In June, Alopecia UK attended the European Hair Research Society (EHRS) conference in Sheffield. During this three-day meeting of hair researchers from around Europe, and some even far beyond, we learned all about the latest developments in hair research. There were over 25 presentations, and almost 70 research posters, too much to discuss in-depth, but I will try my best to share some of my key takeaways from this research conference on all things to do with hair. Hopefully this will give you an idea of the research that’s been happening, and make you feel as inspired as we were!

After Professor Andrew Messenger opened the conference, our CEO Sue Schilling delivered a heartfelt address, thanking the researchers for all their efforts in understanding how hair works and the hope that their work brings to people affected by alopecia. She also highlighted the importance of involving people with lived experience in the research process and all the work Alopecia UK do in the research arena.

The opening session on day 1 was all about alopecia areata, with the first presentation at the conference by Professor Kevin McElwee (one of the newest members of our Research Committee). He talked about the history of alopecia areata (AA), how this has been a condition that has been around for thousands of years, and how in some cultures they used to think it was evil spirits that would come and cut people’s hair (pic left of a Kamikiri 'hair-cutting spirit' from the 17th century. For Kevin's full overview of AA history, see his review from 2020).

There are many different suggestions for the causes of alopecia areata throughout history, including deficiencies, infections, nerve disorders, psychological disorders, toxins, hormones, inflammation and autoimmunity. However, a definite answer to this age-old question has not been found. We do now know that immune cells called T-cells attack the hair follicles, leaving them unable to continue growing hair. It does not destroy the hair follicles, as in scarring alopecias, and hair loss may be reversed in some people by treating the inflammation.

However, we still don’t know what triggers this upset in the immune system, and some researchers now believe that there are likely different pathways for alopecia areata to develop. It is also likely that there are ‘redundancies’ in these mechanisms, meaning that in more severe cases, there can be many overlapping mechanisms that would need to be treated to restore natural hair growth – meaning one treatment alone is unlikely to be effective. There are suggestions that people with other allergy-related (atopic) diseases are more likely to develop AA, and in this group it may also be harder to treat the hair loss. This suggests a different pathway of onset in people who do not have other allergic conditions. Another factor is whether someone has a family history, as AA is more likely to develop in this group. This may indicate that in these people the genetic component driving the disease is stronger than in those who do not have a family history. While that would make them more likely to develop it, a trigger would still be needed to set off the hair loss.

Professor McElwee also hypothesised that besides the now widely-supported belief that alopecia areata is an autoimmune condition, in some people it may also develop through a different pathway. This has to do with how the immune system functions. The immune system is made up of the innate and adaptive systems. The innate system is our core defence system that protects us from harmful materials, and it is non-specific: it forms barriers that keep harmful substances out, such as in the skin. It can also activate inflammation responses to make the environment unsuitable for harmful substances to survive. But, by producing chemical signals (cytokines), it can also recruit the adaptive immune system. The adaptive system is made up of cells that are specifically trained to recognise hostile materials, and do this through antigens that are present on the outside of cells. For example, after being infected with a virus, or receiving a vaccine, the adaptive immune system learns to recognise the specific antigen and can destroy it much more easily before the infection takes hold the next time it comes around. However, in autoimmune conditions, the adaptive immune system will mistakenly attack cells of our own body, by targeting cells with auto- (self) antigens. For some reason, these cells are seen as harmful by the trained immune cells. When this happens, T cells attack the hair follicles, leading to hair loss.

The ‘inflammasome’ theory of alopecia areata suggests that alopecia areata can also develop as a result of the innate immune system being wrongfully or overly activated, resulting in recruitment of the adaptive immune system, followed by attack on hair follicles. In this scenario, the trigger does not have to be auto-immune. This theory would support the idea that alopecia areata is not the same disease in all people, and may explain some of the difficulties in finding effective treatments. One of our earlier blog posts explores this further. 

Prof McElwee also posed the question: will there ever be a cure for AA? In his mind it is possible. In a study with mice in 2002, he found that some mice were resistant to AA. Those mice that were resistant had different levels of immune cells and inflammatory signalling molecules (cytokines). Thus, in theory it may be possible to prevent AA by creating a favourable immune profile prior to its development. However, in practice this may be difficult as we won’t be able to predict for everyone whether they will develop AA ahead of time. Curing alopecia areata after it has developed is also another story. It may be that you can restore the immune system to healthy state, but that does not necessarily mean you can prevent it from becoming upset again in the future when another trigger comes along. Again, in terms of a cure, the concept of resistance to AA was only shown in mice, and it may not necessarily carry over to the human setting. Furthermore, as we know from existing treatments, and emerging evidence from treatment with JAK inhibitors, each treatment may only be effective in a proportion of people. So, due to different underlying causes, individually tailored treatment approaches may be required. One example of treating alopecia areata by targeting an underlying cause/trigger was recently shown in a study by Zheng and colleagues (2023). The results from this study suggest that the severity of alopecia areata can be reduced in people allergic to house dust mites by treatment against the house dust mite allergy, as it reduces the underlying pro-inflammatory climate created by the allergens.


Dr Buket Basmanav from the University of Bonn presented results from genetic studies on a cohort of 2,900 people with AA in Germany. They are studying the different clinical and genetic presentations of AA subgroups, for example those who also have atopic conditions, or other autoimmune conditions. So far they have found that patients who have AA + atopic dermatitis, asthma or autoimmune thyroid disease have an earlier age of onset, higher severity and stronger persistence of hair loss. The onset of hair loss was on average almost a decade earlier in those people with an co-existing atopic or autoimmune condition. In addition, results from a different study they are working on may help predict the likelihood of a positive response to treatment for various common AA treatments such as corticosteroids, DPCP and PUVA. However these results are not published yet.

Dr Basmanav also mentioned results from a study investigating the overlap between major depressive disorder (MDD) and AA. The study suggests, like previous studies, that people with AA are at higher risk for MDD. Subgroups that were at particularly high risk were females and people with a personal family history of AA. The research also suggests there is a genetic overlap between AA and MDD, in the region coding for the major histocompatibility complex (MHC), which is involved in presenting antigens to T cells. However, there were no similarities in genetic risk factors in other areas.


Professor Ncoza Dlova, from the University of KwaZulu-Natal, South Africa, delivered a keynote presentation on the causes of alopecia in Black South Africans. She highlighted the role of hair in identity, and its ability to show how we feel and think. She talked about different types of hair, which in their building blocks are all the same, but can take different structural forms. She also highlighted that African hair typically has a relatively lower density (amount of hairs in an area) and slower growth rate. In people of African ethnicity, traction alopecia is the most commonly seen form of alopecia, which is the result of excessive pulling due to the hair styles used. She stressed that more education is needed to tackle this issue.

She also talked about a possible link between scarring alopecia and lichen planus pigmentosus, a rare condition that results in dark coloured patches on the skin. She further highlighted the surge in cases of frontal fibrosing alopecia (FFA): in her clinic she had seen 20 patients between 2006-2012, but 100 patients in 2021 alone. And while FFA is called ‘frontal’, in many cases it involves hair loss on the rest of the scalp and other body areas too. She is now doing a study investigating the causes of FFA, and so far has noticed that the age of onset in African people is much lower at ~36 years compared to ~60 years in White populations.


Dr Summik Limbu, from Imperial College London, talked about androgenetic alopecia. This is characterised by a shorter anagen (active growth phase) of hair, with more hair follicles in telogen (resting phase with no hair growth). It also involves a reduction in size of the dermal papilla (DP), followed by a reduction in the size of the hair follicle itself, in a process called miniaturisation. The dermal papilla is located at the base of the hair follicle and regulates hair growth, and determines the width of the hair shaft. A smaller DP, thought to be caused by increased androgen hormone activity, therefore leads to ‘normal’ hair growth being suppressed. The hair follicles that do still grow hair usually only produce smaller and finer ‘vellus hairs’ as opposed to the normal, thicker ‘terminal hairs’. She hypothesised that there were differences in the DP of hair follicles in the ‘occipital’ scalp (back of the head) and frontal scalp. In frontal DP, there is a higher level of androgen receptors and 5-alpha-reductase enzymes (these convert testosterone to the stronger dihydrotestosterone). Because of this, the effects of androgen hormones on the DP are increased in this region and this leads to suppressed hair growth. The research found that there were differences in the genes of frontal and occipital scalp DP. These differences between the front and back of the scalp therefore may explain the differences in the risk of developing androgenetic alopecia in these regions.


Professor Jeff Biernaskie, from the University of Calgary, Canada, presented on his work on hair follicle dermal stem cells. These stem cells are recruited to repair damage and travel into the dermal papilla (DP) to maintain its regeneration. With aging, the capacity for hair follicle stem cells to regenerate the DP is reduced due to a lower ability to maintain the stem cell pool. There is an increased demand to repair damage, but the stem cells are also less capable of adopting a DP fate. He suggested treatments to prevent age-related hair loss may target preservation or rejuvenation of hair follicle dermal stem cell health to maintain the regenerative capacity of the dermal papilla.


Professor Tom Dawson, of the Skin Research Institute, Singapore, spoke about menopause and the role of the microbiome on hair. He highlighted that 80-90% of the organisms on skin are bacteria, although in terms of total mass this is similar to fungi, which are much larger. This microbiome produces fat-based substances called ‘eicosanoids’ which have important signalling functions, including influences on gene expression, inflammation and cardiovascular functions like blood flow and clotting. This results in our microbiome having an important regulatory function on our immunity. During our lifetime, there may be changes in the microbiome, i.e. the bacterial and fungal species that populate our skin and gut. Especially during puberty and menopause, changes in the species can be observed. This may be a target for therapy in the future: by identifying the types of fatty substances missing in unhealthy skin we may be able to reintroduce these through nutrition or other strategies.


This is just a small selection of the many talks that took place over the three-day conference. Topics for the talks included hair structure, hair follicle macroenvironment (nerves, blood flow, surrounding tissue), hair aging, growth cycling, microbiome, and the psychology of hair loss (including talks from our very own Dr Kerry Montgomery, and AUK-funded researcher Dr Fabio Zucchelli).

Alopecia UK is very grateful to have been invited to attend and speak directly to the wonderful world of hair researchers. To support this community that is working so hard on finding answers to all of our questions, we sponsored two early career researchers to attend the conference: Dr Matthew Wynne, a trainee dermatologist of Salford Royal NHS Foundation Trust; and Leah Redmond, PhD student at Imperial College London, who ended up winning best ‘Basic Science’ poster!  

Alopecia UK also gave out a poster prize, for the research project ‘most likely to impact patients’, which was won by Dr Matthew Wynne for his project titled: ‘Vibration assisted analgesia during intralesional corticosteroid therapy for alopecia’. We know that the pain from corticosteroid injections can put people off starting or continuing treatment and felt this simple solution, i.e., applying vibration to the skin while doing the injections, could benefit many people affected by alopecia.

All in all, it was a very successful conference!