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The overlooked hormones in thyroid disturbance

Most practitioners of the various disciplines in health would or should have a sound working knowledge of the TSH, T4 and T3 (1) flow and ‘feedback loop’.

Some may be aware of the importance of optimising Vitamin D, Cortisol and T3 thyroid hormone in balance to each other, with emphasis on T3 levels (Van Zanden 2012). T3, Vitamin D and Cortisol exert their actions by binding to receptors on genes in the cell nucleus; Vitamin D has a qualitative effect on T3 intra-nuclear receptors (i.e.: within the cell nucleus).

Cortisol has a quantitative effect by increasing intra-nuclear T3 receptor density, whilst there is also a constant ‘cross talk’ between Vitamin D and T3 intra-nuclear nuclear receptors (Van Zanden: 2017).

What seems to have been forgotten is the importance of the female sex hormones – Oestrogen and Progesterone – in their ability to disrupt or enhance the thyroid conversion process.

Oestrogen and Progesterone – an overview:

Both Oestrogen and Progesterone are sex steroid hormones, with opposite and balancing influences within the female body.

  • Oestrogen stimulates target cells to grow and proliferate endometrium, ovaries, breasts, vaginal tissue and lower bladder. Pubertal female secondary sex characteristics (2) emerge from oestrogen’s influence, as do the secretion of necessary hormones such as Prolactin and Aldosterone (3). Skeletal bone cells (4) are influenced by oestrogen – as is mood and cognition. Oestrogen exerts an inhibiting effect on thyroid hormone by increasing thyroid transport protein which binds and inactivates the thyroid hormone (5). 
  • Progesterone is the 3rd tier in the human body’s hormonal cascade; the oestrogens, other sex hormones and the corticosteroids are all derived from progesterone (6). Progesterone controls and modifies the actions of oestrogen – increasing oestrogen receptor sensitivity to safe levels whilst restricting its adverse, excessive effects. Progesterone is overwhelmingly produced from the corpus luteum after ovulation; its function is to develop and mature the uterine wall to sustain and maintain a pregnancy.

Clinical signs of a suspect under-active thyroid function are lethargy, weight gain, scalp hair loss, mood disturbance, fluid retention, breast tenderness, headaches, and decline in libido –they are also common symptoms of oestrogen dominance (7).

When Oestrogen-Progesterone ratios are imbalanced, oestrogen inhibits with the action of T3 thyroid hormone binding to its receptor (Lee: 1996), whereas progesterone is known to enhance the action of thyroid hormone. In symptomology and its influence on metabolic function oestrogen and thyroid hormone fundamentally oppose each other (8).

Another theory to oestrogen’s obstructing effects on T3 is both hormones carry ‘phenol/phenyl rings’ (9) at the corner of their molecules (Lee: 1996). Because unopposed oestrogen is believed to compete at the thyroid receptor site, it displaces or partially blocks the binding of T3 to its receptor, so receptor ‘expression’ is incomplete. Symptoms of hypothyroidism may result despite outwardly normal serum thyroid hormone levels (10).

How Progesterone deficiency influences scalp hair loss:

When a woman is not ovulating – or producing insufficient amounts of progesterone to respond to oestrogen, she will commence to mobilise androgens (11) from the ovaries and adrenal glands. Because male hormone opposes oestrogen, these are the body’s back-up defence against the undesirable effects of oestrogen in the absence of sufficient progesterone.

Some of these androgens will up-regulate to the most potent male hormone – dihydrotestosterone (DHT) – which then exerts androgenic effects on ‘androgen-sensitive’ scalp hair, the frontal hairline margins, as well as to increase facial hair and sebaceous gland activity (12).

This ‘acquired’ pattern thinning can appear at any age after puberty, but is most common in peri-menopausal women, or women who are anovulatory due to illness or other factors (13).

One only need observe the hair and nails of a healthy pregnant woman when progesterone levels are ten times higher to appreciate the importance of progesterone on these significant skin appendages (14).

Lastly – in many peri or early post-menopausal women a distorted hormonal image of androgen dominance relative to oestrogen-progesterone can arise. This occurs because progesterone levels fall away – followed by oestrogen to a lesser extent – but androgen levels remain constant or temporarily increase.

Elevated androgens will then exert their androgenic effects on scalp and body hair (15), and increasingly promote insulin resistance and weight gain. Both elevated androgens and insulin resistance tend to create ‘hormonal disorder’ by lowering sex hormone binding globulin and stimulating the ovaries to generate more androgens (16).

Copyright Anthony Pearce 2024

  1. TSH: Thyroid stimulating hormone, T4: Thyroxine – the ‘inactive’ thyroid hormone produced in the thyroid gland, T3: Triiodothyronine – 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.
  2. Breast and pubic hair development and mature the uterus for the onset of menses (periods).
  3. Prolactin stimulates breast cell growth and lactation in the pregnant woman. Aldosterone directs the kidneys to increase sodium and water retention to help prevent dehydration.
  4. Osteoclasts – which are responsible for breaking down old bone.
  5. Thyroid binding globulin transports thyroid hormone through the body’s circulatory system to target cells. Inhibiting the action of thyroid hormone slows metabolism resulting in fat storage for energy production during pregnancy.
  6. Progesterone is derived from Sterol Pregnenolone which in turn is drawn from Cholesterol.
  7. i.e.: oestrogen levels not sufficiently balanced by progesterone – aka unopposed oestrogen.
  8. One example: food calories tend to be stored as fat reserves when a woman is in an oestrogen dominant state. By contrast thyroid hormone converts stored fat to usable energy.
  9. Both T4 and T3 thyroid hormone have a phenyl ring attached via an ether linkage to a tyrosine molecule. T4 has two iodine atoms on its phenyl (outer) ring, whereas T3 has only one. Oestradiol (E2) has a distinguishing phenolic A ring with two hydroxyl groups (in positions 3 and 17)
  10. This condition was commonly known as ‘Euthyroid sick syndrome’.
  11. Androgens are hormones which produce male characteristics: dehydroepiandrosterone (DHEA) – the body’s weakest most abundant male hormone and a marker for adrenal reserves. Testosterone is 2nd most potent male hormone (after DHT).
  12. As an oily T-zone and scalp.
  13. Anorexia nervosa, endurance sports such as running marathons, or morbidly obese females who are found to be oestrogen dominant and have Insulin Resistance.
  14. Skin appendages are hair follicles, sweat glands, sebaceous (oil) glands and nails.
  15. There is an inverted relation with androgen-sensitive scalp hair and facial body hair. Androgens cause a thinning of the scalp hair but increase facial and body hair.
  16. Sex hormone binding globulin (SHBG) is the blood carrier protein for circulating hormones: Oestrogen, Testosterone and T4 thyroid hormones. A low SHBG causes increased levels of ‘free’ or unbound Testosterone to be released and have a disruptive effect on the female body. A low SHBG can also suggest an under-active thyroid, as the body attempts to compensate by using male hormone (Testosterone) to drive metabolic activity in the absence of optimal thyroid functioning.


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