 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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