Stop the clock: nutrition and skin ageing

Ageing is a natural process which cannot be avoided. However, most of us would like to slow down the ageing process and hold on to our youthful vitality for as long as possible. Every cell in our body is continuously ageing, but the skin (which is the most exposed organ to the external environment) is where we can see the visible signs of ageing. Radiant, glowing skin is something we aspire to at all ages, but how can we maintain it throughout the years?

There are 2 aspects of ageing. Firstly, intrinsic ageing, which is part of the chronological ageing cycle, affects skin in the same pattern as all internal organs, which are affected and heavily influenced by genetic and metabolic factors. Secondly, extrinsic ageing, which is influenced by external factors including pollution, UV radiation, nutrition, stress and smoking to name a few. As the skin is heavily exposed to these environmental stressors, they can have a significant effect on the appearance of the skin as we age.¹

It can be seen from the list above that much of extrinsic ageing can be ameliorated by reducing exposure to environmental factors that can contribute to ageing. However, lifestyle and nutritional interventions have the ability to help combat effects of both intrinsic and extrinsic ageing. In this blog we look at elements that can contribute to skin ageing and highlight interventions to help slow down the clock and reduce the signs of ageing skin.

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What happens to our skin as we age?

There are multiple factors that occur and can have an effect on the appearance of skin during ageing:^2,3

• Dermis thickness decreases with age, associated with a decrease in both vascularity and cellularity, including fibroblasts as well as reduction in glycosaminoglycans and hyaluronic acid.
• Decrease in collagen turnover (due to a decrease in fibroblasts and their collagen synthesis) as well as elastin. Collagen fibres can also become cross linked which disrupts their normal structure and reduces their ability to support the skin. This leads to a sagging and wrinkling effect on the skin.
• The loss of molecular integrity of the dermis leads to increased rigidity, decreased torsion extensibility, and diminished elasticity.
• Senescence of fibroblasts and melanocytes can lead to pigmentation changes and hence age spots.

Factors contributing to skin ageing

Oxidative stress^1,4

Occurs when there is an imbalance between the production of free radicals (reactive oxygen species (ROS)) and the ability of the body to counteract or detoxify their harmful effects using antioxidants. ROS play a critical role in alterations of the dermal extracellular matrix, both in the case of intrinsic and photo (extrinsic) ageing.

Photoaging is associated with excess exposure to UV radiation and increases the production of ROS within the skin. ROS have been shown to increase the production of matrix metalloproteinases (MMP); enzymes which increase the degradation of collagen, leading to loss of structural integrity within the dermis and promoting wrinkles. In summary, exposure to UV radiation excessively increases ROS and therefore MMP production promoting collagen degradation and ageing skin.⁵

Advanced glycation end products (AGEs)^1,4,6

Glycation is involved in both intrinsic and extrinsic ageing. AGEs are proteins or lipids which become glycated as a result of exposure to sugars; accumulation of these can result in tissue stiffening and reduced elasticity. Glycation can occur in collagen fibres, causing cross linking of collagen and loss of structural integrity.

Cell cycle dysfunction^1,4,7

In all organ system of the body there is cell turnover, where there is a balance between apoptosis (cell death) and cellular regeneration or mitosis. As we age, many factors influence this balance and drive them further towards cell degeneration, i.e. increased apoptosis and endurance of dysfunctional cells and a loss of cell regeneration. This leads to cell loss, driving skin thinning and can also allow an excess of damaged cells, which can increase the risk of cancer formation.

Cell cycle dysfunction can be driven by:^1,6

• DNA damage: persistent exposure to UV radiation increases DNA damage and mutations, which can lead to premature ageing
• Telomere shortening: telomeres act as buffers at the end of our chromosomes, protecting our genes from damage during cell division. UV radiation leads to excessive ROS production, resulting in telomere mutations and further cell death or senescence
• microRNA (miRNA) regulation: in genetics, an miRNA is a form of single-stranded RNA that regulates the expression of other genes. In the skin, miRNA plays a key role in regulating the balance between a cell’s proliferative capacity (ability to regenerate injured cells and tissues) and replicative senescence (how many times a cell can divide). Fibroblasts, which are responsible for collagen synthesis and structural tissue framework in the skin also show increased miRNA activity with age

• Genetic mutation: there is an extremely rare genetic mutation which can cause progeria, a type of premature ageing, which often results in: i) an accelerated skin ageing phenotype, including skin atrophy and sclerosis; ii) poikiloderma (a condition which causes skin discolouration and breakdown) and iii) alopecia, thinning, and greying of the hair

Inflammaging

Chronic, low-grade inflammation is recognised as a major characteristic of the ageing process and is often referred to as ‘inflammaging’. It plays a role in the initiation and progression of age-related diseases such as type II diabetes, Alzheimer’s disease, cardiovascular disease and skin ageing.¹

Hormonal changes

Oestrogen receptors are found in nearly every tissue in the body and influence the function of all organ systems in a woman. This is especially true of the largest organ, skin. Women’s skin, due to the oestrogen depletion associated with menopause, ages at an accelerated pace as compared with men, with both structural and functional deterioration observed. Oestrogen therapy reverses the thinning of ageing skin by both increasing collagen synthesis and retarding collagen degradation, decreases wrinkles by stimulating the synthesis of type III collagen and hyaluronic acids, and increases skin hydration and barrier function, making ageing skin less dry. Therefore, supporting hormone regulation during menopause may have beneficial effects on skin ageing.²

Thyroid hormone is responsible for cell turnover and metabolism and therefore plays a role in the maintenance of skin integrity. Hypothyroidism is associated with thinning and dry skin as there is a reduced capacity for cells to regenerate. Therefore, supporting thyroid function should be considered to help reduce the effects of ageing, if required.⁸

Cortisol is a catabolic hormone, hence it increases tissue regeneration. It can also increase oxidative stress, DNA damage and is associated with shorter telomeres. Therefore, excess stress and the associated increase in cortisol can contribute to ageing of skin. Interventions which include supporting adrenal function, aiding a healthy stress response and relaxation may be helpful.⁹

Key nutrient considerations for mitigating skin ageing

Now that we know how skin ageing occurs and the key factors of influence, let’s look at the agents which research has shown may mitigate these effects and slow the natural skin ageing cycle:

Vitamins

Vitamin C: acts as a co-factor for the enzymes responsible for the stabilisation and cross-linking of collagen molecules. With sunscreen capable of blocking only 55% of the free radicals produced by UV exposure, antioxidants like vitamin C are essential for neutralising the ROS formed due to UV exposure. A double-blind, placebo-controlled study on 10 subjects using 10% topical vitamin C over a 12-week period showed a statistically significant reduction in photo-aged scores and improvement in wrinkling in vitamin C-treated patients compared to placebo.⁷

The most commonly described cutaneous manifestations accompanying vitamin C deficiency are attributed to the impaired collagen synthesis.¹⁰

Tocopherols and tocotrienols (vitamin E): the natural vitamin E complex comprises a group of 8 compounds called tocopherols and tocotrienols. Vitamin E is a strong anti-inflammatory agent in the skin, with its primary photoprotective role being to prevent damage caused by free radicals and ROS.

While vitamins E and C can provide photoprotection alone, they work best in conjunction.  For example, vitamin E quadruples the action of vitamin C. Hydrophilic vitamin C helps to regenerate vitamin E, a lipophilic antioxidant. Together, these antioxidant vitamins protect both the water and lipid compartments of the cell. When working synergistically, they limit chronic UV damage by reducing both cell apoptosis and thymine dimer formation (this is where two adjacent thymine bases in DNA become abnormally bonded). As well as vitamin C, CoQ10 and glutathione can also recycle vitamin E.⁷

Vitamin D: this well-known vitamin is in fact a prohormone; a substance which the body converts to a hormone. The skin, as the primary site of vitamin D production, is one of the central tissues in the prohormone vitamin D endocrine system. It contains a cholesterol-like substance called provitamin D3 which reacts with UVB light to form vitamin D3. Several studies have demonstrated the protective effect of calcitriol (the hormonally active metabolite of vitamin D) against UVB-induced skin damage and carcinogenesis. Research conducted by Chang et al., further suggests a strong association between skin ageing and levels of calcifediol, another precursor of vitamin D.¹¹ This makes sense considering the broad variety of vitamin D’s physiological functions. Not only does it protect skin cells from UV-induced cell death and apoptosis, but it inhibits the activation of stress-activated protein kinases (controls cellular survival, differentiation and apoptosis), and suppresses production of the proinflammatory cytokine, IL-6.⁷

The capacity of the skin to produce vitamin D declines with age, with concentrations of 7-dehydrocholesterol—a vitamin D3 precursor—declining by approximately 50% between the ages of 20-80.

Skin cancer is also the fifth most common form of cancer in females. Studies have indicated that oral vitamin D treatment demonstrates clear skin cancer prevention capabilities, with links to anti-ageing effects.⁷

Carotenoids refer to vitamin A derivatives (such as beta-carotene), astaxanthin, lycopene and retinol; all highly effective antioxidants which hold distinct photoprotective properties. In fact, in comparison to other antioxidants such as lutein and zeaxanthin, the human skin is relatively enriched with carotenoids like beta-carotene and lycopene, possibly reflecting a more specific photoprotective function.⁷

• Beta-carotene: while its primary role is its provitamin-A activity, beta-carotene is an endogenous photoprotector, and its efficacy to prevent UV-induced erythema formation has been demonstrated in various studies. It also significantly reduces the rate of mitochondrial mutation in human dermal fibroblasts after UV irradiation.
• Astaxanthin: is found in microalgae, yeast, salmon, trout, krill, shrimp, crayfish and crustacea. Algal extract containing 14% astaxanthin was found to prevent UVA-induced alterations in cellular superoxide dismutase activity (an antioxidant enzyme) and the subsequent decreases in cellular glutathione content. It also shows pronounced photoprotective effects and an ability to counteract UVA-induced alterations such as skin sagging or wrinkling.
• Lycopene: while it has no vitamin A activity, lycopene is technically a carotenoid. Significant amounts of lycopene are destroyed when skin is exposed to UV light stress, suggesting a role in mitigating oxidative damage in skin tissues.¹⁰

Botanical antioxidants: polyphenols, anthocyanosides & isoflavones

Over the last decade, polyphenols have become a central feature in anti-ageing research. Natural polyphenols, anthocyanosides or flavonoids are not only plant pigments, but also powerful antioxidants which protect plants against disease. With potent antioxidant capabilities, increasing research is demonstrating their protective affects against UV-induced skin inflammation, oxidative stress and DNA damage. ⁷

• Resveratrol: this small polyphenol found in the skin of red grapes, fruits and red wine is often cited for its potential anti-carcinogenic effects; attributable to its ability to scavenge free-radicals and induce anti-inflammatory effects. It has a demonstrated ability to protect against the depletion of endogenous antioxidant defence enzymes, suppress lipid and protein oxidation and inhibit apoptosis.
• Soybean isoflavones: also known as a phytoestrogen due to its structural similarity to oestrogen. Mice fed soy isoflavones showed significantly less wrinkling in their UV-irradiated skin versus controls. Interestingly, collagen deposition was also increased as a result of the dietary isoflavones. Similar results have been demonstrated in human trials, with significant decreases in fine facial wrinkles after 12 weeks of soy isoflavone supplementation.¹²
• Curcumin: predominantly extracted from turmeric spice and a member of the ginger family, curcumin shows a pronounced ability to attenuate oxidative stress and suppress inflammation. In human fibroblasts, curcumin induced cellular antioxidant defences.^13,14
• Cocoa flavanols:  are naturally occurring antioxidant and anti-inflammatory compounds. A double-blind in vivo study looked at the impact of cocoa flavanols on individuals’ minimal erythema dose (MED, sensitivity to the sun) and discovered that after 12-weeks of cocoa flavonol intake, participants’ MED more than doubled, suggesting significant photoprotection. Cocoa flavanol consumption also increased dermal blood flow and oxygen which may help to reduce accelerated ageing.¹⁵
• Anthocyanides (e.g. found in bilberries): have potent antioxidant and photoprotective activity. These have also been found to minimise UV-induced erythema or sunburn.¹⁰

Ubiquinol (coenzyme Q10)

CoQ10 is a fat-soluble, vitamin-like substance; mainly stored within the body’s adipose tissues. While it has a plethora of functions within the body, in the skin it is primarily found in the epidermis, where it forms part of the initial barrier to oxidant assault in combination with other enzymatic and non-enzymatic substances. In animal studies, supplementation resulted in elevation of CoQ homologs in tissues and their mitochondria, causing a selective decrease in protein oxidative damage and an increase in antioxidative potential. ^7,16

Collagen peptides

Consuming oral collagen has been expressed to improve skin elasticity, resulting in increased levels of Type I collagen. Numerous studies exhibit positive effects on skin elasticity, including improvements in surface elasticity. Collagen peptides have been found to increase collagen content and improve skin laxity in a variety of animal and human studies.¹⁷

Omega-3 fatty acids

Eicosapentaenoic acid (EPA) and other omega-3 fatty acids reduced levels of proinflammatory mediators, reduced DNA damage and strand breaks and increased sunburn threshold (thus reducing the likelihood of sun damage), when taken in high doses of between 4-10g/d.¹⁰

Sea Buckthorn Oil

A study demonstrated that sea buckthorn oil can alleviate skin ageing by enhancing the total antioxidant capacity in the body, thereby strengthening the body’s antioxidant defence capability. It can also regulate the production of MMPs thereby protecting collagen against degradation, maintaining the stability of collagen fibre and elastic fibre structure.¹⁸

Probiotics

In an effort to find alternatives to antibiotic skin treatment, probiotics are emerging as a viable therapy. Oral administration of Bifidobacterium breve prevented UV-induced transepidermal water loss (loss of moisture from the skin which can make appearance of fine lines and wrinkles more pronounced) compared to mice receiving placebo.  Additionally, the UV-induced increase in hydrogen peroxide levels, oxidation of proteins and xanthine oxidase in the skin was supressed, suggesting an ability to at least partially alleviate UV-induced barrier changes and oxidative stress in the skin. Lactobacillus plantarum preserved procollagen expression in human fibroblasts. Oral administration of L. plantarum reduced the number and depth of wrinkles in hairless mice.¹⁰

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References

1. Chaudhary M, Khan A, Gupta M. Skin Ageing: Pathophysiology and Current Market Treatment Approaches. Curr Aging Sci. 2020;13(1):22. doi:10.2174/1567205016666190809161115
2. Farage MA, Miller KW, Elsner P, Maibach HI. Characteristics of the Aging Skin. Adv Wound Care (New Rochelle). 2013;2(1):5. doi:10.1089/WOUND.2011.0356
3. Kim JC, Park TJ, Kang HY. Skin-Aging Pigmentation: Who Is the Real Enemy? Cells. 2022;11(16). doi:10.3390/CELLS11162541
4. Shin SH, Lee YH, Rho NK, Park KY. Skin aging from mechanisms to interventions: focusing on dermal aging. Front Physiol. 2023;14. doi:10.3389/FPHYS.2023.1195272
5. Pittayapruek P, Meephansan J, Prapapan O, Komine M, Ohtsuki M. Role of Matrix Metalloproteinases in Photoaging and Photocarcinogenesis. Int J Mol Sci. 2016;17(6). doi:10.3390/IJMS17060868
6. DiLoreto R, Murphy CT. The cell biology of aging. Mol Biol Cell. 2015;26(25):4524. doi:10.1091/MBC.E14-06-1084
7. Schagen SK, Zampeli VA, Makrantonaki E, Zouboulis CC. Discovering the link between nutrition and skin aging. Dermatoendocrinol. 2012;4(3):298. doi:10.4161/DERM.22876
8. Safer JD. Thyroid hormone action on skin. Dermatoendocrinol. 2011;3(3):211. doi:10.4161/DERM.3.3.17027
9. Chen Y, Lyga J. Brain-Skin Connection: Stress, Inflammation and Skin Aging. Inflamm Allergy Drug Targets. 2014;13(3):177. doi:10.2174/1871528113666140522104422
10. Schagen SK, Zampeli VA, Makrantonaki E, Zouboulis CC. Discovering the link between nutrition and skin aging. Dermatoendocrinol. 2012;4(3):298. doi:10.4161/DERM.22876
11. Chang ALS, Fu T, Amir O, Tang JY. Association of facial skin aging and vitamin D levels in middle-aged white women. Cancer Causes Control. 2010;21(12):2315. doi:10.1007/S10552-010-9646-Y
12. Rizzo J, Min M, Adnan S, et al. Soy Protein Containing Isoflavones Improves Facial Signs of Photoaging and Skin Hydration in Postmenopausal Women: Results of a Prospective Randomized Double-Blind Controlled Trial. Nutrients 2023, Vol 15, Page 4113. 2023;15(19):4113. doi:10.3390/NU15194113
13. Benameur T, Frota Gaban SV, Giacomucci G, et al. The Effects of Curcumin on Inflammasome: Latest Update. Molecules. 2023;28(2). doi:10.3390/MOLECULES28020742
14. Kasprzak-Drozd K, Niziński P, Hawrył A, et al. Potential of Curcumin in the Management of Skin Diseases. Int J Mol Sci. 2024;25(7). doi:10.3390/IJMS25073617
15. Mogollon JA, Boivin C, Lemieux S, Blanchet C, Claveau J, Dodin S. Chocolate flavanols and skin photoprotection: a parallel, double-blind, randomized clinical trial. Nutr J. 2014;13(1):66. doi:10.1186/1475-2891-13-66
16. Ayunin Q, Miatmoko A, Soeratri W, Erawati T, Susanto J, Legowo D. Improving the anti-ageing activity of coenzyme Q10 through protransfersome-loaded emulgel. Scientific Reports 2022 12:1. 2022;12(1):1-13. doi:10.1038/s41598-021-04708-4
17. Rahman A, Rehmani R, Pirvu DG, Huang SM, Puri S, Arcos M. Unlocking the Therapeutic Potential of Marine Collagen: A Scientific Exploration for Delaying Skin Aging. Mar Drugs. 2024;22(4). doi:10.3390/MD22040159
18. Liu X, Yuen M, Yuen T, Yuen H, Wang M, Peng Q. Anti‐skin aging effect of sea buckthorn proanthocyanidins in D‐galactose‐induced aging mice. Food Sci Nutr. 2024;12(2):1082. doi:10.1002/FSN3.3823

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Last updated on 4th July 2024 by cytoffice