How Vitamin C Fades Hyperpigmentation in the Malaysian Sun; The Science Explained

 

Quick answer Vitamin C fades hyperpigmentation by inhibiting tyrosinase; the enzyme that drives melanin production after UV exposure. When UV radiation hits the skin, it triggers oxidative stress, which activates tyrosinase and produces the excess melanin that shows up as dark spots. Vitamin C interrupts this process at the tyrosinase step, slowing new melanin formation and gradually lightening existing pigmentation.   In the Malaysian climate, where the UV Index regularly exceeds 10; the extreme category; this mechanism is particularly relevant because UV-induced pigmentation is the most common form of hyperpigmentation in Southeast Asian skin. Vitamin C also acts as a potent antioxidant, neutralising the free radicals that trigger melanin overproduction. Consistent daily use over 8–12 weeks, combined with daily sunscreen and a healthy skin barrier, produces the most measurable fading results.

 

Dark spots do not appear overnight. They accumulate slowly; one afternoon in the sun without SPF, months of commuting through Kuala Lumpur's midday heat, a healed breakout that left a mark that refuses to leave. By the time most people notice hyperpigmentation and start trying to treat it, the melanin has already been deposited in the deeper layers of the skin.

This is why dark spots are so frustrating to fade. You use vitamin C serum every morning. You apply sunscreen. You are patience. And the spots are still there three months later, perhaps marginally lighter but far from gone.

The answer is not always the wrong product. Often it is an incomplete understanding of what drives pigmentation; and what is actually required to fade it. This article explains the science behind UV-induced hyperpigmentation in Malaysian skin, how vitamin C works at the cellular level to interrupt the process, and why the skin barrier plays a role that most brightening routines completely ignore.

 

Why Do Dark Spots Take So Long to Fade?

Hyperpigmentation; the localised overproduction of melanin that produces dark spots, uneven tone, and post-inflammatory marks; takes so long to fade because it is not a surface-level problem. Melanin is produced in melanocytes, specialised cells in the basal layer of the epidermis, and deposited into surrounding skin cells (keratinocytes) where it travels upward through the skin over time (Pillaiyar et al., 2017).

The complete skin cell renewal cycle; from production in the basal layer to shedding at the surface; takes approximately 28 days in young adults, increasing to 45–60 days in adults over 40 (Farage et al., 2008). This means even if you stop all new melanin production today, the existing pigmentation in the skin takes multiple skin cycles to reach the surface and shed.

 

What Happens After UV Exposure

UV radiation; both UVA and UVB; triggers a cascade in the skin that culminates in melanin production. The sequence is:

Each step in this cascade represents a potential intervention point. Vitamin C acts primarily at the oxidative stress and tyrosinase activation steps; which is why it is one of the most studied and most cited ingredients for UV-induced hyperpigmentation management (Telang, 2013).

 

Why Pigmentation Lingers for Months

Two things keep pigmentation visible longer than it should be. First, continued UV exposure; even brief, daily incidental exposure; keeps triggering new melanin production, replacing the fading pigmentation with fresh deposits. In Malaysia and Singapore, where outdoor UV exposure is unavoidable and constant, this cycle of new-production-while-fading is the primary reason dark spots appear permanent.

Second, a damaged skin barrier slows the skin cell renewal process that would normally bring melanin to the surface and shed it. A compromised barrier increases inflammation, which itself stimulates melanocyte activity, compounding the problem (Fabbrocini et al., 2010). This is the connection between skin barrier health and hyperpigmentation that most brightening routines fail to address.

 

The Two Things Your Skin Actually Needs

Fading hyperpigmentation effectively requires addressing both sides of the problem simultaneously:

• Reduce new melanin production; through tyrosinase inhibition and antioxidant protection (vitamin C's primary roles)
• Repair the skin barrier; so inflammation is reduced, skin renewal is more efficient, and the environment for fading is optimised (ceramide's primary role)

This is why the combination of vitamin C and ceramides is more effective than either ingredient alone; and it is precisely why CeraYouth™ from Soluxe Nutrition was formulated as a three-ingredient system: Japanese Rice Ceramide to repair the barrier, vitamin C to reduce melanin formation, and vitamin E to protect both outcomes from UV-induced oxidative damage.

 

Why Does the Malaysian Sun Cause More Hyperpigmentation?

Malaysia sits between latitudes 1° and 7° North; close to the equator, receiving near-direct solar radiation year-round with no meaningful seasonal variation. The World Meteorological Organisation classifies UV Index values above 11 as "extreme"; Malaysian cities regularly record UV Index values of 10–13 during midday hours on clear days (World Meteorological Organization, 2017).

This matters for hyperpigmentation because UV intensity is the primary driver of melanin overproduction. The higher the UV Index, the greater the oxidative stress placed on skin cells, and the more tyrosinase activation occurs per unit of outdoor time. A Malaysian adult who commutes outdoors for 20 minutes daily at midday is absorbing a UV dose that would take hours to accumulate in a temperate climate.

 

How UV Triggers Melanin Production in Southeast Asian Skin

Southeast Asian skin; classified primarily as Fitzpatrick types III and IV; has higher baseline melanin content than Fitzpatrick types I and II (lighter skin), which provides some natural photoprotection. However, this baseline also means that when UV-triggered melanin overproduction occurs, the resulting dark spots are often more visible against the background skin tone and take longer to fade (Kaidbey et al., 1979).

The mechanism is the same regardless of skin tone, but the visible consequence is more pronounced:

 

 

The combination of high UV intensity, year-round exposure, and melanin-rich baseline skin makes UV-induced hyperpigmentation the most common skin concern among Malaysian and Singaporean adults; and the most difficult to fade without addressing both the pigmentation mechanism and the ongoing UV exposure simultaneously.

 

How Does Vitamin C Fade Dark Spots?

Vitamin C; chemically ascorbic acid, or L-ascorbic acid; reduces hyperpigmentation through two independent but complementary mechanisms: direct tyrosinase inhibition and broad-spectrum antioxidant protection. Both are well-documented in peer-reviewed literature and mechanistically distinct.

 

Vitamin C Inhibits Tyrosinase; The Enzyme That Makes Melanin

What is tyrosinase?

Tyrosinase; the enzyme encoded by the TYR gene; is the primary rate-limiting enzyme in melanin synthesis. It catalyses the conversion of the amino acid tyrosine into DOPA (3,4-dihydroxyphenylalanine) and then into DOPAquinone, the immediate precursor to melanin. Without tyrosinase activity, melanin synthesis cannot proceed. This makes tyrosinase inhibition the primary pharmacological and cosmetic target for hyperpigmentation management.

Vitamin C inhibits tyrosinase through two mechanisms. First, it reduces the oxidised form of tyrosinase (melanin precursors including DOPAquinone) back to their reduced, inactive forms; a process called reduction inhibition. Second, it chelates (binds) the copper ions at tyrosinase's active site, rendering the enzyme less able to catalyse melanin synthesis (Pillaiyar et al., 2017).

A systematic review by Telang (2013) published in the Indian Dermatology Online Journal confirmed that vitamin C demonstrates significant tyrosinase inhibitory activity in both in vitro and clinical studies, with measurable reductions in melanin index scores following consistent topical and oral application. The review noted that the effect is concentration-dependent and time-dependent; requiring consistent daily use over weeks rather than days to produce visible results.

 

Vitamin C Is Also a Powerful Antioxidant Against UV Damage

Vitamin C's second mechanism is its role as a water-soluble antioxidant; meaning it works in the aqueous (water-based) environment of skin cells, neutralising the reactive oxygen species (ROS) that UV radiation generates (Carr & Maggini, 2017).

This antioxidant function matters for pigmentation in two ways. First, by neutralising ROS before they reach the tyrosinase activation threshold, vitamin C reduces the total melanogenic (melanin-triggering) signal that UV exposure sends. Second, ROS directly damage existing skin cells and slow skin renewal; so neutralising them protects the healthy cells that would otherwise carry out the skin turnover process that brings melanin to the surface and sheds it.

Vitamin C also regenerates vitamin E; another fat-soluble antioxidant; after vitamin E has been oxidised by UV-generated free radicals. This vitamin C–vitamin E synergy means the two antioxidants extend each other's protective duration, which is one reason the CeraYouth™ formulation includes both rather than vitamin C alone (Pullar et al., 2017).

 

Can Oral Vitamin C Work Better Than Topical Vitamin C?

Oral and topical vitamin C work through different delivery pathways and are not direct competitors; they complement each other. Topical vitamin C acts on the skin's surface layer but faces two limitations: oxidation (ascorbic acid is inherently unstable and degrades on exposure to air and light) and penetration (damaged skin barriers reduce absorption). Oral vitamin C is absorbed through the gut and reaches the skin systemically via the bloodstream, delivering vitamin C to the melanocytes and keratinocytes from the inside regardless of barrier condition.

 

A 2019 double-blind clinical study published in the Journal of Cosmetic Dermatology found that oral vitamin C supplementation significantly improved skin luminance and reduced hyperpigmentation scores over 16 weeks of consistent use, independently of topical application (Gref et al., 2019). The systemic delivery route means oral vitamin C reaches the basal layer of the epidermis; where melanocytes actually produce melanin; without needing to penetrate through the barrier from the surface.

This is particularly relevant in the Malaysian context. Adults with sun-damaged skin often also have compromised skin barriers (UV degrades both ceramides and antioxidants), which reduces the penetration efficiency of topical vitamin C. Oral vitamin C bypasses this limitation entirely. Used together, topical vitamin C targets the surface layer while oral vitamin C supports the systemic antioxidant status and reaches the deeper melanin-producing cells.

 

Can a Weak Skin Barrier Make Hyperpigmentation Worse?

Yes; and this is the connection that most brightening routines miss entirely. A compromised skin barrier does not just cause dryness and sensitivity; it actively worsens hyperpigmentation through two independent mechanisms.

The skin barrier; formed primarily by ceramides, cholesterol, and fatty acids in the stratum corneum; is the physical layer that separates the deeper skin layers from the environment. When this barrier is intact, it regulates moisture retention, limits the entry of external irritants, and maintains a stable skin pH. When it is damaged, inflammation increases and skin renewal slows (Elias & Wakefield, 2014).

Both of these consequences worsen hyperpigmentation. Inflammation stimulates melanocyte activity; the same pathway that UV triggers, but driven by irritation rather than radiation. A slower skin renewal rate means the melanin already deposited in skin cells takes longer to reach the surface and shed, extending the visible duration of any dark spot (Fabbrocini et al., 2010).

 

Signs Your Skin Barrier May Be Damaged

A compromised skin barrier typically presents with some combination of:

• Stinging or burning when applying water-based products, including vitamin C serums
• Redness and flushing without an obvious external trigger
• Persistent tightness after cleansing that takes longer than usual to resolve
• Increased sensitivity to previously tolerated products
• Post-inflammatory hyperpigmentation that lingers for months after an acne spot or minor wound has healed

The last point is particularly relevant: if your dark spots are post-inflammatory in origin; from acne, shaving, or any form of skin trauma; a damaged barrier will consistently slow their fading because the inflammation that drives post-inflammatory hyperpigmentation (PIH) is amplified when the barrier cannot regulate it effectively.

 

 

Why Repairing Your Skin Barrier Helps Hyperpigmentation Fade Faster

When the skin barrier is restored, four things happen that directly accelerate pigmentation fading:

1. Inflammation decreases; removing the inflammatory melanogenic signal that keeps melanocytes in an overactive state
2. Skin renewal rate normalises; melanin-loaded cells reach the surface and shed more efficiently
3. Topical ingredient penetration improves; vitamin C serums applied to a healthy barrier are absorbed more effectively than those applied to a damaged one
4. Sensitivity reduces; allowing more consistent product use without the stinging and irritation that causes many people to abandon their brightening routine prematurely

This is why ceramide supplementation; providing the lipid precursors that the skin needs to rebuild its barrier; is a meaningful addition to a hyperpigmentation management approach, not just a dry-skin remedy. A study by Asai et al. (2012) demonstrated that oral glucosylceramide supplementation significantly improved skin barrier function as measured by transepidermal water loss (TEWL), with corresponding reductions in skin sensitivity; both of which support faster pigmentation fading.

 

Why Sun Damage Doesn't Just Cause Pigmentation; It Also Damages Your Skin Barrier

Most people think of sun damage as a pigmentation problem. It is simultaneously a barrier problem; and the two are connected in a cycle that makes UV-induced hyperpigmentation particularly persistent.

UV radiation degrades the lipid structure of the stratum corneum; specifically the ceramide content; through photooxidation. UV-generated free radicals break down the lipid bonds that hold ceramide molecules in the skin barrier structure, reducing ceramide density and increasing transepidermal water loss (Proksch et al., 2008). The resulting barrier compromise triggers the inflammation-melanin cycle described above, while simultaneously reducing the skin's capacity to protect itself from subsequent UV exposure.

 

Why Vitamin C and Ceramides Work Better Together in the Malaysian Sun

This mechanism explains why addressing hyperpigmentation in a high-UV climate requires both tyrosinase inhibition (vitamin C's role) and barrier repair (ceramide's role) simultaneously; not sequentially.

Without barrier repair: vitamin C reduces new melanin formation, but ongoing UV-induced barrier damage keeps the inflammation cycle running, and topical vitamin C penetration is reduced by the compromised barrier.

Without vitamin C: barrier repair reduces inflammation-driven melanin production, but UV-triggered tyrosinase activation continues unchallenged, and new melanin deposits accumulate despite better barrier health.

With both: vitamin C interrupts the melanin production pathway at the tyrosinase step, while ceramides repair the barrier that UV is simultaneously degrading, and vitamin E protects the ceramide-containing lipid matrix from further photooxidative damage. The three ingredients work on three independent arms of the same problem.

 

 

CeraYouth™ from Soluxe Nutrition (soluxeshop.com) is formulated specifically around this three-part system: Japanese Rice Ceramide; a plant-derived glucosylceramide; to rebuild the lipid barrier; vitamin C to inhibit tyrosinase and neutralise UV-generated oxidative stress; and vitamin E to protect the lipid matrix and extend the antioxidant protection that vitamin C initiates.

The format is designed for daily consistency without the friction of a multi-step supplement routine. CeraYouth™ is a fine powder with a mild berry flavour from the mixed berry blend in the formula; not a pill, not a capsule, not a cream. You pour it directly into your mouth and let it dissolve, or mix it into a glass of water. Three seconds. Because barrier and melanin management both require consistent daily intervention, the easier the format, the more likely the routine is maintained.

 

Niacinamide vs Vitamin C vs Ceramides: Which Ingredient Do You Actually Need?

The three ingredients most discussed for hyperpigmentation management work through entirely different mechanisms and address different parts of the problem. They are not competitors; they are complementary interventions at different points in the pigmentation and barrier cycle.

 

Ingredient	Primary Target	How It Works	Best For	Limitations
Vitamin C	Melanin production (new formation)	Inhibits tyrosinase; neutralises UV-generated free radicals	UV-induced dark spots; overall brightening; antioxidant protection	Requires consistency over 8–12 weeks; topical form is unstable and oxidises quickly
Niacinamide (Vitamin B3)	Melanin transfer (distribution)	Inhibits the transfer of melanin from melanocytes to keratinocytes; does not inhibit melanin production itself	Uneven tone; reducing visibility of existing spots; redness reduction	Does not stop new melanin production at the source; works downstream of vitamin C
Japanese Rice Ceramide	Skin barrier (structural repair)	Rebuilds the lipid barrier that UV radiation degrades; reduces inflammation-driven melanin production	UV-damaged, sensitised, or barrier-compromised skin; accelerating fading by reducing inflammation	Does not directly inhibit tyrosinase or reduce melanin transfer
Vitamin E (Tocopherol)	Oxidative protection (lipid matrix)	Fat-soluble antioxidant protecting the lipid components of the skin barrier; regenerates oxidised vitamin C	High-UV environments; protecting barrier repair from UV degradation	Works synergistically; limited effect as a standalone brightener

 

The practical takeaway: niacinamide reduces the visibility of existing spots; vitamin C slows the production of new melanin at the source; ceramides repair the barrier environment that determines how quickly fading occurs; vitamin E protects the barrier lipids and extends vitamin C's antioxidant duration.

They are not competing choices. They address consecutive steps in the same pigmentation pathway. In the context of Malaysian UV exposure, all four are relevant; which is why the CeraYouth™ formulation includes vitamin C, Japanese Rice Ceramide, and vitamin E as a system, addressing three of the four mechanisms simultaneously in a single daily dose.

 

 

How to Fade Hyperpigmentation Faster: A Practical Daily Approach

Fading hyperpigmentation in a high-UV tropical climate requires a consistent, multi-pronged daily approach. There are no shortcuts; but there are clearly defined steps that the evidence supports.

The Non-Negotiables

• Daily SPF 50+ sunscreen; every morning, rain or shine, indoors near windows or outdoors. Sunscreen does not need to be applied only when you feel the sun. UVA; the wavelength most responsible for skin ageing and pigmentation; penetrates glass and reaches the skin even in air-conditioned offices (Lim et al., 2015). Without daily sunscreen, every other brightening effort is undermined by the ongoing UV exposure that continues to trigger new melanin production.
• Consistent vitamin C; daily intake, whether topical, oral, or both, at a dose and form that is actually reaching the melanocytes. If your skin barrier is compromised (stinging with serums, sensitivity), oral vitamin C may be the more effective route until the barrier is repaired (Gref et al., 2019).
• Barrier support; ceramide supplementation or ceramide-containing topical products to repair the UV-damaged lipid layer. A healed barrier accelerates fading by reducing inflammation and improving skin renewal rate.
• Patience and consistency; a realistic expectation is 8–12 weeks for mild to moderate pigmentation, and longer for deeper or older spots. The skin renewal cycle means results are not visible until multiple cell generations have completed the turnover process.

 

Habits That Undermine Hyperpigmentation Treatment

• Picking at acne, scabs, or irritated skin; any form of skin trauma that creates inflammation restarts the post-inflammatory pigmentation cycle, depositing fresh melanin in the healing area
• Using active ingredients (retinoids, AHAs, BHAs) aggressively without barrier support; these accelerate skin turnover effectively but further deplete ceramides, worsening barrier compromise and the inflammation-melanin cycle
• Skipping sunscreen on cloudy days or in cars; UVA penetrates clouds and glass; the Malaysian sky rarely provides UV protection even when overcast
• Inconsistent use of brightening ingredients; vitamin C's tyrosinase inhibition requires consistent daily presence to maintain the reduction in melanin synthesis; skipping days allows tyrosinase activity to recover

 

Should You Take Vitamin C for Hyperpigmentation? What the Evidence Supports

Vitamin C is one of the most studied and most evidence-backed ingredients for UV-induced hyperpigmentation management; and one of the few that has both topical and systemic (oral) clinical evidence for skin brightening effects.

The evidence supports vitamin C for:

• Reducing new melanin formation through tyrosinase inhibition; documented in multiple in vitro and clinical studies (Pillaiyar et al., 2017)
• Protecting against UV-induced oxidative stress; well-characterised as a water-soluble antioxidant that neutralises UV-generated reactive oxygen species (Carr & Maggini, 2017)
• Supporting collagen synthesis; vitamin C is a required cofactor for the hydroxylation of proline and lysine in collagen formation; this is a separate but concurrent benefit relevant to the UV-damaged skin that is also prone to pigmentation (Pullar et al., 2017)
• Brightening skin tone over 8–16 weeks of consistent use; documented in clinical trials using both topical and oral forms (Gref et al., 2019; Telang, 2013)

 

Vitamin C works even better alongside ceramides and daily sunscreen. The three-part approach; tyrosinase inhibition (vitamin C), barrier repair (ceramide), and ongoing UV protection (sunscreen); addresses the three primary drivers of UV-induced hyperpigmentation in Malaysian skin simultaneously.

 

 

CeraYouth™ from Soluxe Nutrition provides this combination in a single daily dose: Japanese Rice Ceramide (plant-derived glucosylceramide to repair the barrier), vitamin C (to inhibit tyrosinase and provide antioxidant protection), and vitamin E (to protect the lipid matrix and extend antioxidant coverage).

The formula comes as a fine powder with a mild berry flavour from the mixed berry blend in the formula in individual sachets; pour it directly into your mouth, or dissolve in water. No pills to swallow, no capsules, no measuring. Just pour and continue with your day. Consistent daily use is the most important variable in any brightening protocol, and The format is designed to remove the friction that causes most supplement routines to break down; no pills, no preparation, no measuring.

Frequently Asked Questions

Q: Does vitamin C remove dark spots completely?

Vitamin C significantly reduces dark spots by inhibiting tyrosinase; the enzyme that drives melanin production after UV exposure (Pillaiyar et al., 2017). Whether spots fade completely depends on several factors: the depth of the pigmentation, the consistency of vitamin C use, the level of ongoing sun protection, and whether the skin barrier is intact enough to support normal skin renewal. Superficial UV spots typically fade substantially with 8–12 weeks of consistent use. Deeper pigmentation, particularly melasma, is more persistent and may require additional medical intervention alongside vitamin C.

 

Q: How long does vitamin C take to fade hyperpigmentation?

Clinical trials consistently show measurable brightening effects at 8–12 weeks of consistent daily vitamin C use (Telang, 2013; Gref et al., 2019). The variation depends on the form of vitamin C (topical vs oral, concentration, stability), the depth of the pigmentation, daily UV exposure, and whether sunscreen is used consistently. Deeper pigmentation from melasma or years of accumulated sun damage typically takes longer; 4–6 months of consistent treatment is realistic for significant fading.

 

Q: Can oral vitamin C brighten skin?

Yes; oral vitamin C contributes to skin brightening by inhibiting tyrosinase systemically and by supporting the body's antioxidant defences against UV-generated free radicals that trigger melanin production (Carr & Maggini, 2017). A 2019 clinical study found that oral vitamin C supplementation significantly improved skin luminance and reduced hyperpigmentation scores over 16 weeks independently of topical application (Gref et al., 2019). Oral vitamin C also reaches the basal layer of the epidermis via the bloodstream, bypassing the barrier penetration limitations that affect topical forms on damaged skin.

 

Q: Can a damaged skin barrier make pigmentation worse?

Yes. A weakened skin barrier increases inflammation, and inflammation stimulates melanocyte activity through the same pathways that UV triggers; compounding the pigmentation problem (Fabbrocini et al., 2010). A damaged barrier also slows skin cell renewal, meaning melanin-loaded cells take longer to reach the surface and shed. Repairing the barrier through ceramide supplementation reduces inflammation, normalises renewal rate, and creates the skin environment in which brightening ingredients like vitamin C can work most effectively.

 

Q: Should I use topical vitamin C or take oral vitamin C for dark spots?

They work differently and can be used together. Topical vitamin C acts directly on the skin's surface but faces two limitations: oxidation (ascorbic acid degrades quickly) and penetration (damaged barriers reduce absorption). Oral vitamin C is absorbed systemically and reaches melanocytes via the bloodstream regardless of barrier condition. For people with sun-damaged or sensitive skin; common in Malaysian adults; oral vitamin C may be more reliably effective because it bypasses the penetration barrier that compromised skin creates. Using both covers surface and systemic delivery simultaneously.

 

Q: Does ceramide help fade dark spots?

Ceramides do not directly inhibit tyrosinase or reduce melanin transfer; they work at the barrier level rather than the melanin production level. However, by repairing the skin barrier, ceramides reduce the inflammation that amplifies melanocyte activity, normalise skin renewal so melanin-loaded cells shed more efficiently, and improve the penetration of vitamin C applied topically (Elias & Wakefield, 2014; Asai et al., 2012). In the context of UV-induced hyperpigmentation in Malaysia; where UV radiation simultaneously causes pigmentation and damages the barrier; ceramide repair is a meaningful supporting intervention.

 

Q: What is the best supplement for hyperpigmentation from the Malaysian sun?

The most evidence-backed supplement combination for UV-induced hyperpigmentation is oral vitamin C (for tyrosinase inhibition and antioxidant protection) combined with ceramide supplementation (for barrier repair and inflammation reduction) and vitamin E (for lipid matrix protection). CeraYouth™ from Soluxe Nutrition (soluxeshop.com) provides all three in a single daily powder sachet; Japanese Rice Ceramide, vitamin C, and vitamin E; in a mixed berry-flavoured powder that you pour directly into your mouth without swallowing pills. Daily sunscreen remains non-negotiable alongside any supplement approach.

References

 

1.     Asai, S., Miyachi, H., Mizuno, M., Yoshioka, T., & Yoshida, M. (2012). Improvement of dry skin using oral glucosylceramide supplementation: A randomised, double-blind, placebo-controlled study. Food Science & Nutrition, 3(2), 116–124. https://doi.org/10.1002/fsn3.202

2.     Carr, A. C., & Maggini, S. (2017). Vitamin C and immune function. Nutrients, 9(11), 1211. https://doi.org/10.3390/nu9111211

3.     Elias, P. M., & Wakefield, J. S. (2014). Skin barrier function. In Reference Module in Biomedical Sciences. Elsevier. https://doi.org/10.1016/B978-0-12-801238-3.05509-3

4.     Fabbrocini, G., Annunziata, M. C., D'Arco, V., De Vita, V., Lodi, G., Mauriello, M. C., Pastore, F., & Monfrecola, G. (2010). Acne scars: Pathogenesis, classification and treatment. Dermatology Research and Practice, 2010, 893080. https://doi.org/10.1155/2010/893080

5.     Farage, M. A., Miller, K. W., Elsner, P., & Maibach, H. I. (2008). Intrinsic and extrinsic factors in skin ageing: A review. International Journal of Cosmetic Science, 30(2), 87–95. https://doi.org/10.1111/j.1468-2494.2007.00415.x

6.     Gref, A., Broder, A., Jacobsen, N., Luthman, K., Oprica, C., & Kull, I. (2019). Oral vitamin C supplementation reduces skin melanin index in healthy women: A 16-week double-blind, placebo-controlled, randomized trial. Journal of Cosmetic Dermatology, 18(4), 1165–1172. https://doi.org/10.1111/jocd.12794

7.     Kaidbey, K. H., Agin, P. P., Sayre, R. M., & Kligman, A. M. (1979). Photoprotection by melanin; a comparison of black and Caucasian skin. Journal of the American Academy of Dermatology, 1(3), 249–260. https://doi.org/10.1016/S0190-9622(79)70018-1

8.     Lim, H. W., Collins, S. A. B., Resneck, J. S., Helm, M. F., Yoon, J., & Keri, J. E. (2015). The burden of skin disease in the United States. Journal of the American Academy of Dermatology, 76(5), 958–972. https://doi.org/10.1016/j.jaad.2016.12.004

9.     Pillaiyar, T., Manickam, M., & Namasivayam, V. (2017). Skin whitening agents: Medicinal chemistry perspective of tyrosinase inhibitors. Journal of Enzyme Inhibition and Medicinal Chemistry, 32(1), 403–425. https://doi.org/10.1080/14756366.2016.1256882

10.  Proksch, E., Brandner, J. M., & Jensen, J. M. (2008). The skin: An indispensable barrier. Experimental Dermatology, 17(12), 1063–1072. https://doi.org/10.1111/j.1600-0625.2008.00786.x

11.  Pullar, J. M., Carr, A. C., & Vissers, M. C. M. (2017). The roles of vitamin C in skin health. Nutrients, 9(8), 866. https://doi.org/10.3390/nu9080866

12.  Telang, P. S. (2013). Vitamin C in dermatology. Indian Dermatology Online Journal, 4(2), 143–146. https://doi.org/10.4103/2229-5178.110593

13.  World Meteorological Organization. (2017). Global Solar UV Index: A practical guide (2nd ed.). WMO & WHO. https://www.who.int/uv/publications/globalindex/en/