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Table of Contents 1. What Are Free Radicals? [1] 2. Are Free Radicals the Cause of Premature Skin Aging? [2] 3. How to Effectively Minimize Free Radicals and Prevent Premature Skin Aging |
Premature skin aging or hyperpigmentation isn't solely caused by external factors — internal, endogenous elements within the body also play a significant role. Some experts believe that "an overproduction of free radicals can lead to various health issues and inadvertently accelerate the skin's aging process." Join our doctors at ROHTO AOHAL CLINIC to explore how deeply free radicals affect your overall health and your skin's youthful appearance. This knowledge will help you take early and effective steps in caring for your skin from the inside out.
1. What Are Free Radicals? [1]
Definition
Free radicals are unstable molecules in the body that contain an unpaired electron, making them highly reactive. To stabilize themselves, these molecules either "steal" electrons from other molecules or "donate" their own, triggering a series of chemical reactions in the body. The most common types—such as hydroxyl radicals, superoxide, and peroxynitrite—are particularly aggressive. They attack essential cellular components like DNA, proteins, carbohydrates, and lipids, leading to cellular damage and internal imbalances.
The primary targets of free radicals include lipids, nucleic acids (key components of DNA), and proteins. When these molecules are attacked, skin cells can be damaged, resulting in premature aging signs such as wrinkles, dullness, and loss of elasticity.
Origin of Free Radicals
- Endogenous sources: Free radicals are continuously generated through cellular respiration — the energy conversion process that powers cell functions, primarily fueled by carbohydrates.
- Exogenous sources: These include radiation, inflammatory responses, prolonged stress and fatigue, smoking, environmental pollution, and other external aggressors.
Reactive oxygen species (ROS) encompass not only free radicals but also non-radical oxidants such as O₂, ONOO⁻, H₂O₂, and O₃. These oxidative species are produced and broken down by all aerobic organisms, maintaining physiological levels necessary for normal cellular function. However, when present in excess, they lead to a state known as oxidative stress.
Oxidative stress is an imbalance between the production of reactive oxygen species and the body's antioxidant defense mechanisms. Severe oxidative stress can result in cellular damage and even cell death.
2. Are Free Radicals the Cause of Premature Skin Aging? [2]
The skin is the organ most vulnerable to oxidative stress, primarily due to exposure to sunlight and pollution. Frequent exposure to both exogenous and endogenous oxidative factors prompts the body to activate its antioxidant defense and repair systems to restore balance.
Scientific Evidence
Studies have shown that the skin possesses a diverse antioxidant defense system to protect against various oxidants. The epidermis and dermis have these protective mechanisms, with the epidermis having a higher concentration. Key antioxidant molecules in the skin include ascorbic acid, α-tocopherol, glutathione, and ubiquinol, distributed across different cell layers and in varying amounts.
Aging is an irreversible and inevitable physiological change that alters normal bodily functions. A decline in functional capacity characterizes intrinsic aging, increased susceptibility to disease and environmental stress, and affects all tissues. In the skin, it manifests as dryness, fine lines, and deeper wrinkles.
On the other hand, extrinsic aging is driven by environmental factors such as chronic sun exposure and pollutants. Its visible effects differ from person to person, depending on factors like skin pigmentation, genetics, and lifetime UV exposure. This leads to thickening and dryness of the skin, deeper wrinkles, hyperpigmentation, broken capillaries, and visible lesions (including benign, precancerous, and cancerous growths). Notably, intrinsic aging is often observed even in areas with UV exposure, especially on visible parts like the face, neck, arms, forearms, and hands.
When free radicals damage DNA, they trigger oxidative stress, forcing cells to activate repair mechanisms or adjust the cell cycle. These responses produce intermediates that can interact with other cellular components, altering gene expression and potentially leading to internal dysfunction.
Ultraviolet (UV) radiation from sunlight is a major contributor. It stimulates the production of enzymes called metalloproteinases (MMPs), which break down collagen, the protein that keeps skin firm and smooth. UV rays also suppress the production of procollagen, reducing skin elasticity. Notably, UVB (290–320 nm) and UVA (320–400 nm) rays have high energy and can directly damage sensitive cells like fibroblasts (collagen-producing) and melanocytes (pigment-producing), accelerating skin aging.
Therefore, the role of free radicals in skin aging is well-documented. The accumulation of oxidative reaction byproducts is linked to the aging process. UV exposure activates numerous enzymes that indirectly promote the production of ROS (reactive oxygen species), leading to oxidative stress and visible signs of skin aging.
Further Research
You may also refer to the work of Denham Harman — the father of the free radical theory of aging — as cited by Wickens. Harman proposed that aging is linked to forming free radicals induced by radiation exposure in humans. According to this premise, free radicals are responsible for causing cumulative, small-scale cellular damage that ultimately leads to skin aging.
Free radical species from various sources — including radiation exposure, chemical induction, and physical trauma — are known to damage DNA and promote protein glycation. This latter process contributes to the biological dysfunction of key structural proteins such as collagen and proteoglycans, accelerating skin sagging and the visible signs of aging.
3. How to Effectively Minimize Free Radicals and Prevent Premature Skin Aging
Incorporate Antioxidant-Rich Foods
The body has developed a complex antioxidant defense system comprising both enzymatic and non-enzymatic components to combat free radicals. Numerous studies have shown that consuming antioxidant-rich foods like fruits, vegetables, and nuts can help increase longevity.
Among beverages, green tea—a staple in traditional Japanese diets—has been extensively studied for its anti-aging properties and potential to lower cardiovascular-related mortality. In one study, Hao et al. compared the impact of dietary and water-borne minerals on longevity using demographic data from 18 districts in a Chinese population census. Their findings showed that higher intake levels of copper (Cu), selenium (Se), and zinc (Zn) through diet and water were positively associated with increased lifespan.
Vitamins are essential for both animals and humans. While they do not provide energy, they act as enzyme cofactors and precursors that regulate metabolism. The body must obtain them through diet. Among them, vitamins A, C, and E are known as "antioxidant vitamins" and play a key role in neutralizing free radicals and protecting skin cells from oxidative stress.
Vitamin C – The Antioxidant Bodyguard
Also known as L-ascorbic acid, vitamin C is a lipophobic compound that plays a crucial role in collagen synthesis within the body. Among all vitamins, it exists in the highest concentrations in human tissues and is considered a key regulator of redox (oxidation-reduction) balance.
In a study involving 17,304 middle-aged and older Europeans aged 42 to 82, Lewis et al. reported that adequate vitamin C intake is essential for reducing the progression of frailty and sarcopenia, conditions exacerbated by age-related oxidative stress. Qu et al. further found that vitamin C inhibits the expression of prelamin A and suppresses inflammatory mediators that cause cellular aging in subdural mesenchymal stem cells.
Animal studies using Alzheimer’s disease models have also shown that vitamin C deficiency in the brain can disrupt redox balance and accelerate the production of amyloid-beta, a key trigger of oxidative stress in Alzheimer’s pathology.
On the other hand, a review by Kaźmierczak-Barańska et al. highlighted vitamin C's critical antioxidant role in DNA repair and other biological processes. However, experts noted that its function may vary across different cell types and conditions, making research more complex. The “dual nature” of vitamin C — acting both as an antioxidant and, in specific contexts, as a pro-oxidant — poses challenges in fully understanding its precise biochemical behavior.
Nonetheless, with continued advancements in science and technology, our understanding of antioxidants like vitamin C and their multifaceted effects is expected to deepen significantly in the near future.
Vitamin E and Its Role in Aging
Vitamin E, also known as α-tocopherol, is a fat-soluble compound. While other related compounds such as β-, γ-, δ-tocopherols and α-, β-, γ-, δ-tocotrienols also exist, only α-tocopherol is officially recognized as “vitamin E.” This vitamin is widely regarded for protecting cells against oxidative damage.
The well-known U.S.-based Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a large-scale clinical trial examining cancer prevention, found that supplementation with α-tocopherol and β-carotene did not reduce mortality from liver cancer or chronic liver disease.
However, in 2019, Huang et al. published findings from a 30-year follow-up cohort study of ATBC participants, revealing that higher plasma levels of vitamin E were associated with reduced risk of all-cause and major-cause mortality. A deficiency in vitamin E has been linked to increased fragility of red blood cells and degeneration of neurons, particularly peripheral axons and dorsal horn neurons.
Furthermore, long-term vitamin E intake has been shown to help prevent telomere shortening in peripheral blood mononuclear cells in patients with Alzheimer’s disease, a marker associated with cellular aging.
It is important to note that each vitamin E analog exhibits different biological activities. The proportion of vitamin E compounds present in food, as well as their interactions with other coexisting compounds, may influence the aging process.
Boosting Pro-Vitamin A for the Body
Carotenoids, also known as pro-vitamin A, are lipophilic pigments classified into two main groups: carotenes and xanthophylls, based on their polarity. Blood levels of carotenoids have been found to decline in elderly individuals and patients with Alzheimer’s disease.
Research by Huang et al. confirmed a correlation between serum parameters and mortality rates in a cohort study of 29,103 men from the ATBC study. The findings revealed that higher serum β-carotene levels were associated with lower mortality rates from cardiovascular disease, heart disease, stroke, cancer, and all-cause mortality.
In a separate analysis of 3,660 U.S. participants, Min et al. found that elevated blood levels of β-carotene were positively correlated with longer leukocyte telomere length, a biological marker of aging.
Experimental models using Caenorhabditis elegans showed that continuous intake of astaxanthin from early life led to increased expression of genes encoding superoxide dismutase (SOD) and catalase, while also protecting mitochondria and the nucleus by activating nuclear translocation of the DAF-16 protein, ultimately resulting in extended lifespan.
Additionally, Wu et al. reported that astaxanthin intake had notable anti-aging effects in a D-galactose-induced aging model in mice, by maintaining antioxidant enzyme activity, inhibiting the expression of pro-oxidant enzymes, and increasing brain-derived neurotrophic factor (BDNF), which supports brain function and neuronal health.
Supplementing with Coenzyme Q10
Coenzyme Q10 (CoQ10) is a naturally occurring endogenous antioxidant in the body, crucial for maintaining redox (oxidation-reduction) balance. It is one of the most well-recognized endogenous antioxidants and is also available as a dietary supplement. Supplementation with CoQ10 in aged mice has been shown to delay ovarian reserve depletion and restore mitochondrial gene expression in oocytes, leading to improved related physiological functions.
Zhang et al. reported that CoQ10 delays aging by regulating the Akt/mTOR signaling pathway in mesenchymal stem cells treated with D-galactose. In another aging model using human vascular endothelial cells exposed to hydrogen peroxide, CoQ10 was found to delay aging by suppressing the expression of senescence-associated secretory phenotype (SASP) genes, inhibiting intracellular ROS production, increasing nitric oxide (NO) production by upregulating endothelial nitric oxide synthase (eNOS), and enhancing mitochondrial function.
In conclusion, without over-relying on medication, consuming antioxidant-rich foods, maintaining a healthy lifestyle, and managing stress are effective strategies to reduce oxidative stress, a key contributor to skin aging.
Advanced Skincare Treatments
In addition to essential nutrients and vitamins, you can add more color and excitement to life by indulging in advanced skincare treatments at ROHTO AOHAL CLINIC, featuring some of our most popular therapies:
Based on your skin’s aging level and individual needs, the doctors at ROHTO AOHAL CLINIC will provide a personalized skincare regimen that is scientifically grounded, safe, and effective. We invite you to contact us today for a complimentary premium VISIA skin analysis session with a ROHTO AOHAL CLINIC doctor. Please see the contact information below:
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Source:
1. Lobo V, Patil A, Phatak A, Chandra N. Free radicals, antioxidants and functional foods: Impact on human health. Pharmacogn Rev. 2010;4(8):118-126. doi:10.4103/0973-7847.70902.
2. Silva SAME, Michniak-Kohn B, Leonardi GR. An overview about oxidation in clinical practice of skin aging. An Bras Dermatol. 2017;92(3):367-374. doi:10.1590/abd1806-4841.20175481
3. Finkel, T., & Holbrook, N. J. (2000). Oxidants, oxidative stress and the biology of ageing. Nature, 408(6809), 239–247. doi:10.1038/35041687
4. Miyazawa T, Abe C, Burdeos GC, Matsumoto A, Toda M. Food Antioxidants and Aging: Theory, Current Evidence and Perspectives. Nutraceuticals. 2022; 2(3):181-204. https://doi.org/10.3390/nutraceuticals2030014
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