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Hormonal (contraceptive) Therapy – its Effects on Hair & Health

When reading a younger female patient’s pathology testing, health providers might note ‘elevated-out-of-normal-reference-range’ Copper levels, Sex Hormone Binding Globulin (SHBG) – and if tested – Reverse T3 (rT3).

Conversely they may find this patient has low or depleted iron stores, zinc deficiency (absolute or relative to copper); B12 deficiency – as well as other abnormal pathology results AND thinning scalp hair density.

What’s causing this disturbance in hormonal/nutrient levels in otherwise healthy young Women – is there any correlation? The common denominator is these Women are usually ALL taking prescribed oral contraceptive (synthetic) hormone medication – the ‘Pill’.*

Oral contraception was introduced more than 50 years ago and proclaimed a cornerstone of ‘Sexual Liberation’ for women. In many ways it has allowed greater physical, sexual and ‘choice’ freedom for females of child-bearing age – as well as an aid in stabilising hormonal conditions such as Endometriosis and Polycystic Ovarian Syndrome.

Unfortunately what are also well-documented are the risks and adverse reactions; some with potentially fatal outcomes and others that trigger internal disturbance resulting in hair loss.

Pathology reports where these elevated ranges occur will comment: “A 2 to 3 fold increase in serum/plasma Copper concentration may occur in females taking an oral medication….” Or “SHBG levels are often increased during the administration of synthetic oestrogens…..”

These apparently innocuous statements give no hint as to what the consequences are in continuously elevating Copper and/or SHBG on other vital minerals, vitamins and hormonal balance for the woman’s body.

High range SHBG, Copper, Reverse T3 – the ‘terrible triad’:

A percentage of women* who take an oral contraceptive (OCP) will over time exhibit a continuing elevation in their Sex Hormone Binding Globulin carrier protein and Copper levels. Elevated Copper levels will then cause a rise in Reverse T3 (de-activated T4 thyroid hormone).

This occurs because the synthetic Oestrogen from the oral contraceptive is RETAINED in the body, which in turn has a ‘retention effect’ on Copper (Cu) levels. Rising Copper causes FURTHER Oestrogen retention – leading to yet more elevated Cu levels. Copper ‘dominance’ has an absorption ‘blocking’ effect on zinc, iron, B12 and other nutrients/trace elements.

Oestrogen dominance may also lead to hormone imbalance relative to Progesterone (P4) and Testosterone (TT). Excessive Oestrogen is also a common reason for fluid retention in women.

It’s this ‘across the board’ disruption in nutrient and hormonal balance that ultimately presents as noticeable thinning of scalp hair density, lethargy, mood and cognitive disturbance in the Woman.

What is Sex Hormone Binding Globulin (SHBG)? SHBG is produced in the liver and is the ‘carrier’ protein for 70% of circulating, ‘bound’ (inactive) Testosterone (TT) and Oestrogen. When SHBG is too high it will not allow any ‘free’ TT or Oestrogen to be used by the body – so the Woman may have ongoing issues with TT + Oestrogen ‘availability’ or symptoms of deficiency of these hormones.

A raised SHBG will also cause symptoms of low thyroid function because SHBG partly binds and inactivates the thyroid hormone T4.

Other causes for elevated SHBG are:

  • The taking of (synthetic) oestrogen found in orally-ingested hormone therapy*
  • Pregnancy
  • Hyperthyroidism
  • Cirrhosis of the liver
  • Medication such as Phenytoin Sodium (Dilantin) that induce hepatic enzyme induction

One research paper suggests a rise in SHBG for Women taking Metformin for Insulin Resistance is “one indication” that treatment is working (Kovaceska: 2014)

Factors that decrease SHBG:

  • Male hormone (termed ‘Androgens’)
  • Progesterone (P4) – low P4 is a common concern for peri-menopausal women
  • Cortisol (Stress + anti-inflammatory hormone from our Adrenal Glands)
  • High Protein and (good) dietary Fats.

About Copper (Cu): Copper is regarded as an essential trace ‘heavy metal’. As Copper actively antagonises other nutrients it must be in balance with these nutrients for optimal body functioning.

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, B12; Vitamins C and E, and certain trace elements.

Elevated copper obstructs cell receptor interaction with thyroid hormone, whilst low copper is said to inhibit thyroid gland hormone production.

A deficiency of copper can also hinder the deployment of iron by the red blood cells, resulting in the iron being accumulated (but 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 (Watts: 1995).

A refractory low-range or copper deficiency (with a concomitant Zinc dominance) may also result from Vitamin D deficiency (low Copper + Vitamin D tend to occur 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.

Reverse T3 (rT3): Reverse t3 is an adapted non-active form of Triiodothyronine (t3). 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 (de-activated T4) accumulation 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’ will 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. His research suggests if rT3 rises above 350-400pmol/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 usually exhibited as UNDER-active thyroid-like symptoms; tiredness, thinning scalp hair density, weight + mood disturbance. RT3 adversely affects normal scalp hair growth because it interferes with + blocks T3. T3 has the greatest hormonal influence on hair growth (or loss).

What to do?

Experience has found changing OCP’s to ‘low dose’ brands or changing brands will NOT significantly reduce the nutrient-hormonal disruption originating from the synthetic Oestrogen.

My suggestion to young women whose thinning scalp hair is being caused by their OCP is:

    • Consult your Doctor regarding what your blood pathology has revealed. Be guided by the Doctor on contraception alternatives such as Inter-Uterine Devices (IUD) or the natural fertility-contraception indicator ‘Maybe baby’. Implanted OR injected contraceptives almost ALWAYS cause persistent scalp hair shedding and should NOT be considered (in my opinion).
    • If opting for an IUD, ‘transition’ the ceasing of your OCP with the professional insertion-placement of the IUD. This will usually avoid any hormonal ‘fluctuation’ which is a frequent cause of Telogen Effluvium (TE) ** hair loss one to three months after OCP cessation. IUD’s (such as the Mirena Coil) will assist in regulating heavy or persistent menstrual bleeding, as well as help stabilise sex hormone balance.
    • If for whatever reason the woman decides to discontinue OCP hormonal therapy – and this is a GOOD thing 99.9% of the time – they must be made aware of potential TE hair shedding in the following 1-3months. Topical treatments such as Activance Rhodanide (Professional Series only) or a sophisticated formulation of Minoxidil can help lessen the onset of TE. Laser therapy (as LLLT) is also of proven benefit to prevent or minimise TE scalp hair loss.
    • Once OCP is discontinued, SHBG, Copper (and sometimes) rT3 levels generally fall back within acceptable ranges, and supplementation of low iron, Zinc and other affected nutrients can commence. Zinc Picolinate is the only form of Zinc that will not antagonise Iron; other forms should be taken a few hours away from any iron supplement. Supra-therapeutic supplementation of zinc and selenium (under the guidance of an experienced Health Professional) will facilitate the enzymatic process of T4 – T3 conversion rather than T4-rT3 ‘corruption’ as previously mentioned.
    • Reassure the woman that their diligence is the key to their better health and scalp hair recovery. Treatment milestones usually progress this way:
      • 1st indication of recovery is the Client ‘feeling well’ in herself – improved energy, less tired, improved sleep + concentration.
      • 2nd is excessive hair loss with begin to settle + the quality + lustre of hair will re-emerge. This ‘resetting’ of the growing phase (termed Anagen) and decrease in scalp hair shedding may take up to three months to fully stabilise.
      • Noticeable scalp hair regrowth 3-6 minimum (up to 12months with some autoimmune conditions) months after disturbance is corrected.

6. Supplementation should continue until respective ‘optimal’ levels are achieved with nutrient deficiencies. Pathology re-testing for the previous disturbances should be undertaken 3, 4 or 6 months after OCP cessation and supplementation commencement.

*this observable fact does not seem to occur with IUD contraception, creams or pessaries.
** 20-30% in my anecdotal experience
*** Telogen Effluvium is essentially a self-correcting hair loss condition in normal circumstances, but the severity of the hair loss (up to 60% of scalp hair) is very distressing to the sufferer.

**** Author’s note: Despite more than 90 years of drug company propaganda – synthetically derived ‘Oestrogens’ are NOT the same as the Oestrogens produced in the human female body. Drug companies cannot patent and sell natural Oestrogen; synthetic ‘Oestrogen’ is synthesised from pregnant horse (mare) urine or other equally transmuted sources. These drug manufacturers have spent $$Billions indoctrinating Medical Practitioners, the media + female consumers that synthetic hormones “are just the same” as natural hormones produced by the human body.