Eczema is a chronic inflammatory skin condition, while shingles presents as a painful rash when the virus that causes chicken pox reactivates in the nervous system, particularly later in life or in immunosuppressed individuals.
When researchers analysed 1997–2023 primary care information pertaining to 113 426 267 people listed in a UK database, they found that individuals with eczema had a 28% higher risk of developing shingles after adjusting for other influencing factors such as age, sex, comorbidities, cigarette smoking, and alcohol use. Use of immunosuppressant medications had a minimal effect on shingles risk. Also, shingles risk increased with the severity of eczema.
Mechanistically, an altered skin immune response in people with eczema may put them at risk of developing shingles.
“These findings may inform vaccination guidelines,” the authors wrote.
Adding oral antihistamines to existing eczema treatments is unlikely to lead to clinically important reductions in eczema and itch severity, and may not reduce sleep disturbance or flare-ups, finds a review of the latest trial evidence published by The BMJ today.
Some antihistamines may also increase side effects such as drowsiness and the risk of patients stopping treatment.
The researchers say this review addresses longstanding uncertainty surrounding the role of antihistamines in treating eczema, and the results do not support their use in routine eczema management.
Atopic dermatitis, commonly known as eczema, is a chronic condition caused by an overactive immune system that leads to dry, inflamed, and intensely itchy skin. It also often impairs quality of life, mental health, and social relationships.
Oral antihistamines are one of the most commonly used drugs for managing eczema, with an estimated one in five UK patients and nearly half of patients in the US using them. Yet despite their widespread use, evidence-based assessments of their benefits and harms in treating eczema remain inconclusive.
To address this uncertainty, researchers reviewed the results of 47 randomised controlled trials involving 6,230 children and adults (average age 20 years; 52% female) with mainly moderate to severe eczema.
The trials compared the effects of adding oral H1 antihistamines, H2 blockers, mast cell stabilizers, or their combinations to placebo (with or without background moisturisers or steroid creams) on eczema severity, itch severity, sleep disturbance, flare-ups and quality of life, as well as harms such as sedation and drowsiness.
The trials were of varying quality, but the researchers were able to assess their risk of bias and certainty of evidence using established tools.
The results show that compared with placebo, H1 antihistamines likely result in a small but clinically unimportant reduction in eczema severity and itch severity and may not reduce sleep disturbance or flare-ups.
First generation (sedating) antihistamines also probably increase cognitive impairment such as sedation and drowsiness, and may increase the risk of stopping treatment due to side effects.
The researchers acknowledge several limitations related to the nature of the included trials, but say these were addressed using standardised and systematic approaches.
As such, they conclude: “This systematic review and network meta-analysis addresses the longstanding uncertainty surrounding the role of antihistamines in treating atopic dermatitis, showing they likely do not meaningfully improve patient important outcomes while probably increasing harms.”
They add: “Our findings do not support their use in routine atopic dermatitis management. We have provided a foundation for an evidence based change in practice, supporting the development of updated atopic dermatitis guidelines that prioritise efficacy, safety, and patient centred care.”
How changes in melanocyte attachment to the extracellular layer drive vitiligo Under normal conditions (left), melanocytes adhere to laminin-211 in the basement membrane through dystroglycan, maintaining their mature pigment-producing state. In vitiligo (right), remodelling of the basement membrane increases laminin-332 and promotes integrin α3β1-mediated adhesion, activating signalling pathways, including c-Jun, that drive melanocyte dedifferentiation and loss of pigment production. Credit: Osaka Metropolitan University
Vitiligo is an autoimmune disease in which the body’s immune system attacks and destroys melanocytes, the cells that produce the skin pigment melanin. Once the melanocytes are gone, the skin turns white, leading to the characteristic skin patches of the disease.
However, the standard model of vitiligo doesn’t explain some of its unusual features. Some vitiligo lesions re-pigment and treatments sometimes restore pigmentation even in areas that lack melanocytes, suggesting that the melanocytes may not be fully destroyed.
A team from Osaka Metropolitan University team led by Specially Appointed Professor Ichiro Katayama and Specially Appointed Associate Professor Lingli Yang has found evidence that melanocytes do not completely disappear from vitiligo skin and instead enter a “dedifferentiated-like state” in which the mature cells revert to a more primitive form, losing many of their specialised functions including the production of pigment.
“This study uncovers a new mechanism underlying the development of vitiligo, which could change how we treat the disease,” Dr Yang explained.
Their research adds to a body of research that shows that cells do not just respond to chemical signals, but also to what they are physically attached to. As melanocytes are located on the basement membrane, the thin layer that separates the epidermis from the dermis, the membrane provides instructions that help them remain functional pigment-producing cells.
However, the extracellular matrix surrounding melanocytes is remodelled in vitiligo patients. Usually, melanocytes bond with laminin-211; however, in vitiligo patients, the basement membrane becomes enriched in laminin-332. Because their preferred binding partner is no longer available, melanocytes change how they attach. Instead of using their preferred attachment agent, dystroglycan, they attach through integrin α3β1 instead.
These changes activate pathways that are commonly activated when cells are remodelling. In this process, the actin cytoskeleton of the cell is reorganised, gene expression is altered, including that of genes associated with an immature melanocyte state. The findings suggest a self-reinforcing cycle in which changes to the basement membrane drive melanocyte dedifferentiation, while the dedifferentiated melanocytes become less able to maintain a healthy basement membrane, further promoting the disease process.
“This was an exciting discovery for us, as most current treatments largely focus on suppressing autoimmune attacks and reducing inflammation, but if dormant melanocytes are still present in lesions, that might change the way we treat the disease,” Professor Katayama said. “New treatment avenues such as reactivating existing cells or restoring their normal attachment to the basement membrane may be possible.”
When the researchers used pharmacological inhibitors targeting the signalling pathways activated by this adhesion switch, they were able to restore expression of mature melanocyte markers, recover pigmentation-related gene expression, and reverse many features of the dedifferentiated-like phenotype.
“This was an exciting aspect of our research, as it suggests that changing gene expression isn’t permanent and this process may be reversible,” Dr Yang explained. “We found that drugs were able to restore melanocyte function and pigmentation-related characteristics. The next step will be to perform clinical studies to see if this approach is a viable way to manage the disease.”
Globally, more people are using GLP-1 and other weight-loss medicines, and some are experiencing severe hair loss while taking them. But just because it is happening during treatment does not necessarily mean the treatment caused it. According to Dr Kashmal Kalan, Medical Director at Alvi Armani, “Hair shedding during treatment isn’t always caused by the medicine itself. In many cases, it may be the body’s response to losing weight too quickly. Your body reacts as though food is scarce and thinks: ‘Hair isn’t essential. Let’s save energy’.”
Rapid weight loss can increase the risk of temporary hair shedding, whether it follows GLP-1 treatment, bariatric surgery, a very low-calorie diet, or illness. The trigger is often the speed and extent of the weight loss rather than the treatment itself. Eating much less can also leave patients short of nutrients that hair needs. “Think of hair like a houseplant. If you don’t water it enough with the right nutrients, it grows poorly. It doesn’t necessarily die permanently but simply pauses its growth.”
The concern is becoming more relevant as weight-loss medicine use grows in South Africa. Discovery Bank and Visa’s latest SpendTrend report found that 14% of surveyed higher-income South Africans use prescribed weight-management medication. Clinical research has also found that GLP-1 medicines reduced energy intake on a controlled test day by nearly a quarter compared with placebo, which helps explain why nutritional adequacy may become more important when appetite drops.
Dr Kalan says Alvi Armani is seeing more patients who report sudden hair shedding weeks or months after starting weight loss treatment and assume the medicine is directly responsible. The consultation must then establish when the shedding began, how quickly the patient lost weight, how their eating patterns changed, and whether another medical cause needs to be investigated.
The potential causes behind rapid hair loss
A review of nearly half a million adults on GLP-1 treatment found vitamin D deficiency in 7.5% of patients at six months, climbing to 13.6% by twelve months. That’s why bloodwork and not a shopping list of supplements is the first step in any hair loss consultation at Alvi Armani, whether GLP-1-related or not. Standard testing includes vitamin D, B12, ferritin, and thyroid function as standard.
“Ferritin, the protein that stores iron, is one marker I monitor closely. A level below 30 ng/mL, generally considered indicative of low iron stores in adults, is often enough to cause shedding on its own, even though most labs still call that number normal. Most of these patients feel completely fine elsewhere, so there’s no reason for a routine GP visit to pick it up. By the time the hair’s already falling out, we go back and look for what that visit potentially missed.”
Some patients may also reach for gut-health supplements because they assume hair loss comes from issues in the gut. However, Dr Kalan notes, probiotics will only address the problem if a digestive condition is actually contributing to it. Research remains limited, with the largest randomised trial to date finding reduced shedding among the probiotic group, but no meaningful improvement in hair density or thickness.
“If someone has a diagnosed digestive condition, that’s worth treating, and probiotics may have a place. Outside of that, I’d rather see patients pursue tests that can identify what’s missing than a supplement with no clear indication, strain, or dose.”
Dr Kalan encourages anyone on a GLP-1 medication to take shedding seriously if it continues past three months, worsens noticeably, or comes with fatigue or other symptoms that don’t add up. “These medications genuinely change lives for the right patient. If your registered health professional recommends continuation, stay on it. Just make sure your body is still getting what it needs.”
Students and dermatologists are determined to find how rosemary and rosemary extract can repair damaged skin without leaving scars
Penn undergraduate student Jiayi Pang (left) and Penn PhD candidate Emmanuel Rapp Reyes (right) found that rosemary can help skin wounds heal without causing scars.
The social media trend touting rosemary and rosemary extract as part of skincare routines is now backed by science. A compound found in rosemary leaves may significantly improve the healing of skin wounds and reduce scarring, according to new research published in JCI Insight from the Perelman School of Medicine at the University of Pennsylvania.
“Many skin injuries end in scars, and in some people, it can lead to long-term cosmetic and even functional issues,” said senior author Thomas Leung, MD, PhD, an associate professor of Dermatology at Penn. “Our findings suggest that rosemary extract, and specifically the antioxidant, carnosic acid, can shift the healing process from scarring to healthy skin regeneration. We don’t have proven ways to consistently do that in humans.”
The hypothesis behind the hype
The inspiration for this study stemmed from an unusual place: TikTok and Instagram. After seeing beauty influencers and other social-media users touting the skin-healing benefits of homemade rosemary extract serums and products with rosemary, Penn undergraduate student Jiayi Pang and Penn PhD candidate Emmanuel Rapp Reyes turned to Leung for expertise. Then, they did what all good scientists do: they went to the lab and ran their own tests.
“We hypothesized there was likely something real behind the hype because rosemary contains many antioxidants,” said Pang, co-lead author of the study. “But we knew in order to really uncover its potential, we needed to prove its healing properties and uncover how exactly it was facilitating healing.”
Conducting the research in mice, the researchers made cream with carnosic acid, a naturally occurring antioxidant mostly existing in rosemary, to accelerate wound closure and restore hair follicles, oil glands, and cartilage. They also found that a particular nerve sensor in the skin previously identified as essential to scarless healing, TRPA1, was critical for stimulating the healing in this instance, too. When tested in mice without the TRPA1 sensor, which previous research from Leung showed is responsible for scarless healing, carnosic cream lost its impact.
“We also identified other herbs, such as thyme and oregano, that may activate TRPA1. But rosemary stood out for its potency and safety,” said Rapp Reyes, co-lead author of the study. “Other natural ingredients, such as mustard oil, or the topical medication imiquimod are known to also stimulate the TRPA1 receptor, but unlike rosemary, those can cause irritation and inflammation,”
The researchers also found a localised effect from rosemary; scarless healing only occurred when carnosic acid cream was applied to the site of the injury but not when it was applied to skin far from the wound.
The team at Penn, however, notes that individuals should speak with their doctors before incorporating rosemary skincare products in their daily regimens or mixing up their own rosemary-based concoctions. Nevertheless, given rosemary’s accessibility and low cost, the researchers hope their findings will inspire further investigation into its use in human wound care, especially for patients at risk of excessive scarring.
“If rosemary is part of your skincare regimen and you think it’s working, it likely is,” said Leung. “I’m proud that the young scientists that led this research sought answers to questions in their everyday lives.”
QIMR Berghofer scientists have uncovered hundreds of genes that play a role in the growth of both moles and melanoma, in a discovery that could lead to new ways of preventing and treating the deadliest form of skin cancer.
The world’s largest genetics study of ‘moliness’, published in Nature Communications, is unravelling the complex causes of both moles and melanomas that are not related to well-known risks caused by sun exposure, skin colour, and pigmentation.
The team found risk genes linked to biological pathways that could lead to the development of a mole or melanoma. These include an immune response pathway that may be failing to control cell growth, and genes implicated in harmful cell proliferation in other types of cancer, such as breast cancer, prostate, and brain cancers.
Working out how to stop these risk pathways could lead to new melanoma drug targets and prevention strategies that go beyond sun protection.
“We know how to reduce sun exposure and risk through SunSmart behaviours, and new immunotherapies have greatly improved survival rates. But people still get melanoma and people still die from melanoma,” A/Prof Law said.
“Existing immunotherapies fail to work for half of all patients with late-stage melanoma, so we need to find other ways to target the disease. By studying moles, we’re learning more about the biology of melanoma so we can find new ways of controlling it.”
Moles and melanomas share the same cellular origin, forming from a pigment-producing cell called a melanocyte that gives skin its colour. In moles, the cell multiplies to form a cluster then stops growing, leaving a harmless spot. In melanoma, the cell growth continues aggressively.
Moliness is strongly influenced by your genes and having a high mole count is a major risk factor for melanoma. Around a third of melanomas develop from a mole.
The QIMR Berghofer research analysed data from more than 85000 participants of European ancestry discovering 24 new genetic regions that determine the number of moles someone has. This is a five-fold increase on the five areas found in an earlier 2018 study also led by QIMR Berghofer researchers.
All but one of the genetic regions for mole count also play a role in melanoma. The team pinpointed more than 250 key genes in these regions to prioritise for further research.
One of the new genes, SIKE1, regulates immune responses to viral infections. The researchers think it could enable the development of melanomas by malfunctioning and affecting the immune system’s ability to detect and destroy melanocytes that are multiplying abnormally. This could be a promising target for a potential immunotherapy that could possibly prevent early stage melanoma growth.
“I’m really proud to be continuing this long legacy of research. Our study increases understanding of why some people have a lot of moles and why some people develop melanoma so we can better treat and prevent this skin cancer,” Ms Jayasinghe said.
The researchers used the study insights to create a Polygenic Risk Score (PRS) for moliness to predict those who are genetically more likely to have a large number of moles, which could be integrated into melanoma screening tools in future to improve their accuracy in finding those at high risk so they can receive extra monitoring.
The next step is to analyse even larger data sets to find more genetic regions involved in moliness and melanoma. The researchers are also searching for existing drugs that could potentially target the newly identified biological pathways.
New findings identify keratinocytes as replication hubs and immune responders, contributing to the risk of rabies infection from superficial scratches or minor bites
Skin cell (keratinocyte) This normal human skin cell was treated with a growth factor that triggered the formation of specialised protein structures that enable the cell to move. We depend on cell movement for such basic functions as wound healing and launching an immune response. Credit: Torsten Wittmann, University of California, San Francisco
While it was previously thought that keratinocytes (skin cells) were only passive conductors that allow the rabies virus to pass through, novel research reveals that these cells play a much more active role. The findings of a new study in the Journal of Investigative Dermatology (JID), published by Elsevier, provide direct evidence that keratinocytes can support viral replication and transmit the rabies virus to neurons. The investigators offer a mechanistic explanation for how superficial skin exposures from scratches or minor bites by dogs and bats can lead to neuroinvasion, contributing to the risk of infection.
Rabies is a fatal zoonotic infection caused by rabies virus (RABV), responsible for at least 59 000 human deaths per year. The virus is transmitted through the saliva of infected animals. While most cases are caused by dog bites, superficial exposures such as bat bites or scratches can also lead to infection, although the underlying mechanisms remain poorly understood.
“In our previous work, we discovered that keratinocytes – cells that form the epidermis, the outermost layer of the skin – were infected at the site of entry of the rabies virus, both in natural and experimental infections. This was unexpected, as rabies pathogenesis has traditionally focused on muscle cells and motor neurons,” explains lead investigator Corine H. Geurts van Kessel, MD, PhD, Department of Viroscience, Erasmus Medical Centre, Rotterdam, The Netherlands. “Given the strategic position of keratinocytes at the skin barrier and their close proximity to sensory nerve endings, we wanted to understand whether these cells are simply bystanders or active participants in early rabies infection and neuroinvasion.”
The investigators used primary human keratinocyte cultures to investigate susceptibility to rabies virus infection and characterise the resulting antiviral immune responses. Three viral strains were tested: a vaccine strain and two wild-type (“street”) strains derived from fatal human cases associated with bat and dog exposures. The dog-associated strain caused only minimal infection and limited keratinocyte immune activation, whereas the other two strains infected keratinocytes more readily and triggered a pronounced antiviral response.
To simulate the close contact between keratinocytes and intra-epidermal nerve endings, a co-culture model of keratinocytes and neurons was developed. In this model, virus produced in infected keratinocytes was successfully transmitted to adjacent neurons, giving the virus a direct route into the nervous system. Once the virus has established infection in the central nervous system, it is almost inevitably fatal.
“Our study demonstrates that the skin might play a more important role in rabies infection than previously recognised. We were particularly surprised by the strong antiviral response mounted by keratinocytes to the bat-related rabies virus strain,“ notes co-investigator Keshia Kroh, PhD candidate, Department of Viroscience, Erasmus Medical Centre, Rotterdam, The Netherlands. “Wild-type rabies viruses are known for their immunosuppressive capacities, and we expected an immune evasive effect in keratinocytes. Instead, we observed the opposite. This raises new questions about how keratinocyte-derived immune responses influence overall disease progression in rabies and other viral infections of the skin.”
This in vitro co-culture model is the first to study rabies virus entry to the nervous system across a cell barrier. Future in-depth studies should be performed to provide mechanistic insight into the differential strain tropism, the interactions of infected keratinocytes with immune cells, and the mechanisms of neuroinvasion from superficial skin contact.
According to the World Health Organization (WHO), any transdermal exposure (including small scratches or abrasions) should be assessed as a potential rabies risk and managed appropriately based on exposure category and clinical context.
“Our study provides a biological rationale for these recommendations,” says co-investigator Carmen W.E. Embregts, PhD, Department of Viroscience, Erasmus Medical Centre, Rotterdam, The Netherlands. “At the same time, it is important to emphasise that the risk of rabies virus infection via superficial exposures depends on multiple factors, including the nature of the exposure and the epidemiological setting. Rather than causing alarm, our findings support informed decision-making. Awareness that superficial skin exposures can represent a route of neuroinvasion helps ensure that potential risks are recognised and evaluated appropriately, while treatment decisions remain guided by established public health criteria.”
“The data in this study support the increasingly recognised concept that cells in the skin are in snug communication with the nervous system. That a scratch or bite is needed for the transmission of rabies is further evidence of the importance of an intact skin barrier in health,” observes JID Associate Editor Ethan Lerner, MD, PhD, Associate Professor of Dermatology, Harvard Medical School, and Massachusetts General Hospital, Boston, MA, USA.
Study led by UTSW researchers defines how skin hormones influence bacteria and results in potential treatment for Staph infections
This laboratory image shows Staphylococcus aureus bacteria streaked in the shape of a sex steroid, like testosterone. The left shape is of wild-type S. aureus, with the lighter halo around the shape indicating haemolysis, or the breakdown of red blood cells, releasing their haemoglobin into the surrounding fluid. The right shape is a quorum-sensing mutant strain of S. aureus, which cannot damage blood cells.
Men are more susceptible than women to skin infections caused by Staphylococcus aureus bacteria, but the biological basis for this disparity has remained unclear. A new study led by UT Southwestern Medical Center researchers is the first to reveal that testosterone as a key driver of infection. The sex steroid activates a bacterial communication pathway known as quorum sensing, increasing skin cell death and promoting the destruction of red blood cells and white blood cells called neutrophils.
Published in Nature Microbiology, the study also reported that a mirror-image form of testosterone, known as an enantiomer (ent-T), blocks quorum sensing and prevents S. aureus from damaging tissue in mouse models.
Senior author Tamia Harris-Tryon, MD, PhD, Associate Professor of Dermatology and Immunology at UT Southwestern, and first author Maria S. John, PhD, a UTSW postdoctoral researcher, have a patent pending for an ent-T-based therapeutic along with collaborators at the University of Colorado.
“This research has important implications for treating Staph skin infections and conditions complicated by Staphylococcus, such as atopic dermatitis, pemphigus, abscesses, and wound infections, including the deadliest skin infections caused by methicillin-resistant Staphylococcus aureus [MRSA],” Dr Harris-Tryon said. “It also explains why men are more susceptible to Staph infections.”
S. aureus is the leading cause of skin infections. When it enters the bloodstream, it can cause septicaemia, a life-threatening infection that may lead to organ failure.
During infection, the bacteria use quorum sensing to detect neighbouring cells of the same species. As bacterial density rises, they produce short signalling molecules called auto-inducing peptides (AIP), which activate virulence programs and trigger toxin release, resulting in host-cell damage.
The research team found that male skin cells consistently secrete higher levels of testosterone than female skin cells. They also found the same is true for male mice, which were significantly more susceptible to S. aureus colonisation and skin damage than female mice when exposed to a strain of MRSA. However, mice engineered to secrete less testosterone displayed greater resistance to the bacteria, while applying testosterone to the skin of female mice increased MRSA’s severity.
In laboratory experiments, testosterone activated quorum sensing even in the absence of AIPs. Other sex steroids, including progesterone and oestrogen, had no measurable effect on quorum sensing.
While using ent-T as an experimental control, the researchers unexpectedly identified its therapeutic potential. In lab tests, ent-T inhibited quorum sensing and reduced the bacteria’s virulence. The molecule also inhibited quorum sensing on male and female mice when applied to their skin.
Dr Harris-Tryon won an Innovation Award from the UTSW Office for Technology Development in 2024 to fund development of an ent-T-based transdermal therapeutic for Staph.
“Our exciting finding suggests we can inhibit S. aureus virulence rather than killing the bacteria directly, an approach that prevents infection, preserves beneficial skin microbes, and reduces the selective pressure that drives antibiotic resistance while offering a potential new strategy to treat infections, including MRSA,” Dr. John said.
This work builds on Dr Harris-Tryon’s studies in 2023 and 2025 with Jeffrey McDonald, PhD, Professor in the Center for Human Nutrition and of Molecular Genetics at UTSW, which demonstrated sex-specific differences in skin hormone production. The team also has previously uncovered how the immune system stimulates testosterone production in skin cells. Dr Harris-Tryon said the current research builds on UT Southwestern’s longstanding leadership in steroid and skin hormone biology, a field in which the institution has been a global leader for decades.
A team of researchers at the Icahn School of Medicine at Mount Sinai, Weill Cornell Medicine, and other institutions have uncovered a key biological explanation for why atopic dermatitis (eczema) so often starts in childhood. The study, in young mice, found that some types of immune cells in early-life skin are more reactive than those in adults, a difference that may help explain why children are more vulnerable to inflammation and allergic skin disease.
The findings, reported in Nature, suggest that early childhood represents a critical window for immune-driven skin disease and may shed light on why atopic dermatitis is often the first condition in a broader pattern of allergic disease.
Atopic dermatitis (AD) affects nearly one in four children and often appears early in life. It can also precede other allergic conditions, including asthma and food allergies. Until now, scientists have not fully understood why the disease is so strongly linked to early childhood.
“We found that allergy risk is shaped very early in life, when the skin’s immune system is biologically programmed to overreact to allergens, with important consequences for understanding how immune-mediated diseases emerge and should be treated,” says senior study author Shruti Naik, PhD, Associate Professor of Immunology and Immunotherapy, and Dermatology at the Icahn School of Medicine. “By pinpointing the cells and hormonal signals that control this window of vulnerability, we open the door to strategies that could prevent allergic disease before it spreads from the skin to the lungs, gut, and beyond.”
The researchers discovered that a specific immune cell type, the dendritic cell, in young skin behaves differently than in adults. These cells do not overreact to everything – but when it comes to allergens, they respond faster and more strongly, setting the stage for inflammation and AD early in life. In adult skin, the same cells are far less reactive.
To understand why allergies often start in early childhood, researchers exposed infant mice to everyday allergens such as dust mites and mould. Unlike adult mice, the infants developed strong skin inflammation, revealing a brief early-life period when the skin’s immune system is especially sensitive.
The scientists traced this response to dendritic cells, which are unusually active shortly after birth and triggers allergic inflammation. When this pathway was blocked, the young mice did not develop skin allergies.
The team also found that infants lack normal levels of stress hormones that later help keep immune reactions in check, allowing these allergic responses to take hold. Importantly, signs of the same immune activity were found in skin samples from children with early-onset AD, but not in adults, suggesting this early-life window may also be important in humans.
“This work was only possible through a true clinic-to-lab collaboration – where insights from paediatric patients shaped the questions we asked in the lab,” says study co-author Emma Guttman-Yassky, MD, PhD, professor at the Icahn School of Medicine. “By studying allergic disease where it actually begins, in early life, and by modelling clinically relevant allergens and disease features, lead author Yue Xing, PhD, uncovered immune biology that simply doesn’t appear in adult models. By revealing what’s unique about the early-life immune system, this work explains why eczema so often begins in infancy.”
Next, the investigators plan to explore ways to block this early-life immune pathway to stopallergic disease before it spreads from the skin to other organs.
“Beyond eczema, this study reinforces a critical point for medicine,” says Dr Naik. “Children are not simply small adults when it comes to immunity. Their immune system follows a unique set of rules, and recognising that difference is essential for understanding – and ultimately preventing – allergic, immune-driven diseases that begin in childhood.”
From genetics to stress myths, researchers reveal what really drives greying and the breakthroughs pointing to natural colour restoration
Photo by Ravi Patel on Unsplash
Grey hair is more than a cosmetic concern – it drives a booming industry, influences how people are perceived, and can affect confidence. Globally, the hair colour market was valued at nearly USD 28 billion in 2025, with over half of purchases linked specifically to concealing greys. In South Africa, spending on hair colourants is projected to grow from roughly USD 172 million in 2021 to over USD 228 million by 2028, highlighting the demand for solutions that go beyond temporary cover-ups.
By age 50, roughly 50-70% of adults have visible grey hair, while premature greying can appear in some as early as the 20s. The psychological weight is clear: studies indicate grey hair can make people appear 20-30% older, influencing workplace perception, social interactions, and self-esteem. Studies show faces with grey hair are consistently perceived as more subdued than the same faces without greys, confirming that hair colour alone can shape social impressions.
“Many popular beliefs about greying hair are misleading,” says Dr Kashmal Kalan, Medical Director at Alvi Armani. “Stress does not turn hair grey overnight, plucking one strand won’t trigger several more, and no supplement or home remedy has been proven to restore pigment reliably. The reality is far more biological – genetics and pigment cell behaviour are the keys we are finally beginning to understand.”
At the heart of greying are melanocyte stem cells (McSCs) within hair follicles. In youth, these cells migrate and maintain melanin production, the pigment responsible for hair colour. With age, many become inactive or “trapped,” interrupting pigment delivery and causing grey strands. In mouse models, freeing these cells restored pigment production in roughly half of cases – a major step toward therapies that could reawaken natural colour without dyes.
Emerging research aims to tackle the root cause rather than just the appearance of grey hair. Scientists are exploring topical agents that target dormant pigment cells, metabolic modulators that influence follicle behaviour, and activation therapies designed to revive pigment production. These innovations could allow hair to regain its natural shade – not just cover it – while supporting overall follicle health.
“We are witnessing science that was once purely theoretical become reality,” says Dr Sunaina Paima, aesthetic and hair-restoration physician at Alvi Armani Johannesburg. “For patients, this could mean seeing grey strands regain their original shade naturally – a moment the hair science world has long dreamed of. The potential impact on confidence and self-esteem is enormous, because this isn’t just about covering colour, it’s about restoring it at a biological level.”
While most pigment-restoring therapies remain in development, advances in genetics, dermatology, and biotechnology are converging at unprecedented speed. “For decades, grey hair was seen as an irreversible hallmark of ageing,” adds Dr Kalan. “Today, that assumption is being seriously challenged. We’re on the brink of options that rejuvenate hair from the inside out, not just cosmetically.”
These breakthroughs signal a new era in hair science: ageing hair may no longer be inevitable or purely cosmetic, but a biological process that can be understood, guided, and ultimately restored.
