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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. |
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