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2/1/2026 Comments Is skin purging real? The word “purging” is currently frequently used on social media for almost any breakout after starting a new product and often framed as skin needing to get worse before it gets better.¹ In medicine this is not an official diagnosis, however dermatologists do sometimes see a short phase where acne gets a bit worse in the first weeks of treatment and then clearly improves.¹⁻³ This pattern has been documented mainly for topical prescription retinoids, oral isotretinoin and superficial chemical peels.¹⁻⁵ By contrast, ingredients such as niacinamide, cosmetic strength retinal, retinol and bakuchiol do not show the same clear “purge curve” in controlled studies, even though they are often labelled as “retinoid like” online.⁶⁻¹³ This article explains what purging is, which ingredients truly cause it, how long it tends to last and what the science says about popular actives like niacinamide, vitamin C, retinal, retinol and bakuchiol. HOW ACNE FORMS AND WHY PURGING CAN HAPPEN Every acne lesion starts as a tiny blocked pore under the skin, called a microcomedone.¹˒¹⁴ Over time this can develop into a visible whitehead or blackhead and then sometimes into an inflamed papule or pustule.¹˒¹⁴ Treatments that change how skin cells shed inside the pore or that strongly normalise follicular keratinisation can speed up the transition from microcomedone to visible lesion.¹⁻⁴˒¹⁴ This includes retinoic acid strength prescription retinoids and some chemical peels. When they are started, many hidden clogs can surface within a short period, making it look as though “new” acne has appeared.¹⁻⁵  In a true purge, the breakout: ▌Appears in areas where you already get acne ▌Looks like your usual type of acne ▌Starts soon after beginning or increasing a comedolytic treatment ▌Then slowly settles as overall acne improves In contrast, allergic or strong irritant reactions often bring burning or stinging, marked redness and sometimes bumps in new areas that were not acne prone. AGENTS WITH SOLID EVIDENCE FOR EARLY FLARES Prescription topical retinoids (tretinoin, adapalene, etc.) Topical retinoids are first line treatments for comedonal and inflammatory acne and act by normalising cell turnover within the follicle.¹˒²˒⁴ In a pooled analysis of phase 3 trials, tretinoin 0.025% gel used in mild acne caused a measurable early flare in some patients, defined as at least a 10% increase in inflammatory lesions at week 2.² About 15.4% of patients on tretinoin alone met this flare definition compared with 8.7% on vehicle.² In the same analysis, a clindamycin 1.2% and tretinoin 0.025% fixed combination did not show a statistically significant flare at week 2, suggesting that adding an anti inflammatory and antibacterial partner can mitigate this effect.² Clinical reviews summarise that redness, dryness and a small temporary rise in spots are most common in weeks 1 to 3, while overall lesion counts typically fall over 8 to 12 weeks.¹˒²˒⁴ Oral isotretinoin Oral isotretinoin is reserved for severe, scarring or treatment resistant acne. It reduces sebum production and exerts strong comedolytic and anti inflammatory effects.¹˒⁵ Early flares are well described. They tend to occur in patients with many large comedones and in younger males.⁵ One study found that multiple comedones, male sex and young age were linked to a higher risk of flare, while very severe flares remained uncommon.⁵ Guidelines therefore recommend starting isotretinoin at about 0.5 mg/kg/day and increasing to 1 mg/kg/day as tolerated.¹˒⁵ This gradual approach helps control early worsening and mucocutaneous side effects while preserving long term efficacy.¹˒⁵  AGENTS WITH SOLID EVIDENCE FOR EARLY FLARES Prescription topical retinoids (tretinoin, adapalene, etc.) Topical retinoids are first line treatments for comedonal and inflammatory acne and act by normalising cell turnover within the follicle.¹˒²˒⁴ In a pooled analysis of phase 3 trials, tretinoin 0.025% gel used in mild acne caused a measurable early flare in some patients, defined as at least a 10% increase in inflammatory lesions at week 2.² About 15.4% of patients on tretinoin alone met this flare definition compared with 8.7% on vehicle.² In the same analysis, a clindamycin 1.2% and tretinoin 0.025% fixed combination did not show a statistically significant flare at week 2, suggesting that adding an anti inflammatory and antibacterial partner can blunt this effect.² Clinical reviews summarise that redness, dryness and a small temporary rise in spots are most common in weeks 1 to 3, while overall lesion counts typically fall over 8 to 12 weeks.¹˒²˒⁴ Superficial chemical peels and strong AHAs or BHAs Superficial chemical peels using glycolic acid, salicylic acid or salicylic–mandelic blends are widely used in acne and post acne marks.³˒¹²⁻¹⁵ A systematic review of superficial peels for acne identified multiple randomized controlled trials and found that these procedures do improve acne severity but that flare ups can occur as adverse events.³ In one glycolic acid trial about 12% of patients in the peel group experienced flares while no flares occurred in the placebo group, although this difference was not statistically robust.³ Other studies comparing 35% glycolic acid with 20% salicylic–10% mandelic or phytic acid peels showed significant lesion reductions by 12 weeks.¹³⁻¹⁵ Across these studies, typical side effects included transient flare ups, erythema, dryness and scaling.³˒¹²⁻¹⁵ These data support a picture where peels can both help acne and temporarily make it look worse in some patients early in a treatment course. Benzoyl peroxide Benzoyl peroxide is antibacterial and mildly comedolytic and is a standard treatment for inflammatory acne.¹⁶ Detailed prospective data on week 2 flares are limited, but academic patient guidance notes that acne can look worse at first on benzoyl peroxide and that improvement is usually seen after 4 to 6 weeks.¹⁶ When benzoyl peroxide is combined with adapalene in fixed dose products, clinical trials generally show a steady decline in lesion counts, and early flares appear milder than with tretinoin monotherapy.³˒¹²˒¹⁶ OTHER INGREDIENTS WITHOUT STRONG PURGING EVIDENCE Niacinamide: more helper than trigger Niacinamide is frequently accused online of causing purging, yet its documented clinical profile is largely anti inflammatory and barrier supportive.⁶⁻⁹˒¹¹ A review of nicotinamide in dermatology found benefits in acne and other inflammatory conditions and reported a generally mild side effect profile.⁶ In a split face randomized trial, a ceramide and niacinamide containing moisturizer used alongside adapalene 0.1% and benzoyl peroxide 5% improved lesion counts and barrier function compared with a hydrophilic cream, without a higher rate of early flares.⁷ A clinical study of a dermocosmetic serum containing a multi acid complex plus niacinamide in acne prone skin showed significant improvement in acne severity and texture over 8 weeks. Only a few cases of mild, short lived discomfort were reported.⁸ Niacinamide has also been shown to improve melasma and post inflammatory hyperpigmentation with good tolerability.⁹⁻¹¹ Based on current evidence, niacinamide is better described as a supportive co ingredient that improves tolerance of acne therapies than as a purging trigger.⁶⁻⁸ Do retinal and retinol cause purging? Retinal and retinol are vitamin A derivatives used mainly in cosmetic products for texture and photoageing. They are often grouped with medical retinoids, but their clinical data tell a more nuanced story.¹²˒¹⁷⁻²⁰ Within the retinoid pathway, retinal needs only a single conversion step to become active retinoic acid in the skin, whereas retinol requires two steps and most retinol esters or other derivatives require three, which makes them progressively less potent and slower acting in vivo. A pilot study of a 0.05% retinaldehyde loaded niosome nanoemulsion in 23 participants with mild to moderate acne found a significant reduction in open and closed comedones after 2 and 4 weeks.¹⁷ Sebum levels and desquamation indices decreased, and the product was well tolerated, with no serious adverse events reported and no documented early spike in lesion counts.¹⁷ An earlier randomized trial tested retinaldehyde 0.1% gel used once daily with erythromycin 4% lotion versus erythromycin alone in acne vulgaris.¹⁸ Both groups had significant reductions in papules and pustules. Comedones and microcysts improved significantly in the retinaldehyde plus erythromycin group but not with erythromycin alone. Local tolerance was described as very satisfactory, with only a few irritation cases and no emphasis on initial flaring.¹⁸ Most cosmetic retinol data come from photoageing studies, which mainly report irritation signs such as scaling, burning or stinging.¹⁹˒²⁰ These studies do not show a reproducible pattern of early acne flares followed by clear improvement in the way seen with tretinoin in acne trials.²˒⁴ Taken together, the existing evidence for retinal and retinol suggests: ▌They can improve comedones or photoageing signs over several weeks.¹⁷⁻²⁰ ▌They often cause some irritation at higher strengths.¹⁹˒²⁰ ▌They have not been shown to cause a consistent, quantifiable “purge then improve” acne pattern like prescription tretinoin.²˒⁴ What about bakuchiol
Bakuchiol is a plant derived compound that influences many of the same genes as retinol and is often called a “natural retinol alternative”.²¹⁻²³ In a 12 week randomized, double blind trial, 44 patients applied either bakuchiol 0.5% cream twice daily or retinol 0.5% cream once daily for facial photoageing.²¹ Both groups showed significant reductions in wrinkle surface area and pigmentation, with no statistical difference in efficacy, but retinol users reported more scaling and stinging.²¹ A comprehensive review of topical bakuchiol concluded that it behaves as a functional retinol analogue for photoageing with minimal side effects and better tolerance.²²⁻²³ In vivo and ex vivo work shows multi directional activity on collagen, pigmentation and oxidative stress but does not report early acne worsening as a consistent feature.²²⁻²³ So while bakuchiol is “retinol like” in terms of gene expression and anti ageing, the available data suggest: ▌It is often better tolerated than retinol.²¹ ▌It does not show a clear acne purge pattern in clinical studies.²¹⁻²³ Vitamin C and other trendy actives Vitamin C serums are often blamed online for “purging”, but clinical studies of topical ascorbic acid focus mainly on photoageing and pigmentation rather than acne.³˒⁹˒²⁴ These trials sometimes report stinging, burning or erythema as side effects, yet they do not show the characteristic early acne flare with later improvement that is documented for prescription retinoids and isotretinoin.¹˒²˒⁵˒²⁴ Vitamin C is not a proven purging agent, and breakouts after starting a vitamin C product are more likely due to irritation, the vehicle or an underlying acne fluctuation than to a true mechanistic “purge”.¹˒²˒³˒⁵˒²⁴ PURGING VS IRRITATION
HOW LONG DOES PURGING LAST WHEN IT HAPPENS Across agents that truly cause purging, the pattern is broadly similar. Purging, if it occurs, tends to appear in the first 1 to 3 weeks of a new treatment and then settles over the next 4 to 12 weeks as total lesion counts drop.¹⁻⁵˒³˒¹²⁻¹⁵ With topical prescription retinoids, the peak of dryness, redness and extra spots is usually between weeks 1 and 3, with clearer improvements by weeks 8 to 12.²⁻⁴ With isotretinoin, early flares are most common at higher starting doses and in those with many macrocomedones.¹˒⁵ With peels, selective patients may notice a flare after the first or second treatment, while repeated sessions over several weeks show net reductions in lesions.³˒¹²⁻¹⁵ Provided the treatment is continued at a tolerable intensity and there are no signs of severe reaction, purging generally resolves without leaving new scarring.¹˒²˒⁵ IS PURGING AN OILY-SKIN TYPE PROBLEM Clinical data do not support the idea that only oily skin can purge. In the isotretinoin flare study, the main risk factors were multiple comedones, male sex and younger age. Seborrhoea as such was not singled out as a separate predictor.⁵ In the tretinoin flare analysis, flares occurred in some patients with mild acne regardless of skin type.² Peel trials included a mix of Fitzpatrick phototypes and baseline skin characteristics, with flare ups reported across this spectrum.³˒¹²⁻¹⁵ In practice, any person with a significant microcomedone burden can experience purging when a strong comedolytic therapy is started, even if their skin is not very oily.¹˒³ MANAGING AND MINIMISING PURGING Dose and frequency For isotretinoin, starting at about 0.5 mg/kg/day and then increasing as tolerated is standard to reduce early flares and mucosal side effects.¹˒⁵ For topical retinoids, beginning with every second night application, or using a lower strength and increasing slowly, is widely used to lower irritation and perceived flares.¹⁻⁴ Combinations and barrier support Combining tretinoin with clindamycin reduced flare rates compared with tretinoin alone in a phase 3 analysis, showing the value of pairing retinoids with anti inflammatory therapy.² In severe nodulocystic acne at high risk of fulminant flares, short term systemic corticosteroids with isotretinoin can be helpful.¹˒⁵ Barrier supportive skincare also matters. In the split face study, a ceramide and niacinamide moisturizer used with adapalene and benzoyl peroxide improved barrier function and acne outcomes without increasing flares compared with a hydrophilic cream.⁷ Gentle cleansers, non comedogenic moisturizers and sunscreen lower irritation and help patients stay on course through any mild purge.⁶⁻⁸ When to seek medical review Mild, temporary worsening of usual type acne in usual areas can often be managed with dose or frequency reductions and supportive skincare.¹⁻⁴ Red flags include sudden painful nodules, many new cysts, spread to new body areas or systemic symptoms such as fever or joint pain, which require medical review and often a change in therapy.¹˒⁵ CAN PURGING BE PREVENTED Purging cannot always be avoided, but several steps can reduce the risk and severity. ▌Treat large comedones before starting isotretinoin, for example with extraction. This may reduce the chance of sharp early flares.¹ ▌Start both isotretinoin and topical retinoids “low and slow” and increase only as tolerated.¹⁻⁵ ▌Add anti inflammatory and barrier supportive partners such as clindamycin with tretinoin or ceramide and niacinamide moisturizers alongside retinoid or benzoyl peroxide regimens.²˒⁷ ▌Avoid stacking multiple strong actives at the same time. Peel studies show that even one peel can cause flare ups, so combining peels with strong retinoids and high strength benzoyl peroxide from day one is often unnecessary and risky.³˒¹²⁻¹⁵ Setting realistic expectations is equally important. Patients who know that a short, limited flare is possible and temporary are less likely to abandon effective therapy early.¹⁻⁴ KEY POINTS ▌Purging is a short lived, treatment linked increase in visible acne that happens when potent comedolytic therapies push already clogged pores to the surface faster.¹⁻⁵ ▌It has been clearly documented for topical prescription retinoids, oral isotretinoin and superficial chemical peels, and is sometimes seen with benzoyl peroxide; niacinamide, cosmetic retinal or retinol, bakuchiol and vitamin C do not have comparable purge data.¹⁻⁸˒¹²⁻¹⁷˒²¹⁻²⁴ ▌Niacinamide does not show a purge pattern in trials and instead often improves inflammation and barrier function.⁶⁻⁸ ▌Cosmetic retinal, retinol and bakuchiol can irritate at higher strengths but have not been shown to cause a consistent, quantified acne purge like tretinoin or isotretinoin.¹⁷⁻²³ ▌Purging is not limited to oily skin and depends more on comedone load and treatment strength and schedule.¹⁻⁵ ▌Smart dosing, thoughtful combinations and barrier support can reduce flares and improve adherence so that patients reach the real benefits of therapy.¹⁻⁵˒⁷ This content is for informational and educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease, nor to replace individual medical advice; always consult a qualified healthcare professional to determine the most appropriate approach for your personal needs and goals. Take care! Anne-Marie References
Comments
 Lipid peroxidation is a chemical process that involves the oxidative degradation of lipids, particularly polyunsaturated fatty acids (PUFAs), such as arachidonic acid. It´s initiated when free radicals, especially reactive oxidative species, "steal" electrons from lipids, resulting in the formation of lipid radicals and cell damage. This process occurs through three stages: ▌Initiation: A free radical (often hydroxyl radical) abstracts a hydrogen atom from a PUFA, creating a lipid radical. ▌Propagation: The lipid radical reacts with molecular oxygen to form a lipid peroxyl radical, which can then abstract hydrogen from another lipid, continuing a chain reaction and forming lipid hydroperoxides. ▌Termination: The chain ends when two radicals combine or antioxidants (like vitamin E) neutralise them, forming non-radical products. [1][2] Uncontrolled lipid peroxidation leads to membrane damage, cell dysfunction, and death. While it occurs naturally during aging, external factors such as UV radiation, pollution, and cigarette smoke accelerate lipid peroxidation by generating reactive oxygen species (ROS). These ROS interact with PUFAs (Polyunsaturated Fatty Acids) in cell membranes, initiating a cascading chain reaction that produces toxic aldehydes like malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE), which contribute to oxidative stress, cellular damage, and programmed cell death mechanisms like apoptosis and ferroptosis [1][2][3]. Sebum is primarily composed of saturated fatty acids (e.g., palmitic acid at ~31%) and monounsaturated fatty acids (e.g., sapienic acid at ~21%), but it also contains smaller quantities of PUFAs such as linoleic acid [4][5]. Despite their lower abundance, sebum PUFAs are highly susceptible to peroxidation due to their double-bond structure [1][3]. For example, in acne patients, reduced sebum PUFA levels correlate with inflammatory states, while increased saturated fatty acids exacerbate pro-inflammatory cytokine production [4]. This highlights the dual role of sebum lipids in maintaining skin barrier function and contributing to oxidative damage when peroxidation occurs [4][5]. Lipid peroxidation plays a role in various skin conditions, including acne and signs of photoaging [6][7], rosacea, psoriasis, and eczema.  OILY SKIN AND LIPID PEROXIDATION Oily skin is more susceptible to lipid peroxidation due to increased sebum production and lipid accumulation at the skin surface [8]. The higher concentrations of sebum provide more substrate for oxidation, increasing the risk of barrier damage (membrane disruption), inflammation (triggering cytokine release), breakouts, and cell death.
While lipid peroxidation is a natural byproduct of UV exposure, it is harmful at elevated levels. ▌UV-mediated oxidation: UVA primarily drives non-enzymatic lipid oxidation through free radical pathways and oxygen/ozone reactions. UVB activates enzymatic pathways (phospholipases, lipoxygenases) producing eicosanoids from PUFAs like arachidonic acid (AA), linoleic acid, EPA, and DHA [9]. These bioactive signaling molecules regulate inflammation and immunity. Visible/blue light generates singlet oxygen that oxidizes squalene and unsaturated fatty acids in sebum. ▌Antioxidant depletion – lowered capacity: Oily skin types often experience an imbalance in antioxidant defenses. Also, acne-prone skin has lower vitamin E levels, weakening protection against oxidative damage, including squalene peroxidation [8][12]. A hallmark of sebum in acne patients is the presence of lipoperoxides, mainly due to the peroxidation of squalene and a decrease in the level of the major sebum antioxidants [13]. ▌Acne inflammation cycle: Excess sebum attracts immune cells (neutrophils) that release damaging reactive chemicals, worsening oxidative stress [8]. This stress triggers lipid peroxidation, where oxidized fats act as inflammatory signals, directly worsening acne. Studies show higher levels of these oxidized fats in acne patients, strongly linked to inflamed lesions [14][15]. OILY SCALP AND HAIR The scalp, like facial skin, follows cyclical lipid rhythms that maintain barrier integrity and microbial balance. UV exposure, oxidative stress, or seasonal shifts disrupt these cycles and trigger squalene peroxidation, destabilizing the sebum matrix and impairing water retention, plus irritation defense. This lipid imbalance causes dryness, sensitivity, or excess oiliness, while oxidized sebum promotes follicle apoptosis and catagen induction, the signaling cascade that shifts hair from anagen growth to catagen regression, compromising fibre strength, lustre, and cycle duration. To prevent scalp and hair lipid peroxidation, you can use antioxidant-enriched shampoos (e.g., with zinc pyrithione or tocotrienols) and serums daily alongside UV-protective habits like hats or scalp sunscreens. Tocotrienols have stronger membrane integration and antioxidant potency than tocopherols due to their unsaturated side chain. For oily scalps, washing 5–6 times weekly helps reduce oxidized sebum, best paired with lipid-stabilizing topicals. FERROPTOSIS AND SKIN HEALTH Ferroptosis is a type of cell death caused by the toxic buildup of damaged fats in cell membranes and is triggered by iron-driven lipid peroxidation when cells can’t neutralize harmful lipid peroxides, mainly due to glutathione peroxidase 4 (GPX4) failure. GPX4 activity depends on selenium availability. This happens through two key mechanisms:
 STRATEGIES FOR MANAGING OILY SKIN Effective skincare strategies for managing oily and acne-prone skin focus on at least three key objectives [13]: ▌Inhibit the excessive secretion of sebaceous glands / reduce skin surface lipids ▌Improve the quality of sebum ▌Reduce the occurrence of lipid peroxidation 1. Antioxidant-rich skincare: Lipid-soluble antioxidants like vitamin E, CoQ10, carotenoids, and Silymarin naturally blend into the skin’s oils and cell membranes, where they help stop free radicals before they can damage lipids. Water-soluble antioxidants such as vitamin C, glutathione, ferulic acid, and plant polyphenols (like oxyresveratrol, EGCG) work in the skin’s watery layers to neutralize oxidative stress before it reaches the cell membrane. Since oxidation happens in both oily and watery parts of the skin, using a mix of these antioxidants offers the best all-around protection. For people with oily or acne-prone skin, where oil oxidation is more common, products rich in membrane-protecting antioxidants like vitamin E, CoQ10, and Silymarin are especially helpful. ▌Licochalcone A or Glycyrrhiza inflata Root Extract (has both water-loving and fat-loving parts) has been shown to inhibit lipid peroxidation in keratinocytes (the main cell type in the epidermis) induced by UV radiation [20], and in human dermal fibroblasts exposed to hydrogen peroxide [21]. My personal favourites: ACWELL Licorice pH Balancing (Serum Intense Ampoule): Delivers mild antioxidant soothing via licorice root water (glycyrrhizinate) + niacinamide + vitamin E for lipid protection, paired with glutathione/pycnogenol for ROS defence. Lightweight emulsion calms oily skin inflammation while supporting even tone [41]. Complements their cleansing toner/toner pads to fit seamless any daily routine. I'm From Licorice Ampoule: Ultra-light gel with 73% licorice root extract (100 million licorice exosomes) + ammonium glycyrrhizate provides soothing antioxidation. Glycyrrhizin derivatives calm inflammation, support Nrf2 activation, and reduce post-acne pigmentation while panthenol/HA hydrate without greasiness. Downside: this product has a short shelf-life [42]. ▌Vitamin E (tocopherol - highly lipid-soluble) inhibits chain-propagating peroxidation in stratum corneum lipids; human studies show 30-50% reduction post-UV exposure when combined with vitamin C [6]. ▌Vitamin C (ascorbic acid): Reduces 4-HNE adducts (peroxidation marker) by 40-60% in ozone-exposed skin models; synergizes with vitamin E for oily skin protection [26]. My personal favourite: Tir Tir Pure Vitamin C24 Serum offers a potent 24% L-ascorbic acid with calming cica and bisabolol. It´s high concentration might irritate more sensitive skin [43]. Fridge storage (4-8°C) after opening slows oxidation by cutting molecular kinetic energy; slashing reaction rates 50-100% to preserve antioxidant/brightening power for weeks longer, especially recommended in warmer climates. ▌Vitamin C Derivatives (e.g., Tetrahexyldecyl Ascorbate, Ascorbyl Palmitate): Stable vitamin C derivatives like tetrahexyldecyl ascorbate (lipid-soluble) penetrate skin to quench free radicals and support antioxidant defense against oxidative stress [31], though ascorbyl palmitate may promote peroxidation under UVB exposure due to its lipid component forming toxic oxidized metabolites [32] . ▌Oxyresveratrol: Suppresses sebum lipid peroxidation in keratinocyte models, outperforming resveratrol with dose-dependent TBARS* inhibition [27]. ▌Resveratrol: Resveratrol modulates hydrogen peroxide-induced ROS in skin fibroblasts and suppresses UV/oxidant-triggered lipid peroxidation via MAPK/Akt pathways. ▌Ferulic acid: Boosts vitamin C/E stability, cutting UV-induced peroxidation by 45-90% in ex vivo skin [28]. Skinbetter Science Alto Defense Serum combines multiple proven antioxidants (ferulic acid, Vit C/E derivatives, polyphenols) into a potent peroxidation shield. Pricey but comprehensive for serious oxidative stress defense [44]. ▌Ubiquinone (CoQ10 - highly lipophilic): Mitochondrial-targeted, reduces H2O2 and 4-HNE by 50% in pollutant-exposed epidermis [29]. A personal favourite is Timeless Coenzyme Q10 Serum (2% CoQ10 + 8% Matrixyl 3000 + Vitamin E + HA), which delivers potent mitochondrial lipid peroxidation protection plus ATP energy boost, and collagen stimulation, in a lightweight, non-greasy formula ideal for oily skin [40].  ▌Ectoin: This extremolyte forms a protective hydro-complex around proteins/cell membranes, preventing UV/pollutant-induced lipid peroxidation while boosting endogenous antioxidant enzymes (SOD/catalase). Clinical studies show 30-50% ROS reduction in stressed skin. ▌Prickly Pear (Opuntia ficus-indica): Prickly pear seed oil reduces topical lipid peroxidation in inflammation models, linked to vitamin E (tocopherols) and polyphenols with radical scavenging activity and is rich in beta-carotene. It lowers TBARS* and AOPP (protein oxidation), while increasing SOD, CAT and GPx activities (in animal model) [30]. A personal favourite for oily skin is Glow Recipe's Prickly Pear Peptide Mucin Serum (81% prickly pear stem/fruit extracts + peptides, ectoin, tocopherol) as it hydrates oily skin while delivering lightweight antioxidant protection and barrier support [38]. ▌Silymarin: Silymarin from milk thistle reduces lipid peroxidation and sebum oxidation in acne-prone skin, improving inflammatory lesions, redness and post-inflammatory hyperpigmentation in clinical testing [33]. ▌ Linoleic acid (~60% in safflower oil): A highly lipid‑loving polyunsaturated fatty acid that is reduced in oily/acne‑prone sebum (about 12% vs 25% in healthy sebum). It helps normalize sebum composition, making it thinner and less likely to clog pores, sacrifices its own double bonds to take the hit from free radicals before they attack your sebum, strengthens the skin barrier without feeling greasy, and helps calm acne inflammation.  ▌Green Tea Polyphenols (EGCG): EGCG blocks UV-induced epidermal lipid peroxidation (41–84% inhibition) by reducing hydrogen peroxide and leukocyte infiltration in human skin [34]. A personal favourite is Authentic Ego Tidy Pores Serum, a water-jelly lipid peroxidation serum, safe for acne-prone skin, rocasea, eczema, fungal acne with pH between 4.0-4.5. Key Ingredients: 5% Acetamidoethoxyethanol (next-gen NMF hydrator), 2% Betaine (osmoregulator), 2% Glyceryl Glucoside (deep moisture), 1% Portulaca Oleracea (soothing antioxidant), 0.5% Phloretin (brightening), 0.5% Silymarin (sebum protection), 0.5% Glycyrrhetinic Acid (DNA repair and anti-inflammatory), 0.5% Camellia Sinensis (ROS quencher), 0.2% Tetrahydrodiferuloylmethane (potent antioxidant), 0.1% Aminopropyl Ascorbyl Phosphate (stable vitamin C), 0.1% Tremella Snow Mushroom (barrier hydration), 0.05% Dimethylmethoxy Chromanol (lipid peroxidation blocker) [37]. 2. Melatonin: The hormone melatonin is widely present in various tissues, including the skin, and regulates circadian rhythms and promotes sleep. Melatonin can penetrate membranes and mitigate lipid peroxidation and protein oxidation, as well as oxidative damage to the mitochondria and DNA caused by UVR [22]. 3. Daily cleansing and regular exfoliation: Gentle exfoliants such as salicylic acid (a beta hydroxy acid) or glycolic acid (an alpha hydroxy acid), combined with regular cleansing, effectively remove oxidized lipids, pollutants, and debris from the skin's surface. This reduces the risk of oxidative stress and helps prevent pore congestion and reduces acne risk [14]. However, overcleansing or excessive exfoliation should be avoided, not due to the debunked "rebound sebum production" myth, however because these practices can compromise the stratum corneum's barrier function, increasing transepidermal water loss (TEWL) and irritation potential. 4. Sun protection: Sun protection prevents UV-generated ROS from triggering sebum lipid peroxidation, which forms barrier-disrupting peroxides and inflammation [10]. Daily tinted broad-spectrum sunscreens with iron oxides protect against both UV and visible light oxidative stress that drives lipid peroxidation [7]. This is particularly beneficial for oily skin of color. Broad-spectrum SPF50+ delivers ~85-95% total UV oxidative stress reduction when applied properly. Antioxidants may address the remaining 5-15%. Sunscreens with antioxidants like Licochalcone A provide even greater protection with reduction of visible light damage. Sunscreen efficacy directly correlates with reduced UV-induced lipid peroxidation. Stable filters (Tinosorb S/M, Mexoryl XL) maintain photostability without generating ROS. Unstable filters like avobenzone and OMC/octinoxate break down into free radicals if unstabilized [36]. Personal favourites are 3 ultralight sunscreens, using a combination of modern European filters, most of which are photo-stable: Eucerin Oil Control Sun Serum SPF50+ which contains multiple antioxidants including Licochalcone A, sebum-regulating L-Carnitine and mattifying pigments, Eucerin HydroProtect Tinted SPF50+ [45] and Dr. Bouhon Sun Serum SPF50 with soothing cucumber extract, hydrating glycerin and vitamin E (tocopheryl acetate) [39]. 5. Healthy diet: Consuming a diet rich in omega-3 fatty acids, fruits, and vegetables can enhance the skin's antioxidant defenses and reduce inflammation associated with lipid peroxidation [6]. 6. Avoiding environmental stressors: Minimising exposure to (airborne) pollutants and tobacco smoke significantly reduces cutaneous oxidative stress. When avoidance is impractical or impossible, (broad-spectrum sunscreen paired with) topical antioxidants provide essential protection.  7. Sebum-regulating topical ingredients: There are several evidence-based skin care ingredients. I will highlight one called L-Carnitine. L-Carnitine is a skin’s own amino acid derivative that is produced from the amino acids lysine and methionine. It supports sebum regulation through several mechanisms:
▌Increased β-oxidation (“fat burning”): L-carnitine significantly augments β-oxidation in human sebocytes, which is the process by which fatty acids are broken down [23]. This leads to a decrease in intracellular lipid content. ▌Sebum secretion reduction: Topical application of a 2% L-carnitine formulation for 3 weeks significantly decreased the sebum secretion [23]. ▌Bio-availability: Topically applied L-carnitine is bioavailable and can reach the dermis, allowing it to interact with sebaceous glands [23]. New in vitro data shows 86% sebum reduction for even a low concentration of L-carnitine [24]. 8. Mattifying oil absorption: Mattifying agents formulated for oily skin work by absorbing excess sebum and reducing shine through ingredients like perlite (lightweight, porous volcanic glass mineral), clays, silica, and polymers (like starch). Overuse can lead to product buildup, potentially trapping impurities on the skin's surface. 9. Blotting papers are thin, absorbent sheets designed to absorb and thus remove excess oil from the skin's surface, providing a temporary matte appearance [25]. Daily broad-spectrum SPF50+ use is essential to prevent (UV-induced) free radical damage and lipid peroxidation. It provides your ultimate first-line defence before antioxidants can tackle residual ROS. Always consult a dermatologist to tailor the perfect approach for your skin health and beauty. Take care Anne-Marie *TBARS (thiobarbituric acid reactive substances) measures malondialdehyde (MDA), a byproduct of lipid peroxidation in cell membranes, serving as a common biomarker for oxidative stress in skin and other tissues. [1] Ayala et al. Oxid Med Cell Longev. 2014;360438. [2] Endale et al. Front Cell Dev Biol. 2023;11:1226044. [3] Su et al. Oxid Med Cell Longev. 2019;5080843. [4] Cao et al. Front Physiol. 2022;13:921866. [5] Sinclair et al. Nat Commun. 2021;12:1592. [6] Briganti & Picardo (2003) J Eur Acad Dermatol Venereol. 17(6):663-9 [7] Niki (2015) Free Radic Res. 49(7):827-34 [8] Wong A, et al. J Clin Dermatol Ther. 2016;3(1):020. [9] Gruber F, et al. Front Endocrinol. 2020;11:607076. [10] Picardo et al. (2009) Dermatoendocrinol. 1(2):68-71 (was 5) [11] Kostyuk V, et al. PLoS One. 2012;7(8):e44472. [12] Briganti & Picardo (2003) J Eur Acad Dermatol Venereol. 17(6):663-9 [13] Ottaviani et al. (2006) J Invest Dermatol. 126:2430-2437 [14] Bowe & Logan (2010) Lipids Health Dis. 9:141 [15] Yadav et al. (2019) Sci Rep. 9:4496 [16] Tang, D. et al. (2021) Cell Res 31, 107–125. [17] Veeckmans, G. et al. (2023) The FEBS Journal. [18] Li, J. et al. (2020) Cell Death Dis. 11, 88. [19] Feng et al. (2023) Mol. Biomed. 4, 33. [20] Kim et al. (2005) J Invest Dermatol. 125(5):1009-16 [21] Huang et al. (2013) Mol Med Rep. 7(6):1977-82 [22] Bocheva et al. (2022) Int J Mol Sci. 23:1238 [23] Peirano et al. (2012) J Cosmet Dermatol. 11(1):30-36 [24] BDF data on file, Dr. Dorothea Schweiger [25] Wu et al. (2019) J Food Drug Anal. 27(2):610-61 [26] Pecorelli et al. Arch Dermatol Res. 2021;313:139-146. [27] Likhitwitayawuid. Molecules. 2021;26:4212. [28] Wortzman & Nelson. J Cosmet Dermatol. 2021;20(4):1160-5. [29] Pecorelli et al. Arch Dermatol Res. 2021;313(3):139-146. [30] Bardaa et al. Biomed Res Int. 2020;2020:5643465. [31] Swindell et al. Int J Mol Sci. 2021;22(16):8756. [32] Meves et al. J Invest Dermatol. 2002;119(5):1103-8. [33] Draelos et al. J Drugs Dermatol. 2024;23(4):233-8. [34] Katiyar et al. Carcinogenesis. 2001;22(2):287-94. [35] Jagdeo et al. J Drugs Dermatol. 2010;9(12):1523-6. [36] Gaspar LR, Campos PMBG. Photochem Photobiol Sci. 2010;9:402-13. [37] https://www.authenticego.com/products/tidy-pores-serum [38] https://www.glowrecipe.com/products/prickly-pear-peptide-mucin [39] https://drbouhon.com/THE-SUN-SERUM-SPF50 [40] https://www.timelessha.com/products/coenzyme-q10-serum- [41] https://acwell.global/product/acwell-licorice-ph-balancing-ampoule/ [42] https://imfromglobal.com/collections/allproducts?filter=licorice#ingredient [43] https://tirtir.global/products/pure-vitamin-c24-serum [44] https://www.skinbetter.com//antioxidants/alto-defense-serum [45] https://int.eucerin.com/products/sun-protection/hydro-protect-ultra-light-sun-fluid-spf-50-tinted-medium Transparancy-disclaimer: The personal favourite products are ones I genuinely love, purchased and use(d) myself. I contributed to developing Eucerin Oil Control Sun Serum SPF50+ and HydroProtect Tinted SPF50+ and created its scientific and communication materials and studies. I receive no financial benefit from recommending any of the mentioned products. 
Blue light, is also known as high-energy visible (HEV) light and is the most energetic part of the visible light spectrum (380 - 700 nm) with wavelengths ranging from indigo or ultramarine light 420-440 nanometers, blue light 450-495 nanometers to cyan light 480 - 520 nanometers. Blue light has lower energy than ultraviolet (UV) radiation (280–400 nm) and can reach further into the dermis, up to the depth of 1 mm. [1] Sunlight is the primary natural source of blue light. Up to 50% of the damaging oxidative stress in human skin is generated in the VIS spectrum and the other 50% by UV light [2], contributing to premature ageing, ox-inflammageing and hyperpigmentation like age spots.
Blue light from electronic devices The use of electronic devices has led to increased exposure to artificial blue light sources, however the amount of blue light emitted during the conventional use of electronic devices is by far not enough to trigger harmful skin effects. If you sit in front of a monitor uninterrupted for a week at a distance from the screen of approximately 30 cm, this would be the same as the blue light intensity of spending one minute outside on a sunny day in Hamburg Germany at around midday at midsummer. If you hold a smartphone right next to the skin, the intensity does increase, but it would still take approximately 10 hours of uninterrupted use to match the effect on the skin of just one minute of sunlight. The emissions from electronic devices are barely noticeable in comparison to natural blue light directly from the sun and are, thus negligible. However, blue light or HEV light from sunlight can be harmful for skin. Dr Ludger Kolbe Chief Scientist for Photobiology and his team at Beiersdorf AG did pioneering research regarding the harmful effects of HEVIS. [3-4] I would also like to take the opportunity to debunk an important myth at the start of this article as infrared or near infrared light does not induce damaging free radicals (even in high amounts), there is no such thing "infra-ageing" as a result or IR and in fact red light photobiomodulation supports skin rejuvenation. Read more Direct effects of blue light and HEV Light on skin Blue light and HEV light can have both beneficial and detrimental effects on the skin. The most significant direct effects are mediated through their interaction with chromophores, such as flavins, porphyrins, and opsins, which can trigger the overproduction of reactive oxygen species (ROS), reactive nitrogen species (RNS). and hyperpigmentation. Reactive oxygen and nitrogen species cause DNA damage and modulate the immune response. [1] This oxidative stress can lead to: Photo-ageing: Exposure to blue light and HEV light can induce premature skin aging, causing wrinkles, fine lines, and loss of elasticity. Hyperpigmentation: Blue light and HEV light can stimulate melanin production, leading to uneven skin tone and the development of age spots or other forms of hyperpigmentation. DNA damage: The ROS and RNS generated by blue light and HEV light can cause DNA damage, plus potentially increase the risk of skin cancer. Inflammation: The oxidative stress triggered by blue light and HEV light can cause an inflammatory response in the skin, exacerbating conditions like acne, eczema, and psoriasis. Molecular and physiological mechanisms of direct blue light effects on the skin [1]
Indirect effects of blue light and HEV Light on skin Blue light and HEV light can also have indirect effects on the skin by disrupting the body's circadian rhythms. This occurs via both the central mechanism, which involves stimulation of light-sensing receptors located in the retina, and via the peripheral mechanism, which involves direct interaction with skin cells. By disrupting the normal circadian rhythm, blue light can negatively affect the skin's natural overnight repair and regeneration processes. [1] The circadian rhythm has been shown to affect multiple cellular and physiological processes occurring in the skin:
Molecular mechanisms of indirect effects of blue light on the skin [1]
Ideal daytime & nighttime skin care regimen When considering cosmetic interventions, a strategy of daytime protection plus defense and night-time repair may be optimal. The skin's own repair mechanisms, such as base excision repair and nucleotide excision repair, attempt to mitigate blue light induced DNA damage. [12] Daytime protection plus defense Of course prevention and/or reduction of blue light exposure from sunlight is key. Reduce the time spent on electronic devices, especially before bedtime, can help minimize the disruption of circadian rhythms and the indirect effects of blue light and HEV light on the skin. Against premature ageing and hyperpigmentation an evidence based effective approach could be the daily use of tinted broad-spectrum sunscreen preferably containing Licochalcone A (the most effective anti-oxidant reducing damaging free radical activity from both UV and blue light and moreover protects against collagenase MMP-1 expression) strengthening skin's biological defense [4-5-6-7], while iron oxides in colour pigments provide physical protection against blue light. Against hyperpigmentation there are (tinted) sunscreens which on top contain the most potent human tyrosinase inhibitor found in dermatological skin care called Thiamidol® [8-9] and one of the 3 ingredients in the "new Kligman Trio" (NT) [18] and Glycyrrhetinic Acid which supports skin's DNA repair and skin pigmentation [10] and inhibits hyaluronidase activity (HYAL1). Most regular sun filters used in sunscreen don't offer any protection against blue light, however according to the website of BASF the chemical UV filters Tinosorb® A2B and Tinosorb® M can reduce the exposure to blue light. [11] Ectoin or ectoine has shown positive effects against high-energy visible light by decreasing the levels of OPN3 or Opsin-3, a photoreceptor involved in light perception, after HEVL exposure, suggesting role in mitigating light-induced stress on skin cells. Although ectoin does not act as an anti-oxidant or provide a physical barrier, it effectively preserves cellular integrity and function under HEVL stress conditions. [19] However, ectoine exhibits a complex effect on DNA damage, protecting against some forms of radiation-induced damage while potentially enhancing structural changes in DNA under certain conditions. [20] More data would be needed. Scattering and absorption of blue light [5] The penetration depth of visible light is influenced by the reflection, scattering, and absorption mediated not only by the skin’s physical barrier but also by the VL chromophores in the skin and Fitzpatrick skin or photo-type (FST). The primary VL-scatter and absorption molecules in the skin include hemoglobin, melanin, bilirubin, carotene, lipids, and other structures, including cell nuclei and filamentous proteins like keratin and collagen. Melanin and keratins are the primary VL absorbers and scatterers in the epidermis, while hemoglobin is the dominant absorber, and collagen is the major VL scatter in the dermis. Melanin's absorption spectrum ranges from 200 to 900 nm, with the peak absorption varying based on melanin moiety. This means that individuals with darker skin types, which have higher melanin content, are more prone to hyperpigmentation from blue light or VIS due to the greater absorption and scattering of VIS in their skin on top of the previously mentioned higher levels of tyrosinase–DCT complexes leading to increased melanogenesis, leading to both transient and long-lasting pigmentation [13], dependent upon the total dose and exacerbation of melasma especially in individuals with FSTs III to VI. Blue light tanning Recent data demonstrate synergistic effects between VL and UV-A on erythema and pigmentation. VL-induced pigmentation is more potent and more sustained than UVA1-induced pigmentation in darker skin tones.Typically, three mechanisms are involved in the responsive reaction of melanocytes to VL, with increased melanin content: immediate pigment darkening (IPD), persistent pigment darkening (PPD), and delayed tanning (DT). [15] Read more. VL can also exacerbate post inflammatory hyperpigmentation (study with FST IV and V). [16] Blue light therapy While the detrimental effects of blue light and HEV light on the skin have been well-documented, these wavelengths have also shown promise in the treatment of certain skin conditions. In controlled clinical settings, blue light has been used to: Treat Acne: Blue light can reduce the growth of Propionibacterium acnes, the bacteria responsible for acne, and has an anti-inflammatory effect. Manage Psoriasis and Atopic Dermatitis: Blue light has been found to have an anti-inflammatory and antiproliferative effect, making it potentially beneficial for the treatment of these chronic inflammatory skin diseases. Reduce Itch: Some studies have suggested that blue light may help alleviate the severity of itching in certain skin conditions. Vitiligo: Blue light therapy via LEDs can stimulate repigmentation in patients with vitiligo with minimal adverse events, however larger studies are needed. [17] The optimal protocols for blue light therapy are still being developed, and the long-term safety of this treatment modality requires further investigation and should not be initiated without HCP recommendation and monitoring. Overall, the research suggests that prolonged or excessive exposure to high-energy blue light, can have negative long-term effects on skin structure, function, and appearance in all phototypes. As our understanding of the individual variations in skin's response to blue light exposure deepens, the development of personalised or tailored effective solutions become increasingly more tangible. Always consult a qualified healthcare professional or dermatologist to determine what the most suitable approach is for your particular skin condition and rejuvenation goals. Take care! Anne-Marie
References
If you've scrolled through Instagram, you may have caught a glimpse of dermatologists raving about LED masks emitting red light, the secret, evidenced based weapon behind skin rejuvenation known as photo biomodulation. It uses low-powered light within the red to near-infrared range (wavelengths from 632 to 1064 nm) to induce a biological reaction aka stimulate cellular processes. The wonders of red light, also known as LLLT (low-level laser therapy), PBM (red light photo-biomodulation), or PBMT (photo-biomodulating therapy), extend far beyond non-invasive skin rejuvenation. I am not a fan of devices for home use, mostly because of lacking safety and/or efficacy, PBM definitely earned it's prominent spot in my skincare routine.
A summary of the benefts of red light with and without near infrared light for skin Numerous studies have demonstrated the effectiveness of red and infrared light therapy for skin rejuvenation. A combination of red light and near IR light has proven to stimulate the production of collagen (I & III) plus elastin production (Li WH et al Int J Cosmet Sci 2021), enhance mitochondrial ATP production, cell signaling, growth factor synthesis, rebalance ROS (reactive oxidative species) and reduce inflammation. Stem cells can be activated allowing tissue repair and healing. Wrinkle and scar reduction was observed and it can reduce UV damage both as treatment and prophylactic measure. In pigmentary disorders such as vitiligo, it can increase pigmentation by melanocyte proliferation and reduce depigmentation by inhibiting autoimmunity (Pinar Avci et al. Semin Cutan Med Surg. 2013 & Mitchell J Winkie et al. Review Photodermatol Photoimmunol Photomed A focused review of visible light therapies for vitiligo 2024). It has the potential to activate both keratinocytes (epidermis) and fibroblasts (epidermal junction and dermis). With consistent use, you can expect a reduction of lines and wrinkles, improvement of skin tone and texture. PBMT (when done effective and safe) will compliment both your skin rejuvenating and regenerating at home skincare regimen and in-office procedures or even post-surgical skin recovery. ATP ATP (adenosine triphosphate) is the primary source of energy for cellular processes and plays a crucial role in various biological functions. When red light with specific wavelengths (630 nm to 638 nm and 810 nm) is absorbed by the skin cells, it stimulates the mitochondria, which are the powerhouses of the cells responsible for ATP synthesis. This increase in ATP production is providing cells with more energy to carry out their functions effectively and has several beneficial effects on the skin like boosting cellular metabolism, promoting more efficient nutrient uptake and waste removal. The increased ATP levels facilitate collagen synthesis by fibroblasts, a vital component for skin structure, elasticity and firmness and reduction of lines and wrinkles.. ATP aids in the repair and regeneration of damaged skin cells. It accelerates the healing process, making it beneficial for wound healing, post-surgical recovery, and addressing skin issues such as acne scars. ROS (Reactive Oxidative Species) By modulating ROS levels, red light therapy helps reduce oxidative stress and its detrimental effects on the skin. ROS are highly reactive molecules that are naturally produced by cells as byproducts of metabolic processes. While low levels of ROS play important roles in cellular signaling and immune responses, excessive ROS can lead to oxidative stress and damage to cells and tissues. Restoring the balance of ROS result in improved skin health, reduced inflammation, and enhanced skin rejuvenation. Red light therapy has been shown to modulate reactive oxidative species (ROS) levels in the skin by promoting antioxidant defense mechanisms and reducing oxidative stress:
The difference between LLLT and PBM LLLT refers specifically to the use of lasers, which produce coherent, focussed and an intense beam of monochromatic light, while PBM has a broader range of light sources, may include laser as well as light-emitting diodes (LEDs) and other non-laser devices. LEDs are often used in PBM because they are cost effective, versatile and have the ability to cover large treatment areas. LLT uses higher power densities with more energy and has a shorter treatment duration in comparison to PBM to achieve desired therapeutic effects. While there are similarities in terms of mode of action", there is a difference of light source, treatment application and parameters. Based on consensus, PBM and PBMT are considered the correct way to describe this photonic specialty for therapeutic applications. In this post I will focus on PBM and specifically LEDs. A home device claiming to use cold near infrared laser light or Low-Level Laser Therapy is called LYMA laser. It is sold for several thousand euro´s. LED masks and LED panels LED masks specifically produced by the brand Omnilux (FDA cleared) are currently very popular for very good reasons; they are safe and effective when the LEDs emit the right wavelengths and used in the recommended frequency. Omnilux combines 2 therapeutically effective and complimentary wavelengths: 633nm and near-infrared 830 nm. Both wavelengths (more precise 630nm + 850nm) I would recommend to minimally look for in any red LED device, which will disqualify most LED masks and panels in the market! I've include some (not affiliated) links to devices below. Both masks and panels can be effective, however most panels are stronger in comparison to masks 60 mW/cm² vs mW/cm²), hence have the benefit of a shorter treatment time to get a similar result. Intensity and power of red light therapy devices are typically measured in terms of irradiance (measured in milliwatts per square centimeter, mW/cm²) and radiant flux (measured in watts, W), which quantify the amount of light energy emitted by the device. Wearing a mask during a hot summer or in a warmer climate will make you sweat and depending on the materials of the mask and straps, they may be very uncomfortable to wear. Panels have the benefit that they give a more even distribution of emitted light as masks are worn on the face and thus the LED bulbs are pushed on a small skin surface area, panels can cover a larger area (depending on their size) and are more versatile in use, as area's like neck, décolletage, or knees are easier to treat with a panel. With a mask you may be more mobile, although I would not recommend walking around while using the mask. My personal preference would be a panel for the reasons mentioned before and panels are more suitable (more hygienic) for family sharing. My son can use it after an intense workout to speed up his recovery and I like to use it for purposes beyond photo-biomodulation or skin rejuvenation, for example to improve my sleep. With a panel I get more "bang for my buck". 
Red light and NIR (Near Infra Red light) have the ability to penetrate varying depths of the skin, resulting in distinct benefits, thus combinations of wavelengths will provide complementary effects.
630 nm Wavelength This wavelength is often used for its skin rejuvenation benefits. It has a relatively shallow penetration depth and is absorbed closer to the surface of the skin primarily affecting the epidermis. 630nm light is associated with increased circulation, reduced inflammation, reduced sebum production, improved skin tone & texture, aiding in the delivery of nutrients and oxygen to skin cells, and stimulating the production of collagen, leading to improved skin elasticity and a reduction of the appearance of fine lines & wrinkles. 660 nm Wavelength At 660nm, red light can penetrate a little deeper into the skin, reaching the dermis. It is known for its ability to stimulate collagen production, enhance cellular metabolism, and promote anti-inflammatory effects, helping to reduce redness and inflammageing. It also promotes wound healing, making it beneficial for post-surgical or post-trauma skin recovery. 810 nm Wavelength Improve healing & recovery & accelerate wound healing. 830 nm Wavelength Accelerate healing, reduce infection, improve aesthetic outcome following plastic surgery, increase endorfines (mood-enhancing), improve bone repair and growth. 850 nm Wavelength Improve general inflammation body, enhance muscle recovery, improve wound healing, reduced fine lines, wrinkles and hyperpigmentation. Always consult a qualified healthcare professional or dermatologist to determine if and what the most suitable red light therapy approach is for your particular skin condition and rejuvenation goals. Take care! References: Hamblin, Michael R. "Mechanisms and applications of the anti-inflammatory effects of photobiomodulation." AIMS biophysics 4.3 (2017): 337-361. Barolet, Daniel. Regulation of Skin Collagen Metabolism In Vitro Using a Pulsed 660 nm LED Light Source: Clinical Correlation with a Single-Blinded August 2009Journal of Investigative Dermatology 129(12):2751-9 Wunsch A, Matuschka K. (2014). A controlled trial to determine the efficacy of red and near-infrared light treatment in patient satisfaction, reduction of fine lines, wrinkles, skin roughness, and intradermal collagen density increase. Journal of Cosmetic and Laser Therapy, 16(5), 232-237. Avci P, et al. (2013). Low-level laser (light) therapy (LLLT) in skin: stimulating, healing, restoring. Seminars in Cutaneous Medicine and Surgery, 32(1), 41-52. Links to some devices which combine 630 nm and 850 nm: FDA-approved devices ensure safety and regulatory compliance, however the panels are more powerful: Omnilux(tm) Mask (FDA clearance) Very affordable panel (no FDA clearance) Affordable panel (no FDA clearance) 
Glycation is one of the basic root causes of endogeneous (intrinsic) skin ageing and a very challenging one or almost impossible one to reverse. Glycation is an ageing reaction which begins in early life, developing clinical symptoms at around 30, and progressively accumulates in tissues and skin due to the glycated collagens that are difficult to be decomposed. Glycation occurs naturally in the body when sugars react with proteins and lipids to form advanced glycation end products (AGEs). AGEs can be exogenously ingested (through food consumption), inhaled via tobacco or endogenously produced and formed both intracellularly and extracellularly. AGE modifications lead to dermal stiffening, diminished contractile capacity of dermal fibroblasts, lack of elasticity in the connective tissues, contribute to hyperpigmentation and a yellowish skin appearance. The formation of AGEs is amplified through exogenous factors, e.g., ultraviolet radiation.
AGEs cause changes in the skin through 3 processes:
One study published in the Journal of Investigative Dermatology found that levels of AGEs were higher in the skin of older individuals compared to younger ones. The study also showed that there was a correlation between the level of AGEs and the severity of skin ageing. This suggests that inhibiting the production or accumulation of AGEs in the skin is a potential target for anti-ageing interventions or skin ageing management. AGEs are complex and heterogeneous, more than a dozen AGEs have been detected (however not all) in tissues and can be divided into three categories according to their biochemical properties. AGEs are formed through four pathways:
GLYCATION INHIBITION IS KEY AGEs can be crosslinked through side chains to form a substance of very high molecular weight, which is not easily degraded. The consequences from skin glycation are irreversible. This makes prevention or inhibition of the process the best potential strategy to maintain skin health and ageing skin management. One way to do this is by altering the diet to reduce the intake of sugars and carbohydrates, which are known to contribute to glycation. Several studies have found that reducing sugar intake can result in significant improvements in skin health, including reducing wrinkles and improving skin texture.  Sugar molecules bind to dermal fibers, forming advanced glycation end products (AGEs) over time Left: dermis filled with hyaluron, collagen and elastin Right: dermis with less hyaluron, broken elastin and collagen fibers
AGE inhibitors
Another potential strategy is the use of topical agents that inhibit the formation or accumulation of AGEs in the skin. One study published in the Journal of Cosmetic Science found that a cream containing carnosine, a peptide that inhibits glycation, improved skin elasticity and reduced the appearance of wrinkles in individuals with ageing skin. Skincare containing NAHP or Acetyl Hydroxyproline inhibits the formation of AGEs significantly (in vitro), most likely through a mechanism where NAHP competes with the proteins for the sugar. Finally, NAHP sacrifices itself in place of the proteins and gets (at least partially) glycated. NAHP also prevents loss of cellular contractile forces in a glycated in vitro dermis model and counteracts the diminished cell-matrix interaction that is caused by glyoxal-induced AGE formation. Take-aways from a study published in the International Journal of Cosmetic Science [2]: 1. NAHP significantly and dose-dependently inhibited the formation of advanced glycation end-products (AGEs) in a protein solution. 2. NAHP dose-dependently inhibited the formation of N-(carboxymethyl)lysine (CML), a specific AGE. 3. In fibroblast-populated collagen lattices, NAHP prevented the glycation-induced disturbance of fibroblast contractile capacity. 4. Ex vivo application of NAHP to skin explants decreased AGE fluorescence compared to glucose-treated samples. Anti-Oxidants I would suggest to combine those ingredients with an ingredient like Licochalcone A. Numerous high ranked publications support that Licochalcone A protects cells from oxidative stress mediated by e.g. UV and HEVIS (blue light) induced reactive oxidative species (ROS). Due to the activation and nuclear translocation of the transcription factor NrF2, the expression of anti-inflammatory, antioxidant and detoxifying enzymes are induced. These enzymes protect the skin cells (like keratinocytes and fibroblasts) from ROS-induced damage, like lipid peroxidation and DNA as well as protein damage. If Licochalcone A is combined with L-Ascorbic Acid, (the most active form of Vitamin C), it supporting skin's own collagen production, provides superior biological cell protection amongst other relevant benefits. Vitamin C (and E) has shown to inhibit protein glycation [4]. SPRAY TAN A study in Redox Biology indicates that sunless tanning with dihydroxyacetone (DHA) causes glycation and potential DNA damage in the epidermis [1].: 1. Glycation: DHA exposure led to the formation of advanced glycation end products (AGEs) in epidermal cells, confirmed by mass spectrometric detection of N-ε-(carboxyethyl)-l-lysine (CEL). 2. DNA damage: DHA induced a cellular stress response, including activation of stress-related genes and phosphoprotein signaling. While not directly measuring DNA damage, these responses are often associated with cellular stress that can lead to DNA damage. 3. Significance: The effects were observed at low millimolar concentrations of DHA, relevant to topical application. The stress response was rapid and pronounced, occurring within minutes of exposure. 4. Location: The effects were primarily observed in epidermal cells and reconstructs, with no mention of dermal effects. This study suggests that sunless tanning with DHA may not be as safe as previously thought, warranting further investigation into its long-term effects on skin health [1], however no need to panic as this negative effect is only seen in the top layer of the skin. DOUBLE TROUBLE: GLYCATION + UVB [3] The combination of GO-AGEs and UVB exposure has a more pronounced effect on skin inflammation and oxidative stress than either factor alone. This suggests a synergistic relationship between glycation and UV exposure in accelerating skin aging processes. 1. GO-AGEs combined with UVB irradiation significantly increased the secretion of pro-inflammatory cytokines (IL-1β, IL-6, IL-8) in skin cells compared to either GO-AGEs or UVB alone. 2. The GO-AGEs + UVB treatment group showed a more than three-fold increase in IL-6 and IL-8 mRNA levels compared to other groups. 3. GO-AGEs + UVB treatment induced significantly higher release of nitric oxide (NO) compared to other groups. 4. The combination of GO-AGEs and UVB enhanced reactive oxygen species (ROS) release, creating about 1.5 times more oxidative stress compared to control and other groups. 5. Cell viability was notably affected in the GO-AGEs, UVB, and GO-AGEs + UVB treatment groups compared to the control group. These findings are significant as they demonstrate that the combination of GO-AGEs and UVB exposure has a more pronounced effect on skin inflammation and oxidative stress than either factor alone. This suggests a synergistic relationship between glycation and UV exposure in accelerating skin aging processes. Use sunscreen daily. . GLYCATION AND SKIN HEALTH Acne In addition to its role in ageing, glycation in the skin has also been linked to a range of skin health problems. One study published in the Journal of Cosmetic Dermatology found that the level of AGEs in the skin was significantly higher in individuals with acne than in those without acne. The study also showed that treating acne with a topical antibiotic significantly reduced the levels of AGEs in the skin. Atopic Dermatitis Another study published in the Journal of Investigative Dermatology found that individuals with atopic dermatitis had higher levels of AGEs in their skin than healthy individuals. This suggests that glycation may play a role in the development of inflammatory skin conditions. Diabetes + Woundhealing The correlation between high sugar levels and skin ageing can be seen in diabetic patients, where one-third of this population has skin complications. A prominent feature of ageing human skin is the fragmentation of collagen fibers, which severely damages the structural integrity and mechanical properties of the skin. Elevated levels of MMP-1 and MMP-2 and higher crosslinked collagen in the dermis of diabetic skin lead to the accumulation of fragmented and crosslinked collagen, thereby impairing the structural integrity and mechanical properties of dermal collagen in diabetes. Collagen crosslinking makes it impossible for them to easily repair, resulting in reduced skin elasticity and wrinkles. Keratinocytes and fibroblasts are the main cells involved in wound healing, but due to the high glucose (HG) microenvironment in diabetics, the functional state of these cells is impaired, thereby accelerating cellular senescence (programmed cell death). Conclusion We can't completely stop the glycation process, therefore it's important that we inhibit it from a young age onwards, hence monitor the sugar intake of our children, use daily SPF and invest in good dermo-cosmetic products containing ingredients like NAHP and powerful anti-oxidants like L-Ascorbid Acid (Vitamin C is needed for the production of collagen) and Licochalcone A (also anti-inflammatory). Preventing signs of ageing, specifically caused by glycation is most effective. If your skin shows (advanced) signs of ageing, you can get visible improvement using skin component (hyaluron, collagen and elastin) bio-stimulating ingredients like Retinol, Bakuchiol, Arctiin, Creatine or Glycine Saponin. Consult your dermatologist if you wish to improve your skin's appearance or skin health issues. Take care Anne-Marie References [1] Perer J, Jandova J, Fimbres J, Jennings EQ, Galligan JJ, Hua A, Wondrak GT. The sunless tanning agent dihydroxyacetone induces stress response gene expression and signaling in cultured human keratinocytes and reconstructed epidermis. Redox Biol. 2020 Sep;36:101594. [2] Knoblich C, et al. N‐acetyl‐L‐hydroxyproline – A potent skin anti‐ageing active preventing advanced glycation end‐product formation in vitro and ex vivo. Int J Cosmet Sci. 2023;1-10. doi:10.1111/ics.12930 [3] Sultana, R., Parveen, A., Kang, MC. et al. Glyoxal-derived advanced glycation end products (GO-AGEs) with UVB critically induce skin inflammaging: in vitro and in silico approaches. Sci Rep 14, 1843 (2024). https://doi.org/10.1038/s41598-024-52037-z [3] Sadowska-Bartosz I, Bartosz G. Prevention of protein glycation by natural compounds. Molecules. 2015 Feb 16;20(2):3309-34. doi: 10.3390/molecules20023309. PMID: 25690291; PMCID: PMC6272653. Special thanks: Ph.D. dr Julia M. Weise Manager Biological Testing & Dorothea Schweiger Lab Manager Facial Skin Biology Beiersdorf HQ Hamburg 7/22/2018 Comments Chemical or mechanical exfoliation
We can support's skin natural exfoliation process in various ways, for example with mechanical or chemical exfoliation.
Desquamation (shedding of skin cells thus exfoliation) is an important part of the skin's natural regeneration or renewal process. Already in our twenties, this process slightly, however increasingly starts to slow down (Kligman 1983). As a result, the cells on the surface of our skin (corneocytes) become bigger (Kligman 1989) and a little disorganised. This leads to a duller appearance (loss of radiance) and a more rough texture of our skin. A very comprehensive comparison of both methods:
The word "acid" unfortunately sounds very harsh and skin-unfriendly. Many acids are actually skin's own, like for example lactic acid is a skin's own natural moisturising factor (NMF) and so is hyaluronic acid. The level of NMF's decrease as we age and our skin my lose the ability to maintain well hydrated. Many years ago the benefits of lactic acid were capitalised by using baths filled with donkey milk. Citric acid is commonly used in skin care products and toners to balance skin's pH. Gluconolactone is only gradually penetrates skin and is very gentle.
It's unfortunate that "acids" have such a negative connotation, as our skin (healthy and problematic) can benefit if we use them regularly. Moreover, I prefer this method over mechanical exfoliation for all skin types, however particularly if you have dry skin, acne- or redness prone skin, sensitive skin or mature skin. The risk of exfoliation is over-exfoliation. Over-exfoliation is damage of our skin barrier and the symptoms are very comparable to dry or (hyper) sensitive skin symptoms, which are: redness, irritation, tightness, excessive dryness, dry patches, flaking skin, uncomfortable stinging, or even burning sensation. Whenever you experience one or more symptoms of over-exfoliation, it's recommended to reduce the number of times you exfoliate and support the skin barrier repair with a moisturiser. Hope you enjoy healthy skin & take care. 
Understandably we want to get rid of pimples as soon as possible and sometimes apply harsh products to our skin in order to shrink them.
Depending on which ingredient is used, you might inflict injury to the skin and it's barrier which is very comparable to a mild burn. There is even a phenomenon called "toothpaste burn". During the healing process there is a risk of scarring. A study published by Tan J. et al in JJD 2017 shows that up to >87% of patients with mild to moderate acne reports atrophic scarring (sunken scar) to some degree. A healthy skin barrier and well hydrated skin will support a the healing process. However, as the barrier is impaired and the skin dried out, the skin's regeneration and healing process will take longer. Therefore be careful with "shrinking" pimples. The same applies for "popping" pimples, as this method by definition will cause injury to the skin. Picking and squeezing pimples will further irritate the skin tissue and delay proper healing. The risk of scarring is increased when the tissue is inflamed. A recent study of prevalence and risk factors of acne scarring confirmed that there is a relationship between the time between onset and effective treatment. Acne scars can be more difficult to treat than acne! It's better to seek expert advice if you have problematic skin. Take care. 7/12/2018 Comments Relation skin pH and ageing process
A high pH value contributes to premature ageing skin!
A study published in British Journal of Dermatology showed that women with an alkaline stratum corneum (outer layer of the skin) developed more fine lines and crow's-feet (wrinkles at the outside corner of the eyes) than those with acidic skin over an eight-year period. This might be in part because an alkaline epidermis (top layer of the skin) tends to be drier and more fragile than an acidic one. Irritants can enter the skin and water can evaporate more easily. People with hydrated skin showed a 50% lower rate of wrinkling than those with dry skin. If the acid mantle is not intact, it can make skin more susceptible to inflammation (inflammaging) and lowered enzymatic activity, which again increases the risk of development of signs of ageing. Last but not least, alkaline skin is more prone to sun damage thus photo-aging, because its protective barrier has been weakened. pH balance is fragile. I just mentioned that alkaline skin tends to be drier, however it’s also known that the oils secreted by our skin impact skin’s pH by increasing it. This is one of the reasons that oily skin types can be more prone to acne, as the skin’s pH influences it's microflora. That's a topic for another blog post. You’ve maybe seen some of my previous posts on skin’s pH and it’s actually one of my major topics. This is because healthy skin starts with an optimal pH balance. Click below in the featured categories on “Skin pH” if you like to learn more about pH. If there is a specific topic you are interested in missing, please place a comment below and I will see to it that I address it. Take care. 7/10/2018 Comments Facial toners redundant?
Recently I've read an article in which facial toners were called a redundant step in the cleansing routine. They would not serve any purpose anymore and would be “old-fashioned". I disagree, and will explain why.
Particularly when you prefer wet facial cleansing (water has a pH of 7-8), your skin’s pH goes up and you may consider using a toner to bring it back to normal (~5) before using a moisturizer or serum. This also applies if you use an alkaline cleanser or micellar water. It is common that products which are suitable to be used around the eyes, like micellar water, are adapted to a more “eye-friendly” and less “skin friendly” pH of ~7. Skin prefers a pH of ~5. A review on pH and cleansing summarizes that skin surface pH increases after a single washing procedure, even when the skin is only rinsed with water, and that recovery back to baseline can take several hours. (1) Contact with European tap water (typical pH around 8) increases skin pH for up to about 6 hours before it returns to its natural value around 4.7–5. (2) However, with water alone this pH shift is usually modest (on the order of a few tenths of a pH unit, e.g., roughly 0.2–1.0), but still statistically significant in controlled measurements. (2) In my humble opinion, toners are a value adding step in every a.m. and p.m. skin care regimen for both healthy and particularly problematic skin types, where microbiome (microflora or "ecosystem") and skin barrier impairment play a role. They refresh, remove left-over debris and make-up and instantly rebalance skin’s pH value. A balanced pH value is the cornerstone for healthy skin. Toners support skin microbiome and barrier function. Furthermore, the use of a toner usually helps the penetration and thus efficacy of the care product applied directly afterwards and as toner is a "leave-on" product, skin can benefit from all the other actives in a toner formula. Hope you enjoy healthy skin & take care. 1. Blaak J, Staib P. The Relation of pH and Skin Cleansing. Curr Probl Dermatol. 2018;54:132-142. doi: 10.1159/000489527. Epub 2018 Aug 21. PMID: 30130782. 2. Lambers H, Piessens S, Bloem A, Pronk H, Finkel P. Natural skin surface pH is on average below 5, which is beneficial for its resident flora. Int J Cosmet Sci. 2006 Oct;28(5):359-70. doi: 10.1111/j.1467-2494.2006.00344.x. PMID: 18489300. |
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