by Professor Andrew Messenger

It was at a meeting of the Investigative Group of the British Association of Dermatologists (later to change its name to the only slightly less cumbersome British Society for Investigative Dermatology) in 1981 in Cardiff. I was very junior dermatology trainee.  A lecture on the Siberian hamster, one of those animals that exchanges a brown coat in the summer for a white coat in the winter. The lecturer explained the mechanism underlying the change in hair colour which occurs when the animal moults in the spring and autumn. I was fascinated.

Back in Sheffield a few days later I discussed it with my boss, Dr Ronald Church.  He was not interested in hamsters but, on the topic of hair pigmentation, told me he had always been intrigued by the sparing of white hair in alopecia areata (AA). I had never heard of this but shortly thereafter I saw my first case.

Grey hair is typically a mixture of pigmented and non-pigmented hair and if AA occurs in a person with grey hair, only the pigmented hair may fall out, leaving the white non-pigmented hair – this is thought to be the explanation for people ‘going white overnight’. It struck me that this must be telling us something fundamental about how hair follicles are affected in AA and I set out to explore what it may be. 

This first involved learning all I could about hair biology, about the pathology of AA, and what was known about the mechanisms responsible for greying of hair (not very much at the time). Then to taking biopsies from willing patients, and onto various laboratory methods to try to understand how hair pigmentation is affected in AA.  The results supported the idea that the hair follicle is attacked by immune cells in AA and helped to identify the part of the hair follicle that is the target of this attack. This appeared to be where specialised cells in the hair root are starting to form the hair fibre itself and where pigment is being produced by cells known as melanocytes. We were also able to explain how the follicle responded to the attack in a way that meant it was not destroyed. However, it was not possible to fully explain why non-pigmented hairs, which lack melanocytes in the hair root, are usually spared in AA. This is still the case although, as I mention later, we are making some progress.  Nonetheless, my interest in hair growth in general, and AA in particular, had been well and truly sparked.

From there I became more involved in lab-based research, especially in the development of hair follicle cell-culture models. Then, as the demands of being an NHS dermatologist increased, I turned to pursuing more clinically oriented projects which, as in that first case, were often based on seeing patients with hair problems that posed questions or generated new ideas.

For example, female androgenetic alopecia (FAGA) had long been assumed to be the same condition as male androgenetic alopecia (male pattern hair loss/baldness) and due to a combination of genetic factors and androgens (hormones like testosterone). But some women with typical FAGA have no androgens. How could this be explained? Is FAGA truly an androgen-dependent condition? Is it genetic? The research involved measuring hair density and hair diameters in over 400 women, taking family histories of hair loss in women and in 700 men, measuring hormone levels and sebum production and taking DNA samples for genetic studies. The results suggested that, although true androgenetic alopecia does occur in women, this pattern of hair loss, which we now prefer to call female pattern hair loss (FPHL), cannot be fully explained on that basis. Most women with FPHL have normal female levels of androgens and only one of the 12 genes then known to be associated with male AGA, showed an association with FPHL, and then only weakly. We now think that other factors are contributing to FPHL, possibly environmental, but we do not yet know what they are.

Pursuing these ideas would not have been possible without the help and involvement of many others including colleagues in Sheffield and from around the UK (Valerie Randall, Matt Harries, Walter Gibson, Gill Westgate, Kerry Montgomery, Roy Oliver, Andrew McDonagh, Rachid Tazi-Ahnini and Hugh Rushton to name only a few), and beyond (especially Niki Romani in Austria, Silke Redler and Regina Betz in Germany and Rod Sinclair in Melbourne). Here in Sheffield, I am particularly indebted to my researcher colleagues Pattie Birch and Kathy Dobson who did most of the work.

In 2006 Pattie and I organised a meeting of the European Hair Research Society (EHRS) in London. Pattie had previously established an alopecia support group in Sheffield through which she encountered the newly formed charity Alopecia UK. We invited AUK to the EHRS meeting and that was the start of a long and ongoing relationship with the charity. AUK’s Jackie Tomlinson (then McKillop) joined the team producing the 2012 Alopecia Areata Guidelines for the British Association of Dermatologists. I was the Chair of the organising committee for the World Congress for Hair Research in Edinburgh in 2013. We invited Jackie to speak at the event, and she gave an inspirational speech in our opening talks.

Income from that meeting was donated to Alopecia UK and was used to fund the Hair Research Priority Setting Partnership, a team enterprise led by the charity and Abby Macbeth. Alopecia UK has become ever more involved in research in recent years. They can provide the patient input into design, assessment and, increasingly, the running of research projects now usually required by grant-awarding bodies.

AUK has also invested directly in research itself, most recently in the form of supporting PhD studentships, and also provides help to support research by others. In a recent clinical trial of a new topical treatment for alopecia areata sponsored by Soterios, AUK provided invaluable help in recruiting trial participants. Perhaps most importantly the UK hair research community and AUK share a common purpose and working together has undoubtedly helped us to progress more effectively. Over the years, I have been happy to support AUK wherever I can, including speaking at the charity's first ever conference, a precursor to the AUK Big Weekend. 

Finally, back to hair pigmentation and AA. Three recent studies- one in the UK and two in the USA- found varying rates of AA across different population groups, with the highest prevalence observed among individuals of Asian heritage, where the risk was approximately three times greater than those of White ethnicity. Another study in White British people, has found that the darker the hair colour the greater the risk of developing AA. Taken together, these findings suggest that the risk of developing AA is influenced by the amount of melanin (pigment) being produced in hair follicles, although it is clearly not the whole story as people with fair hair do get AA and, although less susceptible, white non-pigmented hair can be affected by the disease. Our understanding of how melanin production makes hair follicles vulnerable to AA is still limited, and we need research to provide the answer. Whether this will lead to better treatments is hard to know but the ideas are out there and being discussed.

The biology of hair growth is a source of great wonder and fascination. Although human hair is regarded by some as trivial and unimportant, as mammals, we would not be here without it. Perhaps an ancient connection with our evolutionary history underlies the impact that alterations in hair growth can have on our psychological wellbeing.

Looking back over the past 40+ years of my career in dermatology, understanding of hair loss conditions has come a long way. I am proud of the part I have played in this and continue to be fascinated by new research findings. Through research we are making progress in treating hair diseases but there is plenty more to do.