Bioderma Congress Reports IMCAS 2026

Report written by Dr Lidiya-Todorova (Dermatologist, Bulgaria) 

Chairs: Dr. Leonor Alda GIRAO (Dermatologist, Portugal) and Dr. Nicolas KLUGER (Dermatologist, Finland), 

Speakers:  Dr. Nicolas KLUGER (Dermatologist, Finland) 

Report written by Dr Lidiya-Todorova (Dermatologist, Bulgaria) 

Chairs: Dr. Suleima Arruda and Prof. Neil Sadick 

Speakers:  Ronda Farah and Pr. Neil S. Sadick 

Report written by Dr Dimitris Motsios (Dermatologist-Venereologist, Greece) 

Speakers: Dr Shadi Kourosh (USA), Dr David Gunn (Netherlands), Dr Yuki Ogura (Japan), Dr Mukta Sachdev (India), Virginie Couturaud (France), Rishabh Kala (India) and Dr Elodie Valin (France) 

Skin Longevity: Separating the Science from Snake Oil 

Speaker: Dr Shadi Kourosh (USA) 

Dr Kourosh opened the session by addressing the rapid proliferation of the term “skin longevity,” emphasizing the necessity of anchoring this concept in measurable biological mechanisms rather than marketing language. She proposed that true longevity in dermatology must be defined by preservation of cellular competence, structural integrity of the extracellular matrix (ECM), and sustained inflammatory equilibrium over time. A central focus of her lecture was inflammaging a chronic, low-grade inflammatory state characterized by persistent activation of NF-κB signalling and increased expression of IL-6, TNF-α, and matrix metalloproteinases (MMP-1, MMP-3). These mediators drive progressive collagen I and III degradation and elastin fragmentation, weakening dermal tensile strength [1]. Importantly, she highlighted the role of senescent fibroblasts expressing p16INK4a and components of the senescence-associated secretory phenotype (SASP), which perpetuate inflammatory amplification and ECM breakdown. Mitochondrial decline was presented as an upstream event in visible skin aging. Reduced NAD+ availability compromises SIRT1 activity, impairing genomic repair mechanisms and increasing oxidative stress burden [2]. This metabolic insufficiency accelerates collagen crosslinking through glycation and enhances dermal stiffness. The result is not simply wrinkle formation but a progressive reduction in tissue resilience. Clinically, Dr Kourosh advocated a shift from corrective strategies toward biologically preventive interventions. Barrier stabilization reduces inflammatory signalling cascades; mitochondrial support and redox balance help preserve fibroblast functionality; and early ECM protection may delay structural collapse. Rather than focusing exclusively on wrinkle depth or volume loss, dermatologists should evaluate durability, structural coherence, and inflammatory control as longevity endpoints. The overarching message was clear: skin longevity must be evidence-driven, mechanistically justified, and rooted in intrinsic biological preservation rather than accumulation of external materials. 

Youthful Looks and Health 

Speaker: Dr David Gunn (Netherlands) 

Dr Gunn presented longitudinal epidemiological data supporting the concept that facial appearance reflects systemic biological aging. Drawing primarily from the Rotterdam Study, he demonstrated that individuals who appeared younger than their chronological age exhibited significantly lower rates of osteoporosis, chronic obstructive pulmonary disease, cataracts, and cognitive decline [3].  

These associations persisted after adjustment for lifestyle factors, suggesting that perceived age reflects underlying biological processes rather than cosmetic variation alone. Further evidence from a Danish twin cohort reinforced this association. In that study, each additional perceived age year increased mortality risk by 14%, exceeding the predictive value of chronological age (11%) [4]. Importantly, controlled image manipulation experiments confirmed that intrinsic facial morphology skin texture, wrinkle distribution, dermal laxity rather than hairstyle or clothing, drove mortality prediction. Mechanistically, dermal aging mirrors systemic aging pathways. Collagen density reduction, elastin fragmentation, and glycation-induced crosslinking increase tissue stiffness and impair biomechanical recovery. Advanced glycation end-products (AGEs) accumulate with age and oxidative stress, promoting fibroblast dysfunction and vascular compromise. Mitochondrial inefficiency and chronic low-grade inflammation further contribute to microvascular fragility and ECM degradation. Dr Gunn also discussed the emerging role of AI-based morphometric analysis. High-resolution phenotyping can quantify subtle structural changes in dermal architecture, potentially transforming perceived age from a subjective metric into an objective biological biomarker. The clinical implication is significant: improving skin structure may reflect systemic health optimization. Dermatology therefore occupies a unique position at the intersection of aesthetics and preventive medicine, where visible skin changes provide early insight into organismal aging trajectories. 

Next-Generation Anti-Aging Strategy for Wrinkle Improvement and Prevention 

Speaker: Dr Yuki Ogura (Japan) 

Dr Ogura presented a biomechanical model of wrinkle formation based on 3D elasticity mapping.  

Two structural alterations were identified in aged skin: the development of an “elastic gap” between a stiffened stratum corneum and a softened papillary dermis, and selective loss of compliance within the superficial dermal layer. Mechanical simulations demonstrated that even modest increases in stratum corneum stiffness amplify stress transmission to deeper dermal compartments. This stress redistribution contributes to wrinkle propagation independent of absolute collagen quantity. A critical molecular finding involved the decline of type V collagen after age 40. Type V collagen regulates fibrillar assembly of type I collagen and contributes to dermal elasticity. Reduction in its expression alters fibril architecture and compromises biomechanical flexibility. Ex vivo studies demonstrated that retinol restored type V collagen expression within 48 hours while simultaneously reducing stratum corneum stiffness [5].Beyond its well-known effect on keratinocyte turnover, retinol appears to modulate papillary dermal biology. By influencing collagen synthesis, reducing MMP expression, and supporting dermal matrix organization, retinoids function as structural regulators rather than superficial exfoliants. Under current European regulatory concentration limits, stabilization technologies become essential to maintain efficacy at lower doses. This highlights the importance of formulation science in achieving biological impact. The lecture reframed wrinkle prevention as correction of mechanical imbalance and restoration of dermal coherence, aligning anti-aging interventions with tissue biomechanics rather than purely cosmetic smoothing. 

The Longevity Aesthetic Blueprint 

Speaker: Dr Mukta Sachdev (India) 

Dr Sachdev described a clear shift in aesthetic dermatology from volumetric replacement toward regenerative sequencing. Patients increasingly request natural outcomes that preserve facial identity while improving tissue quality. 

Regenerative approaches aim to stimulate intrinsic repair pathways rather than introduce inert bulk. Key biological mechanisms include fibroblast activation, TGF-β modulation, neoangiogenesis, and controlled inflammatory signalling. Platelet-rich plasma (PRP) delivers growth factors such as PDGF and VEGF, enhancing collagen synthesis and vascular support. Injectable platelet-rich fibrin (iPRF) provides sustained release of cytokines and growth factors. Polynucleotides (PDRN) stimulate DNA synthesis and promote angiogenesis through adenosine A2A receptor activation, supporting dermal regeneration. Biostimulatory injectables induce controlled collagenesis through mild inflammatory signalling, leading to gradual matrix remodeling. The emphasis is on tissue behaviour rather than volume accumulation. Excessive filler deposition may alter biomechanics and compromise long-term structural coherence, whereas regenerative sequencing supports progressive dermal strengthening. Dr Sachdev highlighted that early intervention sometimes termed “prejuvenation”  may delay structural collapse by maintaining ECM quality before significant volume loss occurs. The overarching principle is biological coherence: interventions should respect tissue physiology, minimize inflammatory burden, and promote durable matrix organization. This approach reflects a maturation of aesthetic dermatology toward long-term structural optimization. 

Reverse Aging Beyond Anti-Aging 

Speaker: Virginie Couturaud (France) 

Virginie Couturaud presented transcriptomic and proteomic insights into aging skin derived from single-cell analysis. Over 800 genes in keratinocytes and more than 1,000 in dermal fibroblasts demonstrated age-dependent modulation. Affected pathways included oxidative stress regulation, circadian rhythm control, mitochondrial metabolism, and ECM structural proteins. Proteostasis decline emerged as a key contributor to aging. Impaired autophagy and reduced proteasome efficiency allow accumulation of damaged proteins, accelerating cellular dysfunction. Concurrent dysregulation of NAD+ metabolism and sirtuin signalling compromises genomic stability and redox homeostasis. Cutaneous aging was also discussed in relation to systemic aging. Recent collaborative research published in Nature Aging suggested that senescent cell accumulation in skin may contribute to broader inflammatory signalling, positioning skin as an active participant in organismal aging rather than a passive reflector. The lecture emphasized precision strategies targeting redox balance, mitochondrial efficiency, and structural protein preservation. Interventions that stabilize cellular metabolism and maintain proteome integrity may extend skin healthspan. This systems-biology perspective reinforces a shift from superficial anti-aging claims toward mechanistically validated longevity interventions grounded in cellular preservation. 

Genomics, Metabolomics and Personalized Skin Aging 

Speaker: Rishabh Kala (India) 

Rishabh Kala explored the integration of genomics and metabolomics in personalized dermatology. Genetic polymorphisms affecting inflammatory mediators, MMP expression, FLG barrier proteins, and aquaporins influence hydration, inflammatory susceptibility, and collagen turnover. Variants in BCO1 may impair conversion of beta-carotene into active vitamin A, altering retinoid responsiveness. Polymorphisms affecting vitamin C transport and recycling influence collagen hydroxylation efficiency. These predispositions partially explain inter-individual variability in treatment response. Metabolomics provides real-time insight into oxidative stress markers, glutathione availability, glycation products, and one-carbon cycle efficiency. Assessment of transsulfuration pathways and methylation capacity may reveal redox vulnerability or accelerated matrix degradation.  

The combination of genetic predisposition and metabolic state enables individualized strategies targeting barrier repair, antioxidant reinforcement, and collagen preservation. Rather than applying uniform protocols, precision dermatology seeks to align interventions with biological variability, improving predictability and long-term outcomes. 

Skin Microbiome and Aging 

Speaker: Dr Elodie Valin (France) 

Dr Valin presented large-scale microbiome data demonstrating reproducible age-related compositional shifts. Aging skin shows reduced abundance of Cutibacterium and Lactobacillus species and increased representation of anaerobic taxa. Cutibacterium metabolizes sebum lipids into free fatty acids and propionic acids, contributing to PPARα activation and maintenance of barrier integrity. Age-related decline reduces beneficial lipid metabolism and may impair hydration and inflammatory regulation. Microbial diversity shifts influence local pH, lipid composition, and immune signalling. Dysbiosis may amplify low-grade inflammation and barrier fragility, accelerating structural decline. Machine learning models applied to microbiome datasets demonstrated accurate prediction of chronological age based solely on microbial composition, reinforcing the microbiome as a biomarker of aging trajectory. Preservation of microbial balance, gentle cleansing strategies, and barrier-supportive formulations emerge as central components of longevity-oriented dermatology. 

References 

1. Franceschi C, et al. Inflammaging and age-related diseases. Nat Rev Immunol. 2018. 

2. Covarrubias AJ, et al. NAD+ metabolism and aging. Nat Rev Mol Cell Biol. 2021. 

3. Gunn DA, et al. Perceived age as predictor of mortality. BMJ. 2009. 

4. Christensen K, et al. Perceived age and survival in twins. BMJ. 2009. 

5. Ogura Y, et al. Mechanical imbalance and collagen V restoration in wrinkle formation. J Dermatol Sci. 2024. 

Summary  

What struck me at IMCAS 2026 is that the entire discussion, whether it came from cosmeceuticals, injectables, devices, microbiome, or genomics, kept converging on the same destination: skin aging is being reframed as a problem of biological durability, and the future is bioregeneration and skin healthspan, not more product and not more volume. The sessions repeatedly moved away from the old correction model and toward a model where we preserve and restore what the skin is supposed to do: maintain barrier competence, regulate inflammation, sustain mitochondrial energy balance, and keep the extracellular matrix mechanically coherent over time. That is the foundation of natural results today, not minimalism as a lifestyle choice, but a clinical philosophy where the most natural outcome is the visible expression of restored physiology. 

At IMCAS, this shift was explicit in the skin longevity and healthspan framing: dermatology is moving from antiaging toward healthspan, emphasizing structure, function, resilience, and prevention rather than purely aesthetic endpoints. That theme appeared again and again in different scientific languages. In the next generation antiaging strategy lecture, wrinkles were presented not as superficial lines but as visible endpoints of deeper mechanical and biological changes.  

The most important message was that modern antiaging does not erase, it normalises mechanics and biology early, before the system collapses into correction. The retinol elasticity lecture then gave the most concrete mechanistic explanation of what this means: wrinkle formation was tied to a previously underrecognized mechanical imbalance, including an elastic gap between a stiffened stratum corneum and a softened dermis, and a selective softened layer in the upper dermis, both of which actively drive wrinkle development. Retinol’s value, in that model, is not marketing tradition; it is its capacity to reduce stratum corneum stiffness, narrow the elastic gap, and restore the upper dermal soft layer, with type V collagen highlighted as a structural component of that functional softness that declines after 40 and can be restored ex vivo within two days. In other words, the future conversation is no longer what ingredient works, but what intervention restores the mechanical architecture that prevents deepening of biological damage.  

This naturally leads to a broader regenerative thesis: the extracellular matrix is not a passive scaffold; it is a living biomechanical signalling system, and fibroblasts are not simply collagen factories; they are decision makers responding to tension, inflammation, oxidative stress, and nutrient state. When the extracellular matrix fragments, through matrix metalloproteinases, glycation crosslinks, oxidative damage, or senescence driven inflammatory signalling, fibroblasts lose their normal mechanotransductive cues and drift toward dysfunction. Modern biostimulation is, at its best, an attempt to re-establish the biological conditions that allow fibroblasts to behave like competent fibroblasts again: to build organized collagen, maintain elastin integrity, and sustain dermal hydration and viscoelasticity. That is why the regenerative aesthetics trends talk resonated with what was repeatedly emphasized throughout the congress as the future: post COVID patients are prioritizing tissue quality and natural outcomes, and the core regenerative mechanisms described, fibroblast activation, controlled inflammatory response, neoangiogenesis, immune modulation, extracellular matrix remodelling, and increased collagen and elastin synthesis, are precisely the biological levers that determine a natural, durable result. The message is not anti-filler in an ideological sense; it is a strategic re balancing where correction is no longer the primary endpoint; tissue biology is. 

The longevity framing gained even more weight when perceived age was linked to systemic health. The congress content described large cohort work showing that those who look younger tend to have lower prevalence of multiple age associated conditions and better cognition, and that looking older does not correspond to fewer diseases. This is consistent with prospective population evidence showing perceived age is associated with morbidity and mortality, supporting the concept that facial aging can function as a biomarker of biological aging, not merely a cosmetic characteristic. This is clinically relevant because it elevates skin longevity from aesthetic preference to biological signal: the face becomes a readout of systemic resilience, inflammatory burden, and tissue integrity. 

From a future looking perspective, IMCAS also made clear that the next decade will be shaped by integration of intercellular signalling therapies, cellular housekeeping biology, and senescence modulation. Exosomes and extracellular vesicles are biologically compelling because they constitute a native communication language between cells, carrying proteins, lipids, and nucleic acids capable of influencing inflammation, angiogenesis, fibroblast behaviour, and wound repair. Reviews summarizing translational and early clinical work support biological plausibility, but they also highlight current limitations: variability in vesicle source, lack of standardized dosing and potency assays, heterogeneity of manufacturing, and insufficient large controlled clinical trials for many marketed claims. There are also public scrutiny and regulatory concern around unapproved exosome products marketed in aesthetic settings, reflecting the reality that a biologically active product category will demand medical grade standardization and oversight if it is to become credible and widely adopted. What to expect, therefore, is not a simple exosome expansion, but a separation between rigorously manufactured, clinically studied extracellular vesicle therapies and non-standardised commercial offerings that may face increasing restriction. 

Proteostasis and autophagy emerged as essential concepts for skin longevity because durability is not only about collagen synthesis; it is also about cellular quality control. Autophagy is the system by which cells clear damaged proteins and organelles, including dysfunctional mitochondria. Impairment of autophagic flux contributes to accumulation of oxidative damage, metabolic inefficiency, and reduced regenerative capacity, affecting keratinocytes and fibroblasts alike. Dermatologic research increasingly emphasizes that autophagy intersects with oxidative stress, senescence, and tissue repair, and that its decline is a hallmark mechanism of aging in skin biology. The practical implication is clear: biostimulation in a metabolically compromised environment produces less predictable outcomes. Regeneration becomes more durable when cellular maintenance systems are supported, redox balance is improved, and mitochondrial function is preserved. 

Senescence modulation is the most direct bridge between longevity science and clinical dermatology. Senescent cells accumulate with age and secrete SASP mediators that amplify inflammation and extracellular matrix degradation. The congress content explicitly referenced senomorphic and senolytic strategies as emerging approaches, alongside mitochondrial fitness and a behaviour targeting treatment philosophy rather than simple volume restoration. In the broader scientific landscape, topical geroscience approaches are no longer theoretical; they have entered human exploratory trials, including topical rapamycin studies reporting measurable changes in senescence associated markers and clinical parameters in skin, supporting proof of principle for topical modulation of aging biology. This is a significant signal: the next generation of antiaging is increasingly likely to be defined by quantifiable effects on senescence burden, inflammatory signalling, and structural preservation rather than by surface smoothing alone. 

The clinical evidence base for collagen stimulation is evolving toward a more mature, trial driven framework. Prospective controlled studies and expanding systematic reviews support the efficacy and safety of biostimulatory agents such as poly L lactic acid and calcium hydroxylapatite for tissue quality and contour outcomes, with increasing attention on protocol variables that directly influence biological remodelling: dilution, depth, session spacing, and objective assessment of dermal change. Hyperdiluted calcium hydroxylapatite is particularly relevant to the longevity conversation because it shifts the modality away from volumisation and toward collagen stimulation and skin quality improvement, aligning it with regenerative goals. What is coming next is not simply wider adoption, but better protocol science and more robust endpoint selection, including ultrasound measures of dermal thickness, elastography, and validated clinical skin quality scales. 

The genomics and metabolomics concepts captured at IMCAS align with how longevity medicine is developing globally: prediction combined with targeted correction. Genomics indicates predisposition while metabolomics reflects real time biochemical activity, allowing clinicians to connect inflammation, glycation pathways, oxidative stress, collagen breakdown, and antioxidant capacity with individualized interventions. This is clinically meaningful because two patients receiving the same biostimulatory protocol may generate different collagen outcomes depending on mitochondrial competence, oxidative stress burden, metabolic status, barrier dysfunction, and inflammatory tone. Longevity focused dermatology therefore becomes a precision discipline, integrating biological state with procedural planning. 

If I had to summarize what IMCAS 2026 felt like scientifically, it was this: regenerative aesthetics is no longer an isolated aesthetic trend; it is becoming the clinical expression of longevity biology. The emerging standard is an evidence-based plan that preserves extracellular matrix architecture, protects mitochondria and proteostasis, reduces inflammaging and senescence burden, stabilizes barrier and microbiome ecology, and uses biostimulatory tools, topical, injectable, device based, and lifestyle linked, not to change the face, but to restore tissue behaviour. That is why natural results are dominating: not because patients want less medicine, but because advanced medicine now aims to make tissue function better, not simply look different. 

What to expect from the future, based on what was visible at IMCAS, is a move toward structured longevity protocols with defined biological endpoints. We will see more integrated sequencing where barrier and microbiome management are treated as prerequisite steps, not adjuncts. We will see wider use of objective imaging and AI phenotyping to stratify aging patterns and predict responders. We will see a stronger evidence gap addressed in areas like exosome biology and senotherapeutics, with regulatory pressure forcing standardization and clinical trials. We will see more emphasis on mitochondrial support and proteostasis as necessary foundations for durable regeneration. Above all, we will see that the most credible antiaging will be the one that proves biological durability. 

From a practical clinical standpoint, this longevity model translates into a different way of selecting patients, planning sequencing, and defining success. The first step is to identify whether the primary limitation is structural extracellular matrix collapse, inflammatory load, barrier fragility, metabolic compromise, or a combination, because each of these conditions changes how the tissue responds to stimulation. In early aging, where fibroblast capacity remains relatively intact, regenerative interventions can be preventive and lighter, focusing on maintaining dermal quality and preventing mechanical imbalance. In moderate aging, where the extracellular matrix is fragmented and inflammation is higher, sequencing becomes critical: barrier repair and inflammation control precede strong stimulation, because stimulating a fibroblast in an inflamed, oxidatively stressed environment risks unpredictable remodelling. In advanced aging, where senescence burden and glycation stiffness dominate, realistic expectations and combination strategies become essential, and the value of senomorphic modulation and metabolic stabilization becomes more relevant. 

Success, in this framework, should be measured as longevity outcomes rather than only cosmetic change. That includes improved skin resilience, improved structural coherence, and durable quality improvement over months rather than transient correction over days. It includes a shift toward objective assessment where feasible, incorporating imaging metrics such as dermal thickness, tissue stiffness patterns, and changes in skin quality parameters. The role of the dermatologist expands: not only to inject or treat, but to curate a biologically coherent plan that preserves function and extends healthspan. 

Bioderma’s relevance within this longevity-oriented model is direct and scientifically coherent because the first layer of skin longevity is barrier competence and inflammatory control. When the barrier is impaired, transepidermal water loss increases, microbial balance destabilizes, and low-grade inflammatory signalling intensifies. That environment accelerates extracellular matrix fragmentation through increased oxidative stress and protease activity, and it reduces the predictability of any regenerative intervention because fibroblasts respond poorly when chronic inflammation, barrier disruption, and metabolic stress coexist. A barrier first strategy therefore becomes foundational, not supplementary. The practical consequence is that medical grade dermocosmetic support is no longer positioned as maintenance after procedures only, but as part of the core longevity protocol that creates the biological conditions required for durable tissue quality improvement. Within this approach, formulations that support lipid restoration, reduce irritant driven inflammation, and respect microbiome equilibrium can be framed as protective measures for dermal structure over time, because they reduce the upstream triggers that amplify inflammaging and accelerate matrix degradation. In a longevity perspective, the most credible skin care is the one that improves functional resilience, reduces inflammatory reactivity, and supports long term stability.  

This aligns with what was consistently emphasized at IMCAS, namely that the future of aesthetic dermatology is built on prevention, preservation, and biological coherence, with natural outcomes emerging as a clinical consequence of restoring tissue physiology rather than imposing external correction. 

Report written by Dr Lev Naidoo, (Dermatologist, South Africa) 

Chairs : Dr Geisa Costa and Dr Edward Lain 

Speakers: Dr Mukta Sachdev (India) and Dr Elodie Valin (France)  

Proteome Protection as the key to skin cellular longevity- A new topical approach inspired by recent discoveries in age-related diseases 

Speaker: Dr Elodie Valin (France) 

Ecobiological Approach 

Dr Elodie Valin , the NAOS scientific director, presented on the concept of proteome protection and its significance in cellular longevity.  

Ecobiology combines ecosystem science with biology, treating the skin as a living ecosystem that interacts with the environment, with a goal of supporting the skin’s biology for long-lasting benefits, rather than merely treating signs of aging. 

Research Background 

The NAOS partnership with world- renowned biologist Professor Radman, provided direction for a change in focus from the genome to the proteome when approaching skin health. Professor Radman’s research demonstrated how extremophilic bacteria were able to survive in the most challenging environments, through the bacteria’s capability to repair damaged DNA via their proteomic make-up that included inoxidable repairing proteins. 

The proteome is the complete set of proteins in a cell or tissue. Proteins are the most abundant component in the body after water and as such are of key importance in supporting skin longevity through their dual structural and functional roles. 

Protein Carbonylation in the Skin

Protein carbonylation is the one type of oxidative damage that is specific to proteins. It freezes a protein into a three-dimensional structure that is non- functional, which in time aggregates into larger structures that are toxic to our cells, making them both a marker and accelerator of cell aging. 

Clinically protein carbonylation in the skin presents with epidermal dehydration, loss of radiance, a decrease in dermal density and rhytid appearance. 

Proteome Protection and Skin Aging 

The exobiological approach of protecting the proteome therefore protects from clinical signs of aging.

Clinical Proof 

A hemi-face 6-month clinical study demonstrated this patented proteome technology’s superior result when used in a serum with a neutral cream in comparison to the sole use of the neutral cream in terms of skin firmness, density, evenness of complexion and rhytid improvement. 

Report written by Dr Lev Naidoo (Dermatologist, South Africa) 

Chairs: Prof Martina J Kerscher and Dr Shadi Kouros 

Speakers: Prof Hassan Galadari, Dr Shadi Kourosh and Dr Barbara Dalbos Bouillard 

Reversing skin age: epigenetic science meets aesthetics  

Speaker: Prof Hassan Galadari 

Introduction to Epigenetics 

Prof. Galadari introduced this lecture on epigenetics by reminding us that whilst our genetic makeup accounts for our diversity, the greater nuances reflected by the epigenetic read on our genes further extrapolates this diversity.  

Key: All the cells in our body have the same genetic make-up. Epigenetics refers to the regulation of gene expression without altering the underlying DNA sequence. It represents the functional interface between the genome and the environment. 

Mechanisms of Epigenetics 

Epigenetic changes allow genes to be expressed in various ways. 

Key mechanisms include: 

1. DNA Methylation: this process involves the addition of methyl groups to DNA, affecting gene activation.
2. Histone modification: this alters the accessibility of DNA for transcription.
3. Non-coding RNA: this affects gene expression post – transcriptionally 

Through evolving epigenetic science, we understand as individuals age, certain genes may become expressed or suppressed. 

Extrinsic factors including UV exposure, toxin, smoke , pollution, stress, altered sleep patterns and suboptimal nutritional intake may turn protective genes off, compromising our overall health, including our skin’s health. 

Protective Factors 

Prof. Galadari went on to highlight that this process may also be positively modified in the skin by the inclusion of key skin practices that turn on reparative gene pathways i.e.: supportive epigenetic pathways. 

1. Sun Protection: Sunscreen helps by preventing UV damage to genes. 

2. Antioxidants: Certain substances e.g.: vitamin C, help shield against oxidative stress.
3. Cell regulators: Ingredients like retinoids support collagen production. 

Clinical Procedures and Epigenetics 

Prof. Galadari further highlighted the synergism of these protective skin ingredients with appropriate clinical procedures including laser and intense pulsed light treatments that also have the capacity to positively affect our epigenetic read. 

Chang et al. J Invest Derm.2013  

Hamelin MR. Photomed Laser Surg. 2018  

Haykal D et al. J Cosmet Dermat. 2025 

Epigenetics in Precision Skincare 

Speaker: Dr Shadi Kourosh 

Introduction 

Dr Adrianne Shadi Kourosh’s lecture was a continuation into how we can practically utilize principles of epigenetics in our clinics. She opened with key supportive skincare and procedures we can include to switch on protective epigenetic reads and further went on to explain the importance of timing select skincare ingredients to the natural circadian rhythm of the skin. 

Epigenetics and hyperpigmentation: how can epigenetics go beyond the classic “anti-tyrosinase” approach? 

Speaker: Dr Barbara Dalbos Bouillard 

Introduction to hyperpigmentation 

Hyperpigmentation is often viewed as an excess of pigment produced by melanocytes following exposure to acute inciting stimuli. Dr Bouillard challenged this perspective, postulating that it may instead be an alteration in melanocyte behaviour with immunological memory cells driving the process of pigment production even beyond the point that the inciting stimulus has passed . 

Epigenetic factors in hyperpigmentation 

Exposure to inflammation modulates the expression of key melanocyte regulators. This modulation affects both the synthesis of pigment and the skin’s sensitivity to pigment-promoting stimuli. 

Key: The skin can remain affected long after an initial melanin-inducing trigger has disappeared. 

Concept of cellular memory 

Hyperpigmentation is initiated by exposure and inflammation but can become self- perpetuating even when the exposing stimuli or inflammatory insult is no longer present. Cellular memory may therefore result in the persistent upregulation of melanogenic pathways, in the absence of ongoing stimuli. 

Clinical Observations 

The process of cellular memory explains how pigmentation can persist for months or even years without ongoing visible inflammation, suggesting a long-lasting functional programming of melanocytes instead of just temporary activation. 

This impact may be more intense in the higher Fitzpatrick skin types, where inflammatory responses lead to greater pigment production, with a slower reset a slower to baseline tone. 

Treatment challenges and importance of upstream intervention 

Many treatments fail as they have focused on decreasing pigment production rather than subduing persistent inflammatory memory. Strategies must focus upstream on controlling inflammation. The prevention and control of cellular memory is crucial for durable results in the context of hyperpigmentation. 

Dr Bouillard highlighted that topical steroid fails as they only temporarily decrease inflammation but do not have the capacity to act on important chronic melanogenic gene promotors like MITF. 

Peels for Skin of Colour- Update and Newer Formulations in 2026

Speaker: Dr Mukta Sachdev 

Key Trends for Skin of Colour in 2026 : Superficial peels are preferred for their safety and efficacy in skin of colour patients. There is a shift toward gentler, lower concentration peels that minimise the risk of both post-inflammatory hyperpigmentation and downtime.

Priming is a Key Step : The priming process should be respected for two to four weeks prior to the procedure. Pre-peel, it allows for detection of potential causes for clinical intolerance and in so doing decreases the risks of adverse effects. It also allows time to establish whether a patient can be compliant with a skincare routine. Priming further facilitates uniform penetration of the peeling ingredient during the peel and allows for a smoother healing process following the peel.

Priming Agents : These may include sunscreen, topical alpha- or beta- hydroxy acids, retinoids or ingredients that subdue the melanogenic pathways.

Report written by Dr Lev Naidoo (Dermatologist, South Africa)

Chairs: Dr Ferial Fabian and Dr Michael H Gold

Speaker: Dr Ross Raduscky

Beyond the scale: the nutritional pitfalls of diet extremes and GLP-1s

Speaker: Dr Ross Raduscky

The Ozempic Face Phenomenon

Ozempic face is a colloquial term, that can be used to describe rapid facial deflation and increased skin laxity resulting in accelerated visible aging, hair shedding and slower post- procedural recovery following the use of GLP-1 agonists or rapid weight loss from extreme dieting. Counselling should occur at the beginning of diet extremes or GLP-1, therapy not after symptoms arise.