Beta-carotene is the orange plant pigment found in carrots and sweet potato. It’s a carotenoid your body can convert into vitamin A, which supports normal skin barrier function and epithelial health. Because it’s fat-soluble, small amounts settle into the outer skin layers where they help neutralise UV-triggered oxidative stress. Over time, that build-up also nudges skin tone slightly warmer to create a food-derived glow.

In a 12-week, placebo-controlled trial, adults taking 24 mg/day beta-carotene or a mixed carotenoid supplement (β-carotene, lycopene, lutein; 24 mg total) showed reduced UV-induced erythema (sunburn response) compared with placebo – evidence that carotenoids can raise the skin’s photoprotective capacity when taken consistently (Heinrich et al., J Nutr, 2003). Mechanistically, carotenoids accumulate in the stratum corneum and quench singlet oxygen and lipid peroxyl radicals, helping limit photo-oxidative damage (Stahl & Sies, Am J Clin Nutr, 2012).

Independent longitudinal work shows that increasing dietary carotenoids shifts skin colour along the b* axis (more golden) within 6 weeks, and perception studies find this carotenoid-driven tone is judged healthier-looking than a darker melanin tan (Whitehead et al., PLoS ONE, 2012; Alaluf et al., J Nutr, 2002). Together, these data support a positioning of beta-carotene as glow + resilience over time, not a rapid tanning agent.

Ever wondered where wild salmon get their colour? It comes from astaxanthin, a red-orange carotenoid made by microalgae like Haematococcus pluvialis that moves up the food chain into salmon and prawns. In people, astaxanthin is fat-soluble and settles into skin lipids and cell membranes, where it helps neutralise UV-triggered oxidation before it can stress the barrier or fray collagen.

In randomised, placebo-controlled trials, daily astaxanthin improved real skin outcomes. Adults taking 4 mg/day had less UV-induced skin deterioration than placebo (Ito, Seki & Ueda, 2018). Independent clinical studies at 6–12 mg/day for 6–8 weeks report smoother-looking wrinkles, better elasticity, improved moisture and lower transepidermal water loss, and some show bigger gains when oral and topical astaxanthin are combined (Tominaga et al., Acta Biochim Pol, 2012; Tominaga et al., J Clin Biochem Nutr, 2017; Zhou et al., Nutrients, 2021).

On a cellular level, astaxanthin lodges in skin lipids and helps neutralise reactive oxygen species like singlet oxygen, supporting the barrier and a collagen-friendly environment. Ex-vivo and cell studies show lower inflammatory cytokines and reduced MMP-1 in dermal fibroblasts, which aligns with the elasticity and wrinkle findings in people (Am J Clin Dermatol, 2014; Tominaga et al., J Clin Biochem Nutr, 2017; Zhou et al., Nutrients, 2021). In singlet-oxygen quenching assays, astaxanthin is exceptionally potent, outperforming vitamins C and E and β-carotene, with reports of up to 6,000× vitamin C for that specific lab test (Molecules, 2022).

Lycopene is the vivid red pigment in tomatoes, watermelon and pink grapefruit. It is a fat-soluble carotenoid that settles into the skin’s lipid layers, where it helps neutralise UV-triggered oxidative stress and supports an even, calm look to skin. With steady intake it also contributes to a warmer, food-derived glow over time.

Human intervention trials with lycopene-rich tomato products show measurable photoprotection. In a randomised study, 55 g/day tomato paste (16 mg lycopene) for 12 weeks increased the minimal erythema dose and reduced UV-induced erythema and mtDNA damage versus control, indicating a real UV-buffering effect (Rizwan et al., Br J Dermatol, 2011). Earlier work providing 16 mg/day lycopene for 10 weeks similarly reduced UV-induced erythema (Stahl et al., J Nutr, 2001). At the molecular level, a tomato nutrient complex modulated UVA/UVB/UVA1-induced stress-response genes in human skin, including pathways tied to inflammation and photoageing (Grether-Beck et al., Br J Dermatol, 2017). Reviews explain that lycopene accumulates in the stratum corneum and quenches singlet oxygen and lipid peroxyl radicals, helping limit photo-oxidative damage that can disturb barrier function and collagen (Stahl & Sies, Am J Clin Nutr, 2012).

Independent longitudinal research shows that raising dietary carotenoids shifts skin colour toward higher b* values within about 6 weeks, and perception studies find this carotenoid-driven tone looks healthier than a darker melanin tan (Whitehead et al., PLoS ONE, 2012; Alaluf et al., J Nutr, 2002).

L-tyrosine is an amino acid your body uses to make melanin in skin and catecholamines like dopamine and noradrenaline. Your body already produces L-tyrosine from the amino acid phenylalanine, so this simply tops up a pathway that already exists. In the melanocyte, tyrosinase acts on L-tyrosine to start the melanin pathway, which is how your natural colour develops with UV exposure. Think of it as a building block for melanin production, unlike Melanotan, which is a synthetic peptide designed to stimulate melanin production in the skin.

Human trials and a systematic review show L-tyrosine can help preserve working memory and cognitive control during stressors like sleep loss, heat and demanding multitask paradigms, consistent with its role as a precursor for brain catecholamines (Jongkees et al., J Psychiatr Res, 2015; Shurtleff et al., Pharmacol Biochem Behav, 1994).   

For skin, L-tyrosine is the starting substrate that tyrosinase converts to DOPA on the way to melanin, placing it at the top of the pigmentation pathway (Pillaiyar et al., Int J Mol Sci, 2016). However, there is no clinical evidence that oral L-tyrosine alone darkens human skin without UV exposure. Reviews of tanning mechanisms and accelerator products emphasise that pigmentation changes depend on UV-triggered pathways and tyrosinase activity, not oral tyrosine by itself (D’Orazio et al., J Invest Dermatol, 2015; J Am Acad Dermatol, 2014).

A tag-team your skin already knows. Vitamin C is a water-soluble antioxidant and a required cofactor for collagen formation, and it also helps recycle vitamin E. Vitamin E (α-tocopherol) is the main fat-soluble antioxidant in skin, concentrating in cell membranes and arriving at the surface via sebum to protect lipids from peroxidation. Together they reinforce your skin’s natural defense network and complement carotenoids for a healthy-looking glow.

Human trials show that oral vitamin C plus vitamin E increases the skin’s minimal erythema dose and reduces UV-induced redness and sunburn cells compared with placebo, indicating meaningful photoprotection when taken consistently (Eberlein-König et al., J Am Acad Dermatol 1998; Placzek et al., J Am Acad Dermatol 1999). Reviews explain how vitamin C directly supports prolyl and lysyl hydroxylases in collagen maturation and regenerates oxidised tocopherol, while vitamin E sits in lipid membranes and sebum to intercept lipid peroxyl radicals, helping maintain a smoother, more resilient appearance (Pullar, Carr & Vissers, Nutrients 2017; Thiele et al., J Invest Dermatol 2001).

Lutein and zeaxanthin are the yellow carotenoids in leafy greens and corn. Your eyes love them, and your skin uses them too. They sit in lipid layers and help filter high-energy light while neutralising reactive oxygen species. In our blend, they’re present in trace amounts to round out the carotenoid spectrum.

In a 12-week, double-blind, placebo-controlled trial, 10 mg lutein + 2 mg zeaxanthin improved overall skin tone and luminance (L)* and raised the minimal erythema dose, indicating better resistance to UV-induced redness compared with placebo (Juturu et al., Clin Cosmet Investig Dermatol, 2016). 

A placebo-controlled crossover study showed a lutein supplement modulated UVA/UVB/UVA1-induced gene expression in human skin toward a less photo-stressed profile, supporting a molecular basis for photoprotection (Krutmann et al., Br J Dermatol, 2017).  Earlier clinical work testing oral and topical lutein + zeaxanthin reported improvements in hydration, elasticity, photoprotective activity and lower lipid peroxidation, with the combined route performing best over time (Palombo et al., Skin Pharmacol Physiol, 2007). 

Zinc and copper are trace minerals your skin uses as working parts of enzymes. In the epidermis, zinc is concentrated where keratinocytes are busy building and repairing the barrier. Copper, meanwhile, is required by lysyl oxidase to help cross-link collagen and elastin and by tyrosinase in the melanin pathway. Together they also sit at the core of Cu/Zn superoxide dismutase (SOD1), one of skin’s frontline antioxidant enzymes.       

In human skin, zinc and copper act as cofactors for enzymes that keep the barrier strong, the matrix resilient and pigment pathways working normally. Zinc supports keratinocyte proliferation, differentiation and repair, and low zinc states are linked with inflamed, impaired skin (Ogawa et al., Nutrients, 2018). Copper is required by lysyl oxidase, which cross-links collagen and elastin to support firmness and elastic recoil (Kagan & Li, J Cell Biochem, 2003). Copper also sits in the active site of tyrosinase, the rate-limiting enzyme for melanin synthesis, placing copper at the heart of normal pigmentation chemistry (Solano, Int J Mol Sci, 2018). As antioxidant partners, zinc and copper combine in Cu/Zn superoxide dismutase (SOD1), a frontline epidermal enzyme that converts superoxide radicals into less reactive species after UV and environmental stress (Altobelli et al., Front Med, 2020).

Clinically, oral zinc has shown dermatology benefits in controlled trials for inflammatory acne, aligning with its immunomodulatory and antioxidant roles (Dréno et al., Dermatology, 2001). Nutrition studies also show that high zinc intakes over time can reduce copper status, which is why balanced formulas pair both minerals (Fischer, Giroux & L’Abbé, Am J Clin Nutr, 1984). At 2.5 mg zinc + 942 mcg copper per serving, you are supplying supportive cofactor levels for collagen cross-link integrity, pigment enzyme activity and antioxidant defense, complementing the carotenoids that drive a healthy-looking glow.