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Vitamins, Minerals and your Thyroid-what your Doctor may not know

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 Practitioners around who understood these apparent complexities.

Although males can (and do) experience different forms of alopecia, overwhelmingly the most commonly seen is Male Androgenic Alopecia – 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 almost always an indication of internal 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skin appendage (in nutrient-metabolic-hormonal terms) hair is often the first tissue to have these supports withdrawn when body levels are becoming depleted.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* 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 to ‘furnace’ them.

Iron storage (termed ferritin) is considered the true indicator of iron status – with an accepted reference range of 20-300ug/L. To aspire to a ‘target’ level about mid-range – i.e.: 120-150ug/L** – could not be considered unrealistic given the importance of iron in the body (Lee: 2007). A post-menopausal woman’s iron stores should be 100ug/L as minimum.

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 Tri-phosphate (ATP) – ‘cellular energy’ is created. Our metabolic activity and Phase II liver detoxification pathways are ATP dependent.

Your health Practitioner should always request a FULL iron studies – not just ferritin (iron stores) – as well as Hemoglobin. Careful assessment of iron studies (following the ‘Rushton Protocol’ – Rushton et al) can reveal:

  1. Depleted iron stores 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 proteins or carbohydrates consumed (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.

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).

Testing Iodine levels is a simple urinary ‘spot-screen’, but is seldom routinely assessed. Low Iodine results in an under-functioning thyroid. There is also a studied correlation between Iodine deficiency and reduced IQ in children, and breast disease in women.

In 2008 Professor Creswell Eastman from the Australian Council of Control (Iodine Deficiency Disorders) – urged food manufacturers to again add Iodine to their products***. 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 300ug/L (target: >150ug/L for adequate Iodine pools) to maximise breast disease protection BUT minimise risk of benign goitre (neck swelling).

The NHMRC recommends Iodine supplementation of 150mcg/day to ensure women who are pregnant, breastfeeding or considering pregnancy have adequate Iodine status. However prominent researchers (Chan et al) suggest 300-600mcg/day for deficiency and up to 900mcg/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 etc) as Iodine has a very short ‘half life’ and will 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 one-two years, with periodic re-testing (via Iodine excretion testing) to optimise Iodine pools.

NOTE to above: There is however a growing concern amongst progressive Health Professionals with patients self-medicating (or being provided) Iodine supplementation without first measuring Iodine levels for deficiency (or not). Whilst Iodine is a crucial trace element nutrient for metabolic functioning, it can potentially be quite harmful because it may exacerbate autoimmune disease (thyroiditis) AND increase risk of thyroid cancer when supplementation is not required. For optimal Iodine synthesis and thyroid hormone conversion, it should be combined with Selenium. Tyrosine + Zinc (Van Zanden: 2014)

Research confirms Vitamin D**** is one of the three most important nutrients to health. Vitamin D is essential for the active absorption, utilisation + regulation of Calcium + 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: <75nmol-50nmol/L is insufficient & potentially compromises calcium retention, whilst levels less than 50nmol/L is deemed deficient.

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

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

A 2009 study found women with Vitamin D levels greater than 85nmol/L had a 50% LOWER RISK of being diagnosed with breast cancer than those women with levels less than 60nmol/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 (maturity). To positively influence any rT3, autoimmune issues or help stabilise blood sugar levels Vitamin D should be maintained at or above 150nmol/L.

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

Progressive medical researchers***** speculate that just by annually testing and maintaining a woman’s Vitamin D and Iodine at respective ‘target’ levels, 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 when Iodine + Vitamin D levels are optimised – allowing the body to operate more efficiently.

Readers who take thyroid medication are advised to acquaint themselves with the latest (unpublished) study summary on Vitamin D daily dosage at my Blog. (www.hairlossclinic.com.au)

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)

Zinc is held to be implicated in at least 150 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.
  • A crucial catalyst in the binding and activation of the active thyroid hormone Triiodothyronine (T3) to receptors on the cell nucleus.
  • Zinc deficiency is thought to contribute to poor thyroid hormone conversion – and deficiency diminishes healthy genetic expression of thyroid hormone.

A refractory zinc deficiency may result from inadequate protein availability (Baratosy: 2006). Amino acid (Tyrosine) derived from protein is a foundation of thyroid hormone production. There is also a synergistic relationship between Zinc + stomach acid (HCL). Sufficient HCL production is required to absorb Zinc, whilst good Zinc levels are required for HCL production (Chan: 2011).

A noted anomaly of zinc deficiency that may be seen is dry, fragile/brittle hair BUT 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 40-50umol/L.

Reviewing Copper (Cu) levels is particularly crucial. Low copper is said to inhibit 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 the iron being accumulated (and unavailable) 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.

A refractory low-range or copper deficiency (with a concomitant Zinc dominance) can be caused by Vitamin D deficiency (low Cu + Vitamin D go together).

If testing reveals BOTH zinc and copper to be deficient – this usually indicates malabsorption. Zinc and copper directly compete for absorption at the gut interface, so if one is elevated the other is habitually low or deficient.

An elevated copper level***** and Sex Hormone Binding Globulin (SHBG) is regularly seen in females using certain types of oral contraceptive. This is largely due to the additional (synthetic) oestrogen found in contraceptives and hormone replacement therapy. Oestrogen retention gives rise to copper preservation – and vice versa – ultimately leading to zinc and other nutrient depletion, and oestrogen dominance. Copper may also be elevated in Cortisol insufficiency (Rebic: 2010)

SHBG is the ‘carrier’ protein for 70% of circulating, ‘bound’ (inactive) Testosterone (TT) and Oestrogen – and is produced in the liver. Other origins for elevated SHBG are:

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

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 metal influence. High copper levels restrict the absorption and utilisation of zinc (particularly), iron, magnesium, Vitamins B3, 5, and 6, Vitamins C and E, and certain trace elements.

Sex Hormone Binding Globulin (SHBG) is the carrier ‘protein’ for 70% of the circulating but ‘bound’ (inactive) testosterone and oestrogen. Elevated SHBG levels may result in symptoms of testosterone and oestrogen deficiency. A raised SHBG will also cause symptoms of low thyroid function because SHBG partly binds + inactivates the thyroid hormone T4.

In the long line of essential nutrients for optimal thyroid function, the importance of Selenium is only shaded by Iron and Iodine (Baratosy: 2010). Several thyroid enzymes are Selenium-dependant to the creation of thyroid hormone. 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 has an integral role in anti-oxidant and immunity defense mechanisms.

There remain some differing opinions on the most reliable form of Selenium testing. Some advocate blood serum; others support hair mineral analysis (HTMA) – still others suggest toe nail clippings.

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 (>100nmol/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 many excellent thyroid texts written by better educated and more qualified folk than me. I simply wish to convey to the lay reader what thyroid hormones they might request tested – and why:

    • 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:
      • TSH does not reflect low metabolic activity; cell mitochondrial energy output and the necessary nutrients to furnace the body.
      • TSH does not reflect sufficient and quality conversion of the inactive thyroid hormone Thyroxine (T4) to the active, cell-influencing Triiodothyronine (T3).
      • TSH does not reflect deficiency of any of the numerous nutrients crucial to T4 – T3 synthesis, conversion, and activation.
      • 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.
      • 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.
      • TSH does not immediately reflect increasing thyroid antibodies in autoimmune thyroiditis.

      Difficulties with any of the above has been termed ‘Euthyroid Sick Syndrome’ – patient’s exhibit symptoms of an under functioning thyroid but their TSH and T4 results are “normal”

  • Thyroxine (T4): T4 is secreted by the thyroid gland in response to hypothalamic-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.
  • Triiodothyronine (T3): although some T3 is produced by the thyroid gland, greater than 80% results from T4 conversion. T3 is our active thyroid hormone which profoundly regulates body metabolism.
  • 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’s normal conversion to T3 is corrupted – and rT3 results. Lee (2005) found 40% of the synthetic thyroid hormone replacement Thyroxine sodium (Oroxine/Thyroxine etc) is altered to rT3*******.In healthy, minimally-stressed people rT3 is quickly 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/Zinc dependent, so supplementing supra-therapeutic levels of these nutrients will aid T4 – T3 conversion over rT3 ‘corruption’ (Chan: 2014)********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 and Fibromyalgia sufferers. Arem (1999) proposes these two debilitating illnesses are manifestations of thyroid dysfunction. A characteristic of ‘Wilson’s Thyroid Syndrome’ is patients’ exhibit high rT3 levels because T4 is continually corrupted to rT3 at the expense of T3.Reverse T3 disrupts thyroid homeostasis by inhibiting the production and function of T3. rT3 binds to – but does not activate – T3 intra-cell receptors; 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 400pmol/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. T3 has the greatest hormonal influence on hair growth (or loss).

Calculating rT3 (for the Practitioner):

Example: Reverse T3 is 379pmol/L & 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 greater, if it’s less than 20 there is a corruption to rT3 at the expense of T3.

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

  • 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 shows 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 their symptoms/pathology suggest the thyroid is over active.

The usual thyroid antibodies tested in Australia are:

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

Question: ‘Why’ does your Doctor not appear concerned about the presence of these elevated antibodies? Although it’s suggest 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 ‘off the chart’ thyroid antibody levels and it supposedly “not be a problem” (Van Zanden: 2011). In reality these antibodies are essentially destroying your thyroid gland and MUST be addressed.

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’ 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).

Simple sugars, alcohol, processed white flour are some dietary issues that erode Cortisol levels. Elevated Insulin levels – as found in some metabolic conditions – 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-Cortico 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’ + the Adrenals are not receiving the ‘signals’ to produce more CC. Thyroid-Adrenal axis must be in ‘balance’ for optimal function of either. The humble Vitamin C is believed to be one of the most important nutrients for CC production as it’s most concentrated in the Adrenal glands (Dr. James L. Wilson: Adrenal Fatigue 21st Century stress syndrome). Also raising vital nutrient levels (such as Iron, Vitamin D + Iodine) 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 400-600nmol/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 dependant, 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: T3, D3 (Vitamin D) and CC (Cortisol). Medication/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 realized, and D3 can drastically alter thyroid blood tests up or down. Of most concern to Practitioners are those patients who do not need much vitamin D – and if given too much – a hyperthyroid state may be induced (Van Zanden: 2011).

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, toxic heavy metals should be an early assessment priority. Accurate and convenient testing is achieved by 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 adequately 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 first tissue to suffer a withdrawal of metabolic and nutrient 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 may be lost from all over (diffuse); in some women a dual picture of female ‘pattern’ thinning with an underlying diffuse hair loss will be evident.

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

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

Influence on Mood:
Appreciation amongst Health Professionals of the scope of mood disturbance created by nutritional, metabolic and hormonal disordering largely remains poor. Scalp hair shedding in females – as a principal indicator of emerging internal disturbance – seems to be viewed (by some) as ‘inconsequential’ or a ‘vanity’ matter.

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” and a 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 distress is known to elicit a wide range of mood disturbance: depression-like symptoms, agitation, anxiety, ‘sensitivity’ and mood-fragility are only some of the emotional responses observed.

Dr. John Lee states: “what could be more stressful for the body than NOT to have the nutritional-metabolic wherewithal it needs to ‘run’ itself” (Lee: 2011 Functional Medicine Conference). Women with thyroid-adrenal or nutritional-metabolic disturbance will frequently relate they “have the perfect/happiest life/marriage – but feel so stressed”.

It should now be appreciated that “gimmicky” single treatments such as laser combs, commercial hair loss programs etc can do nothing to influence nutritional, metabolic or hormonal disturbance. These areas must be individually tested for – and reviewed and treated as part of the person’s total clinical picture.

Copyright Anthony Pearce 2008 (revised February 2015)

*The onset of menstruation in a young female at puberty.
** A Post-menopausal woman should be around 100ug/L.
*** Iodine supplementation to some food products such as bread was re-introduced in 2010/2011
**** Read more in-depth information on Vitamin D at www.hairlossclinic.com.au (Vitamin D – the re-discovered key to illness prevention).
**** Dr. John Lee and ACNEM Doctors/Natural Medicine Practitioner
***** Almost all (plasma) Copper (Cu) 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 and malignant diseases)
*******See Post (‘When the Body Shoots Blanks’) at my Blog www.hairlossclinic.com.au
******** Selenium 300-600mcg/day; Zinc (as Picolinate) 76-115mg/day (Chan: 2014)