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Hair Loss in the Pregnant and Post-Partum Woman

Nothing reveals the unique beauty of a woman quite like a healthy woman displaying her pregnancy. The additional life growing inside her presents a glow that no cosmetic make-over could ever replicate.

Her hair too is usually at its most lush density and soft manageability. A pregnant woman’s scalp hair growth (anagen) cycle – usually a constant 85-90% – may increase to 95% during her 2nd + 3rd trimesters. Only during her young adolescence would a woman’s scalp hair follicles be so active in growth (Dawber+ Van Neste: 1995).

The two dominant female sex hormones (Oestradiol + Progesterone*) increase immensely to help support the growth and development of the unborn child, and these hormonal surges have a ‘flow-on’ effect to hair growth – adding to the expectant mother’s radiance.

As pregnancy progresses it’s generally accepted that higher oestrogen levels (oestradiol + oestrone) are responsible for an increased and prolonged anagen phase, as well as thickened hair shaft density in trichometric studies. Pecoraro et al (1967) also suggested ‘telogen’ (shedding) phase is more rapid in a pregnant woman than the usual 2-3 months of a follicle cycle.

The rate of scalp hair growth in humans is profoundly influenced by the levels of unbound (i.e.: ‘active’) thyroid hormone (Dawber+ Van Neste: 1995). In their excellent text ‘Thyroid Power – 10 Steps to Total Health’, Shames + Shames (2002) note that women at the beginning of their pregnancy used to be given small doses of thyroid hormone to help prevent miscarriage and aid in foetal development. Even a minimal thyroid imbalance may be associated with miscarriage, premature birth, and even birth defects according to Arem (1999). He cites research that suggests 2-3% of pregnant women have an under-functioning thyroid gland. **

Excessive hair fall during pregnancy:

Essentially this should not occur, and is a contradiction of the hormonally mediated influences on hair growth during pregnancy. When excessive scalp hair shed does occur it is likely due to:

1.Nutritional deficiency: iron, Vitamin D, Iodine, zinc or other deficiency.

2.Metabolic disturbance: thyroid gland dysfunction; pregnancy-related glycaemia (blood sugar + insulin) disturbance.

3.Telogen Effluvium from recent illness.

Regrettably – nutritional deficiency in pregnant women is not uncommonly seen, and is due (in my opinion) to NON-specific baseline pathology testing (i.e.: testing ‘Haemoglobin’ instead of a full ‘Iron Studies’ panel). Vitamin D (25 [OH] D), Iodine or Red cell zinc are rarely ever tested unless specifically requested.

It is unacceptable in a modern health system that pregnant women should be allowed to proceed through pregnancy with severe iron, iodine, vitamin D or other nutritional deficiency. One West Australian woman who consulted me was found to have an iron storage (ferritin) of 8ug/L (range: 20-300) at six months pregnancy.

Quite recently a young woman five months pregnant and expecting her first child consulted me for continual excessive hair shedding. Her Vitamin D levels were so low they could not be measured by pathology testing. The 2007 reference range for 25(OH) D is 50-200nmol/L; ‘target’ is to be greater than 100nmol/L – this woman could only register LESS THAN 10nmol/L.

There are now many studies (www.vitamindcouncil.org) which demonstrate that an optimal Vitamin D status (i.e.: >100nmol/L) during pregnancy is essential for both maternal well-being and in-utero development of the child. There is also a growing awareness of the link between gestational Vitamin D deficiency in the pregnant mother and autism in her still-unborn child: Canadian Paediatric Society. Vitamin D supplementation: Recommendations for Canadian mothers and infants. Paediatr Child Health 2007;12(7):583-9 + Cannell JJ. Autism and Vitamin D. Med Hypotheses 2008;70(4):750-9.

We have a known national Iodine deficiency among the general Australian population (Eastman: 2007); women are physiologically more prone to iron, iodine and 25(OH) D deficiency than males because of their ‘femaleness’. The medico-legal implications of this are self-evident.

Chan (2015) believes pregnant Women should supplement sensibly with organic forms of Iron, Zinc (as ‘Picolinate’) and its synergistic partner Selenium; Vitamin D (especially if pregnant through Autumn-Winter months) & Iodine (essential for the baby’s developing brain and future I.Q.)

Post-partum hair loss:

In essence, post-partum effluvium is a withdrawal of specific hormonal influences previously mentioned which hitherto have prolonged the hair follicle’s growth phase and delayed entry into catagen/telogen.

Following childbirth telogen hair count begins to rise and has been reported as high as 65% at two months (Dawber + Connor: 1971) – typically though 30-35% of scalp hair may be in telogen phase at two months postpartum.

A diffuse effluvium – disproportionate hair shed from the entire scalp – may be distressingly excessive for about three months but can continue for as long as a year. In usual circumstances the duration of shed is less than six months, and the majority of women return to normal hair density within a year.

The prolongation and exacerbation of post-partum hair loss is influenced by Prolactin secretion in breast-feeding, blood loss during childbirth, sleep deprivation, nutrition, or the many reasons for emotional stress in a new mother.

Anecdotally I have found post-partum effluvium to be more severe in those women who are continually sleep derived for extended periods of time. Simply put: if we can’t sleep our Pituitary Gland won’t produce sufficient Growth hormone (GH); we won’t stimulate production of Melatonin*** – we’ll be fatigued, weak, suffer mood disturbance – and our hair will fall out (Arem: 1999).

Management:
  • Post partum alopecia is considered the one true moult in humans, and new young mothers who exhibit post-partum effluvium should be reassured that (in time) a full recovery of lost hair density is the expected outcome.
  • If not previously tested, baseline blood pathology should be ordered to assess iron studies, (red cell) zinc, 25(OH) D, Iodine, B12 etc. All levels need to be in the 50-75th percentile of respective reference ranges to facilitate a more rapid ‘resetting’ of follicle anagen phasing.

Activance Rhodanide is a natural ‘leave-in’ treatment (the vitaminoid Rhodanide is the active nutrient) which I have found very effective in accelerating effluvium resolution. Unlike Minoxidil it is completely safe for lactating/breast-feeding women to use (Minoxidil is excreted in breast milk). www.activance.com.au . Breastfeeding mothers have found Activance ‘Blue’ (ultra-hypoallergenic formulae spray) excellent for ‘nipple care’ and to safely cleanse ‘cradle cap’ of new borns.

Photo-biotherapy such as ‘soft/cold’ low level laser light (LLLT) is in my experience most effective in effluvium-type shedding due to its anti-inflammatory and vaso-dilating (blood perfusion) properties. Six-twelve 15-20 minute treatments twice-weekly helps settle post-partum effluvium in the majority of women.

In theory – providing a post-partum woman experiencing effluvium and/or post-natal mood disturbance with a low dose natural Progesterone (P4) cream (1% or less) with a low-dose ‘Biest’ addition – should help to arrest both issues. However earlier studies by Skelton (1966) found ‘no consistent beneficial effect’.

Consult a qualified and experienced hair loss Practitioner only –such as a Trichologist or Medical Practitioner.

*The Corpus Luteum of non-pregnant females may produce 10-20mgs of Progesterone (P4) per day. A pregnant woman’s placenta produces up to 300mgs of P4 per day (Dr. John R. Lee MD; ‘What your Doctor may not tell you about Menopause’: 1996)

**Ridha Arem MD is a noted US Endocrinologist. He cites a study by Glenoer, D (1997) of American pregnant women.

***See article: ‘Melatonin – the essential night tonic’ at this website.

****PS – ‘Professional Series’ strength is 50% stronger, anti-inflammatory + more effective in the treatment of TE than commercially-available forms.

Copyright Anthony Pearce 2009 (revised Jan 2014) References for this article are contained within the body of the paper.