Yes, in the majority of clinical scenarios, you should immediately suspend the use of potent active ingredients when your skin is experiencing an acute flare-up. A flare-up—characterised by erythema (redness), pruritus (itching), or burning—indicates that the stratum corneum is compromised and the skin's immunological response is hyper-reactive [1]. Continuing the application of cellular communicators like retinoids or chemical exfoliants such as Alpha Hydroxy Acids (AHAs) can exacerbate transepidermal water loss (TEWL) and prolong inflammatory signalling, potentially leading to post-inflammatory hyperpigmentation or secondary dermatitis [2].
Instead of active intervention, the primary clinical objective during a flare-up is 'barrier restitution'. This involves a simplified regimen focusing on physiological lipids—specifically ceramides, cholesterol, and free fatty acids—which help to seal the epidermal breach and soothe the inflammatory cascade [1][3]. Once the skin's baseline sensation and visual appearance have normalised for at least 48 to 72 hours, actives can be reintroduced gradually, one at a time, to ensure tolerance and prevent recurrent sensitisation [4].
From a physiological perspective, a skin flare-up represents a disruption of the epidermal permeability barrier. When the lipid matrix that holds corneocytes together is damaged, the skin loses its ability to regulate hydration and shield against external irritants. This breach triggers the release of pro-inflammatory cytokines, such as Interleukin-1α, which orchestrates a broader immune response [2][5].
Active ingredients like L-ascorbic acid or glycolic acid often have a low pH, which can further irritate an already acidified or compromised environment. Furthermore, ingredients that increase cell turnover (mitosis) put metabolic strain on a system that is currently prioritising repair over regeneration [5]. Favouring humectants like glycerine and occlusives like petrolatum during this phase provides the stable environment necessary for the skin's natural enzymatic repair processes to function optimally [3].
For those navigating these moments of reactivity, focusing on barrier resilience becomes the priority rather than high-strength correction. Our Surface Calm was formulated with a complex of ceramides and cholesterol to ensure a non-stripping cleanse, while Balance Biome Crème incorporates Bifida Ferment Lysate to support the microbiome and gently restore hydration without overwhelming sensitised skin.
FAQ
Which specific active ingredients should I stop first?
You should immediately cease use of 'transformative' actives that increase cell turnover or have a low pH. This includes all forms of Vitamin A (retinol, retinaldehyde, tretinoin), exfoliating acids (salicylic, glycolic, lactic), and high-concentration Vitamin C (L-ascorbic acid) [2][4]. These ingredients can be particularly caustic to a compromised barrier, worsening the 'skin burn' sensation often associated with a flare-up.
Are there any 'actives' that are safe to keep using?
Yes, not all 'active' ingredients are irritants. Ingredients classified as 'barrier-repairing' or 'anti-inflammatory' are beneficial. Niacinamide (Vitamin B3) at lower concentrations (2-5%) can actually bolster ceramide synthesis, while panthenol (Pro-vitamin B5) and allantoin are recognised for their wound-healing and soothing properties [1][5]. However, if even these cause stinging, a total 'moisturiser-only' hiatus is recommended.
How do I know when it is safe to restart my actives?
Reintroduction should only occur once the 'clinical signs of inflammation' have subsided. This means no visible redness, no texture irregularities like scaling, and no subjective sensations of tightness or stinging when applying a basic moisturiser [4]. It is best practice to wait an additional 3 days after the skin looks 'normal' before reintroducing one active at a time, typically starting with every second or third night [6].
References:
[1] Del Rosso JQ, et al. Journal of Clinical and Aesthetic Dermatology. 2016;9(12):S2-S8. doi:10.12788/j.sder.2016.035
[2] Elias PM. Journal of Investigative Dermatology. 2005;125(2):183-200. doi:10.1111/j.0022-202X.2005.23668.x
[3] Draelos ZD. American Journal of Clinical Dermatology. 2018;19(1):49-51. doi:10.1007/s40257-017-0331-3
[4] Levin J, et al. Journal of Clinical and Aesthetic Dermatology. 2010;3(2):22-41. PMID: 20725556
[5] Proksch E, et al. Experimental Dermatology. 2008;17(12):1063-1072. doi:10.1111/j.1600-0625.2008.00786.x
[6] Mukherjee S, et al. Clinical Interventions in Aging. 2006;1(4):327-348. doi:10.2147/ciia.2006.1.4.327
