivated thyroid – at the expense of T3 – the body’s most important thyroid hormone.

SHBG is the blood carrier protein for 70% of circulating, ‘bound’ (inactive) Testosterone (TT) and Oestrogen – and is produced in the liver. Elevated SHBG levels may result in symptoms of testosterone and oestrogen deficiency. A raised SHBG may also cause symptoms of low thyroid function because SHBG partly binds and inactivates the thyroid hormone T4.

Other origins for elevated SHBG are:

  • Pregnancy
  • Hyperthyroidism
  • Cirrhosis of the liver
  • Medication such as Phenytoin Sodium (Dilantin) that induce hepatic enzyme induction.

Selenium is an essential trace element for thyroid hormone production and function. Most thyroid enzymes are Selenium-dependent to the creation of thyroid hormone (Baratosy: 2010). Unlike copper and zinc, selenium and iodine are agonists to each other – with optimal levels of both (in balance) essential for a healthy thyroid gland. Selenium also integral to antioxidant and immunity defense mechanisms.

The B-vitamins are essential co-enzymes to maintaining mitochondrial ATP production. Compromised mitochondrial function leads to low metabolic (thyroid) activity.

Thiamine (Vitamin B1), B12, Vitamin D and folic acid are synergistic to copper. Supplementing these nutrients where required helps restore body copper balance. Vitamin D metabolism is enhanced by copper. Adequate Vitamin D levels (>100 nmol/L) are essential for optimal T3 receptor expression (Lee: 2007).

The Thyroid Hormones:

It’s not my intention to detail or even outline the anatomy and physiology of the thyroid-related endocrine system and the hormones involved. There are countless excellent thyroid texts written by better educated and more qualified professionals than myself. I simply wish to convey to the lay reader what thyroid hormones they might request tested – and why:

  1. Thyroid Stimulating Hormone (TSH): produced by the (anterior) Pituitary Gland – TSH regulates thyroid hormone production from the thyroid gland. TSH has long been regarded as the most reliable and sensitive indicator of thyroid function, however its limitations are these:
    1. TSH does not reflect low metabolic activity; cell mitochondrial energy output and the necessary nutrients to furnace the body.
    2. TSH does not reflect sufficient and quality conversion of the inactive thyroid hormone Thyroxine (T4) to the active, cell-influencing Triiodothyronine (T3).
    3. TSH does not reflect deficiency of any of the nutrients crucial to T4 – T3 synthesis, conversion, and activation.
    4. TSH does not reflect T3 interaction with its mitochondrial or DNA receptors within the cell itself. If this interface fails – T3 cannot influence cell activity in any meaningful way.
    5. TSH does not (usually) reflect elevated Reverse Triiodothyronine (rT3) levels which interfere with T4 – T3 conversion and T3’s activation of its intra-cell receptors.
    6. TSH does not immediately reflect increasing thyroid antibodies in autoimmune thyroiditis.
    7. TSH is a brain (trophic) hormone NOT a thyroid hormone – a common misconception.

Difficulties with any of the above has been termed ‘Euthyroid Sick Syndrome’ i.e.: patients’ exhibit symptoms of an under functioning thyroid but their TSH and T4 results are consider ‘within range’.

  1. Thyroxine (T4): T4 is secreted by the thyroid gland in response to hypothalami-pituitary stimulation (TRH/TSH). This secreted T4 then circulates in the blood – bound to a carrier protein – until synthesised (in the liver and kidneys) to T3. T4 possesses no interfacing receptors of its own but is the inactive precursor of T3.
  2. Triiodothyronine (T3): although a slight amount of T3 is produced by the thyroid gland, greater than 80% results from T4 conversion. T3 is our active thyroid hormone which has the most profound effect on regulating body metabolism.
  3. Reverse Triiodothyronine (rT3): rT3 is an adapted non-active form of Triiodothyronine (de-activated T4). In times of protracted physiological and emotional stress or illness, elevated Cortisol, Copper or other heavy metal toxicity – T4 normal conversion to T3 is corrupted – and rT3 results. Lee (2005) found 40% of the synthetic thyroid hormone replacement Thyroxine sodium (Oroxine/Thyroxine) is altered to rT3 (7).

In healthy minimally stressed people rT3 is usually rapidly purged from the body. When rT3 levels are allowed to become excessive they exert a >100 times affinity to convert T4 to rT3 – thus producing further rT3 at the expense of T3.

The enzymatic process which facilitates T4 – T3 conversion is Selenium and Zinc dependent, so supplementing supra-therapeutic levels of these nutrients will aid T4 – T3 conversion over rT3 ‘corruption’ (Chan: 2014) (8)

Elevating levels of rT3 is a ‘biological hibernation signal’ – shutting the body down to “await better times” (Van Zanden: 2012). Elevated rT3 levels are commonly detected in chronic fatigue, fibromyalgia and in ongoing PTSD. Arem (1999) proposes chronic fatigue and fibromyalgia are – at least in part – manifestations of thyroid dysfunction.

A characteristic of the so-called ‘Wilson’s Thyroid Syndrome’ is patients will exhibit high rT3 levels because T4 is continually corrupted to rT3 at the expense of T3. Wilson’s thyroid (temperature) syndrome is NOT considered an evidence-based diagnosis or condition by the American Thyroid Association (Nippoldt: 2015).

Reverse T3 disrupts thyroid homeostasis by inhibiting the production and function of T3. rT3 binds to – but does not activate – T3 intra-cell receptors, thus effectively blocking T3 interface and activation.

Dr. John Lee was the first practitioner to facilitate the testing of rT3 in Australia. He regards rT3 as a “quality control marker for T4 conversion….” (Lee: 2007). Dr. Lee proposes if rT3 rises above 400 pmol/L it will begin to adversely interfere with further thyroid hormone (T4-T3) hepatic conversion; thyroid hormone transport and block the T3 receptors within cell nuclei – preventing thyroid receptor expression by T3.

The consequences of this is UNDER-active thyroid-like symptoms; tiredness, thinning scalp hair density, weight + mood disturbance. rT3 influences normal scalp hair growth because it interferes with + blocks T3. Together with Vitamin D, T3 arguably has the greatest hormonal influence on hair growth (or loss).

Calculating rT3 (for the Practitioner):

Example: Reverse T3 is 379 pmol/L and is divided by T3 which is 3.0.
Calculation: 4.8 times 1000/330=7.92. Adjusted range should be >20 – particularly in times of high stress. The prime diagnostic indicator for rT3 issues is the ratio of Free T3 to Reverse T3. As the ratio of Free T3 divided by reverse T3 should be 20 (or higher) – if it’s less than 20 (again result is 7.92) there is a corruption to rT3 at the expense of T3.

This is the research of Dr. Tom Brimeyer (US MD) which I acknowledge.

4. Thyroid antibodies: thyroid antibodies are detectable indicators within the circulatory system that our immunity is primed against our thyroid gland. The presence of thyroid antibodies is sometimes discounted because a percentage of the population may show low levels of antibodies without any discernible thyroid disease.

Elevated levels typically signify autoimmune thyroiditis: ‘Hashimotos’ if the patient exhibits an under active thyroid state, and ‘Graves’ Disease’ if symptoms/pathology suggest the thyroid is overactive.

The usual thyroid antibodies assessed in Australia are:

  • Thyroglobulin Antibodies (TG Ab.)
  • Thyroid Peroxidase Antibodies (TPo Ab.) – the more sensitive test.
  • Anti-thyroid stimulating hormone receptor antibodies (TSH-thyroid receptor antibodies -TRAB) – is a sensitive + diagnosis-specific test to assess for autoimmune thyroiditis (Graves’ disease). Anti-thyroid stimulating hormone receptor antibodies (TRA) are commonly present in most people with hyperthyroidism – and their continuing incidence after treatment for hyperthyroidism suggests a relapse of the condition. TRA levels should be less than 1.8 IU/L.

Researchers suggest a strong association between autoimmune thyroiditis and Coeliac Disease. Patients exhibiting both conditions were able to eliminate thyroid antibodies by adopting a Gluten-free diet (Baratosy: 2005). It’s believed both thyroid antibodies and Gluten antibodies originate from the gut and tend to go ‘hand-in-hand’. Most people exhibiting elevated thyroid antibodies have a ‘genetic marker’ for Gluten sensitivity when genetically profiled (Cooper: 2011).

An Italian study of female nursing home geriatrics with hypothyroidism found that by eliminating gluten from the diet, the hypothyroid symptoms in these patients diminished or disappeared.

Research (Wentz: 2015) has also found that taking pancreatic enzymes and or Inositol may help diminish thyroid antibodies and improve autoimmune thyroid conditions.

It may take at least twelve months (or longer) for excessive scalp hair shedding to subside in autoimmune thyroiditis due to continuing lymphocytic infiltrate of the thyroid.

Question: Why does your doctor (sometimes) not appear concerned about the presence of these elevated antibodies? Although it’s suggested that 10% of the healthy population may exhibit LOW levels of thyroid antibodies and be ‘asymptomatic’ – it now seems to have broadened that an individual can have significantly elevated thyroid antibody levels with no ill-effects. Left unmanaged these antibodies will eventually obliterate the thyroid gland and MUST be addressed (Van Zanden: 2011).

About Cortisol: Cortisol is the major glucocorticoid (steroid hormone) produced in the adrenal cortex of the adrenal glands. Cortisol is a key stress response hormone – essential for carbohydrate, protein and fat metabolism, anti-inflammatory tasks, blood glucose regulation, and appropriate immune system function. Cortisol is essential for the Triiodothyronine (T3) ‘expression’ because it up-regulates nuclear T3 receptors within the cells.

 Cortisol production varies throughout the day in a predictable rhythm, termed diurnal rhythm. Output is highest in the early morning – falling to its lowest concentration at night as Melatonin rises. Persons suffering ‘Adrenal Fatigue’ (Cortisol insufficiency) exhibit a ‘flattened’ – or even inverted Cortisol profile where ‘morning surge’ is absent.

 Due to its anti-inflammatory actions, Cortisol insufficiency should always be considered where unequally localised inflammatory conditions such as acne, eczema, or other skin rashes; ovarian cyst pain, colitis, swollen joints, or asymmetrical ear infections persist (Rebic: 2010).

 Symptoms of Cortisol insufficiency are:

  • Morning tiredness unrelieved by sleep, often with an energy ‘crash’ in mid or late afternoon.
  • An energy surge early to mid-evening where you feel more energetic, clearer thinking and brighter mood. However you don’t feel ready to sleep until midnight or early hours of the morning.
  • Feelings of light-headedness when standing up; sluggish pupil-contraction when bright light ‘challenged’.
  • ‘Fat pads’ (chronic puffiness) under the eyes
  • Seek out salty or sugary, refined foods as quick energy hits.
  • Younger women may experience quite marked PMS discomfort or mood disturbance.

 Simple sugars, alcohol and processed white flour are known to erode Cortisol levels. Elevated Insulin levels suppress Cortisol due to the antagonist effect of Insulin on Cortisol.

Pathology testing may be evaluated and/or cross-checked through bloods, 24hr Urine collection or Saliva Hormone assay. Blood testing should assess:

  • ACTH (Adreno-Corticoid Trophic Hormone) is produced in the Pituitary gland of the brain to ‘signal’ the Adrenal glands to produce Cortisol (CC) – our stress + anti-inflammatory hormone. A low ACTH indicates Adrenal-Pituitary ‘feedback’ is ‘sluggish’ and the Adrenals are not receiving the signal to produce more CC.

Thyroid-Adrenal axis must be balanced for optimal functioning of either gland. Vitamin C is believed to be one of the most important nutrients for CC production as its most concentrated in the Adrenal glands (Dr. James L. Wilson: Adrenal Fatigue 21st Century stress syndrome). Also raising vital nutrient levels (Vitamin D, Iodine, Zinc and Iron) will help stimulate adrenal-thyroid function, so assessment of these should always be undertaken as part of any investigative process.

  • Fasting AM blood Cortisol: which should fall within a range of 400-600 nmol/L; optimal 400 nmol/L (Van Zanden: 2012). Cortisol is the only hormone that rises as we age.

The crucial roles sex and other steroid hormones play in thyroid homeostasis – particularly Progesterone and DHEA – have not been discussed here. Suffice to say the thyroid-adrenal relationship is mutually dependent, and a Saliva Hormone Assay of these and other relevant hormones is an integral part of the complete investigative process.

When treating thyroid-metabolic issues it’s essential to balance the three key receptors:

  1. T3 thyroid hormone
  2. Vitamin D
  3. Cortisol

Medication or supplementation requirements depend on the interaction of these nuclear receptors – with T3 being the most important (Van Zanden: 2011).

It’s now known Vitamin D modifies thyroid receptors to a greater degree than previously realised, and D3 can drastically alter thyroid blood pathology results up or down. Of most concern are those patients taking prescribed thyroid medication who require little daily Vitamin D. If supra-therapeutic amounts are given by injection or long-term supplementation, a hyperthyroid state may be induced (Van Zanden: 2011): https://hairlossclinic.com.au/hypervitaminosis-d-the-complications-of-excess-vitamin-d-supplementation/

Toxic heavy metals – principally lead, mercury, cadmium, aluminum and arsenic block the function of vitamins and minerals necessary for thyroid homeostasis. Where patients relate long-standing illness, assessing for heavy metal toxicity should be an early priority. Accurate and convenient testing is achieved by a Hair Tissue Mineral Analysis (HTMA).

The thyroid hormone cascade is incredibly involved and complex. Vitamins, minerals, amino acids, trace elements, essential fatty acids (DHA/EPA), sex and steroid hormones, as well as the immune system must all be available – and harmonious to each other – for T3 to accomplish its task. If any one of these vital components are lacking the process will stall – and optimal body functioning diminished. In all this hair is the expendable extravagance: usually the 1st appendage of the integrum to experience withdrawal of nutrient, metabolic or hormonal support.

Scalp hair presentation: In any of these nutritional or metabolic disturbances, scalp hair appearance and feel often varies between individuals. Hair may feel noticeably dry or oily; hair shafts are often thin and fragile. Scalp hair in females may be lost from all over (diffuse) or a dual picture of pattern thinning with an underlying diffuse hair loss will be evident.

Thinning scalp hair resulting from thyroid disturbance frequently presents as pattern thinning – often descending to ear level with an underlying diffuse hair thinning. The hair itself has a fine ‘cotton wool’ feel to it.

Atopic people may exhibit Alopecia areata as a patchy hair loss concern; autoimmune thyroiditis and a. areata are strongly associated. When autoimmune activity is involved (i.e.: autoimmune thyroiditis or a concomitant autoimmune condition) – loss of eyebrows – partially or fully – decreased body hair or a thinning or loss of eyelashes may also be apparent.

Influence on Mood: Appreciation among health professionals of the scope of mood disturbance created by nutritional, metabolic or hormonal disordering remains poor, with scalp hair loss in females – as a principal indicator of emerging internal disturbance –viewed by some as ‘inconsequential’ or one of vanity.

For the woman though, her hair defines her femininity – female balding is not regarded as socially-acceptable in western societies – and many women experience thinning scalp hair density as a ‘loss’ or grieving process.

Stress seems to be the orthodox mantra when shedding scalp hair concerns are raised – it can be – but more often it’s the underlying disturbance responsible for both the hair loss and mood disturbance. Thyroid-adrenal disturbance is known to elicit a wide range of mood disturbance: depressive-like symptoms, agitation, anxiety, sensitivity, or mood-fragility are some emotional responses observed: https://hairlossclinic.com.au/the-stress-hair-loss-correlation/.    

Presenting clients – particularly female – often reveal cool to cold extremities; hands or feet or the tip of the nose. They are often quite sensitive to cooler temperatures or intolerant to changes in temperature. This is the result of low metabolic activity where the body struggles to maintain optimal ‘core’ (basal) temperature. Low nutrient levels (iron, vitamin D or zinc) or disturbance of the thyroid-adrenal axis are mostly the reasons behind low metabolic activity.

Dr. John Lee states: “what could be more stressful for the body than not to have the nutritional-metabolic wherewithal it needs to keep itself alive …” (Lee: 2011 Functional Medicine Conference).

Copyright Anthony Pearce 2008 (revised February 2022)

  1. The onset of menstruation in a young female at puberty.
  2.  Post-menopausal woman should be around 100 ug/L.
  3. Iodine supplementation to food products such as bread was re-introduced in 2010/2011.
  4. Read more in-depth information on Vitamin D at www.hairlossclinic.com.au (Vitamin D – the re-discovered key to illness prevention).
  5. Dr. John Lee and ACNEM Doctors/Natural Medicine Practitioner
  6. Most (plasma) Copper is bound to Caeruloplasmin – the carrier protein for Cu in the bloodstream. Elevated plasma Cu is most commonly secondary to elevated Caeruloplasmin Globulin and seen in cases of acute OR chronic inflammatory disease (including liver, biliary or malignant diseases)
  7. See Post (‘When the Body Shoots Blanks’) at my Blog www.hairlossclinic.com.au
  8. Selenium 300-600 mcg/day; Zinc (as Picolinate) 75-115 mg/day (Chan: 2014)

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