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How Plant Extracts Can Protect Against Photoaging and Skin Cancer.

Nothing ages your skin faster than sun exposure.

Everyday exposure to the sun's ultraviolet rays causes cumulative DNA damage that leads to photoaging and increases the risk of skin cancer. (1) Sunscreens help considerably, but they aren't able to provide total protection.

An extract of a Central American fern plant called Polypodium leucotomos, when orally ingested, helps keep ultraviolet rays from damaging your skin and increasing cancer risk. This plant extract protects skin cells from the inside out!

Two additional compounds--red orange extract and nicotinamide--provide additional protection from photoaging and DNA mutation. Ideally, this "oral sunscreen" should be used alongside a high-SPF topical sunscreen. This unique oral botanical can provide all-day protection.

Sun Exposure Destroys Skin Cells

While most people love the warm glow of sunlight on their skin, these rays are quite damaging. The sun's ultraviolet (UV) light damages skin DNA, suppresses a vital tumor-suppressor gene, and inhibits immune cells. (1-6)

If left unchecked, this onslaught causes skin to age faster and boosts the risk of skin cancer.

Wearing sunscreen is important, but it doesn't provide total protection. It doesn't protect the scalp or eyelids, it may be rubbed off by perspiration or swimming, and most people don't use nearly enough to block the sun's rays. Although clothing is a good means of sun protection, UV rays can still penetrate some fabrics. (7)

A plant extract called Polypodium leucotomos offers an ideal complement to topical sunscreens. Because it is taken orally, it protects all skin areas evenly--and it won't wash or rub off.

Unlike sunscreens applied to the skin, Polypodium leucotomos extract is rich in polyphenols that inhibit oxidative stress and inflammation--while also protecting skin cells against DNA damage caused by ultraviolet radiation. (8)


Sun Protection From the Inside Out

* The sun's ultraviolet rays damage DNA, accelerating photoaging of the skin and increasing the risk of skin cancer.

* Taken orally, a fern extract called Polypodium leucotomos inhibits UV-radiation damage and promotes DNA repair--two actions that help prevent premature skin aging and lower cancer risk.

* When combined with Polypodium leucotomos, nicotinamide and red orange extract provide even greater sun protection.

* This formulation can be taken orally each day to provide a powerful "internal sunscreen" to complement topical sunscreens by protecting all skin areas evenly--from the inside--without any fear that it will wash or rub off.

* In addition to this oral sunscreen, a high-quality topical sunscreen should be used for prolonged sun exposure.

Blocking Sun-Damage Mechanisms

Ultraviolet radiation causes photoaging and skin cancer because of how it impacts your DNA. This occurs through three mechanisms in particular: (9-11)

* First, UV radiation causes initial DNA damage.

* Second, it stops damaged DNA from being removed.

* Third, it prevents damaged DNA from being repaired.

Scientists found that orally administered Polypodium leucotomos protected hairless mice that were exposed to UV radiation by inhibiting all three of these UV-damage mechanisms. (12) It also helped combat inflammation of the skin.

Impressively, this study showed that Polypodium leucotomos helped reduce DNA damage during--and even before--UV exposure. (12)

Anti-Aging Effects

Researchers conducted lab studies on skin cells to investigate the extract's general anti-aging effects on skin elasticity and structure. They found that Polypodium leucotomos was able to:

* Inhibit enzymes that break down the elastin and collagen required for youthful-looking skin,13,14 and

* Protect cells that make the structural framework of skin tissue (the extracellular matrix and collagen).13

In other words, Polypodium leucotomos prevented the key underlying mechanisms involved in skin aging.

Human Clinical Trial

In a human study, healthy volunteers between 29 and 54 years old took 480 mg of Polypodium leucotomos extract orally prior to being exposed to UV rays. Skin biopsies showed decreases in DNA damage--suggesting photoprotective effects on DNA. (15)

When subjected to a low dose of UV light, placebo participants had a 217% increase in damaging DNA mutations, while Polypodium-supplemented participants had a striking 84% decrease. (15) Such DNA mutations and formation of damaging DNA photoproducts are the main cause of prematurely aged skin and skin cancer. (11,16-19)

When subjected to higher UV exposure, DNA mutations in the placebo group increased by 760%. By contrast, these mutations increased by only 61% in the Polypodium-supplemented group. (15) These studies show that orally taken Polypodium leucotomos helps prevent an array of mechanisms involved in UV light-induced skin-cell damage.

Additional UV Protection

UV radiation reduces the production of ATP (adenosine triphosphate), the cellular energy which the body needs to repair damaged DNA. (20)

For additional help in this area, we turn to a form of vitamin B3 called nicotinamide. Nicotinamide helps prevent UV-induced loss of cellular ATP. Protecting ATP (adenosine-triphosphate) helps promote continuous DNA repair mechanisms. (20)

In one study, scientists pretreated skin cells with nicotinamide and then exposed them to UV radiation. The nicotinamide removed and replaced damaged DNA and significantly increased the number of cells undergoing DNA repair. It also reduced the production of damaging DNA photoproducts in cell cultures and in human skin.21

In addition, a clinical trial showed that nicotinamide can also protect against UV-induced immune suppression. (2)

These two actions--repairing DNA and protecting against immune suppression--contribute to nicotinamide's ability to reduce the risk of skin cancer. (3)

Nicotinamide's protective effects against cancer were seen in a clinical study of 386 healthy patients who had been diagnosed with at least two non-melanoma skin cancers in the previous five years. This put them in the "high-risk" category for future skin cancers.

The participants took 500 mg doses of nicotinamide or placebo twice a day. After 12 months, the rate of new non-melanoma skin cancers in the supplemented group was reduced overall by 23% compared to the controls. (22)

A Third Pillar of Sun Defense

Red orange extract is a complement to Polypodium leucotomos because it provides protection against UV-induced inflammation and oxidative stress.

Red orange extract is obtained by a patented process from three pigmented varieties of Citrus sinensis. Its UV-protection benefits are due to its abundant anthocyanins, flavanones, and hydroxycinnamic acids. (23-26)

In a human study, oral supplementation with red orange extract reduced sunburn intensity by 35%. (27) The number of lifetime sunburns is closely correlated with the development of skin cancers. (28)

In another study, researchers applied red orange extract to skin cells and then exposed them to UV radiation. The extract significantly reduced UV-induced cell damage, inflammation, and cell death. (24)


Exposure to ultraviolet radiation starts a chain reaction of events that ends in either prematurely aged skin, skin cancer, or both.

1. First, UV radiation causes DNA damage. It triggers photochemical reactions that produce compounds known as DNA photoproducts (19) Photoproducts can then trigger DNA mutations, the main cause of prematurely aged skin and skin cancer. (11,16-19)

2. UV radiation prevents the natural DNA repair of damaged cells. The photoproducts generated by the sun's rays alter a gene called p53. This vital tumor-suppressor gene is known as "the guardian of the genome." (4-6)

When DNA damage occurs, p53 activates DNA repair. If the damage to the DNA is irreparable, p53 initiates programmed cell-death (apoptosis) to eliminate the damaged cell. (4,29) But when the p53 gene is mutated by UV light, it can no longer do its job. As a result, damaged cells do not undergo normal DNA repair, they escape apoptosis, and they start to multiply. (30)

It's not surprising, then, that p53 is one of the most frequently mutated genes in human cancers. (4)

3. UV radiation inhibits the production of valuable ATP (adenosine triphosphate). (16,20) Without adequate ATP levels, the body's repair systems cannot remove damaged DNA segments.3132 Damaged cells can then continue to multiply.

These mechanisms result in ultraviolet radiation being the main cause of skin photoaging, as well as the main cause of skin cancer. (11) Orally taken Polypodium leucotomos combats UV radiation by promoting both DNA protection and repair. (12,15)


Everyday exposure to the ultraviolet rays of the sun causes cumulative DNA damage that massively accelerates photoaging of the skin and increases the risk of skin cancer.

Research shows that--taken orally--a fern extract called Polypodium leucotomos has protective effects against UV-induced damage to skin cells and supports DNA repair--two key mechanisms that lower cancer risk and help prevent premature skin aging.

Adding nicotinamide and red orange extract provides an even greater level of sun protection.

These nutrients can be taken orally to provide a baseline of protection against the sun's damaging effects and to complement topical sunscreens by protecting even hard-to-reach areas of the body.

They offer evenly distributed skin protection from the inside, and won't rub or wash off.

For prolonged exposure to UV radiation, this potent defense should be combined with a high-quality, high-SPF topical sunscreen for more complete protection. If you have any questions on the scientific content of this article, please call a Life Extension[R] Wellness Specialist at 1-866-864-3027.


(1.) Available at: overview-of-sunlight-and-skin-damage. ( sunlight-and-skindamage/overview-of-sunlight-and-skin-damage) Accessed,

(2.) Yiasemides E, Sivapirabu G, Halliday GM, et al. Oral nicotinamide protects against ultraviolet radiation-induced immunosuppression in humans. Carcinogenesis. 2009;30(1):101-5.

(3.) Nazarali S, Kuzel P. Vitamin B Derivative (Nicotinamide)Appears to Reduce Skin Cancer Risk. Skin Therapy Lett. 2017;22(5):1-4.

(4.) Anna B, Blazej Z, Jacqueline G, et al. Mechanism of UV-related carcinogenesis and its contribution to nevi/melanoma. Expert Rev Dermatol. 2007;2(4):451-69.

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(6.) Available at: ( Accessed March 10, 2017.

(7.) Available at: ( Accessed April 23, 2018.

(8.) Choudhry SZ, Bhatia N, Ceilley R, et al. Role of oral Polypodium leucotomos extract in dermatologic diseases: a review of the literature. J Drugs Dermatol. 2014;13(2):148-53.

(9.) Hussein MR. Ultraviolet radiation and skin cancer: molecular mechanisms. J Cutan Pathol. 2005;32(3):191-205.

(10.) de Gruijl FR, van Kranen HJ, Mullenders LH. UV-induced DNA damage, repair, mutations and oncogenic pathways in skin cancer. J Photochem Photobiol B. 2001;63(1-3):19-27.

(11.) Nishigori C. Cellular aspects of photocarcinogenesis. Photochem Photobiol Sci. 2006;5(2):208-14.

(12.) Zattra E, Coleman C, Arad S, et al. Polypodium leucotomos extract decreases UV-induced Cox-2 expression and inflammation, enhances DNA repair, and decreases mutagenesis in hairless mice. Am J Pathol. 2009;175(5):1952-61.

(13.) Philips N, Conte J, Chen YJ, et al. Beneficial regulation of matrixmetalloproteinases and their inhibitors, fibrillar collagens and transforming growth factor-beta by Polypodium leucotomos, directly or in dermal fibroblasts, ultraviolet radiated fibroblasts, and melanoma cells. Arch Dermatol Res. 2009;301(7):487-95.

(14.) Murphy G, Cockett MI, Ward RV, et al. Matrix metalloproteinase degradation of elastin, type IV collagen and proteoglycan. A quantitative comparison of the activities of 95 kDa and 72 kDa gelatinases, stromelysins-1 and -2 and punctuated metalloproteinase (PUMP). Biochem J. 1991;277 (Pt 1):277-9.

(15.) Villa A, Viera MH, Amini S, et al. Decrease of ultraviolet A light-induced "common deletion" in healthy volunteers after oral Polypodium leucotomos extract supplement in a randomized clinical trial. J Am Acad Dermatol. 2010;62(3):511-3.

(16.) Chen AC, Halliday GM, Damian DL. Non-melanoma skin cancer: carcinogenesis and chemoprevention. Pathology. 2013;45(3): 331-41.

(17.) Pfeifer GP, You YH, Besaratinia A. Mutations induced by ultraviolet light. Mutat Res. 2005;571(1-2):19-31.

(18.) Sage E, Girard PM, Francesconi S. Unravelling UVA-induced mutagenesis. Photochem Photobiol Sci. 2012;11(1):74-80.

(19.) Kim SI, Jin SG, Pfeifer GP. Formation of cyclobutane pyrimidine dimers at dipyrimidines containing 5-hydroxymethylcytosine. Photochem Photobiol Sci. 2013;12(8):1409-15.

(20.) Park J, Halliday GM, Surjana D, et al. Nicotinamide prevents ultraviolet radiation-induced cellular energy loss. Photochem Photobiol. 2010;86(4):942-8.

(21.) Surjana D, Halliday GM, Damian DL. Nicotinamide enhances repair of ultraviolet radiation-induced DNA damage in human keratinocytes and ex vivo skin. Carcinogenesis. 2013;34(5): 1144-9.

(22.) Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention. N Engl J Med. 2015;373(17):1618-26.

(23.) Cardile V, Frasca G, Rizza L, et al. Antiinflammatory effects of a red orange extract in human keratinocytes treated with interferon-gamma and histamine. PhytotherRes. 2010;24(3): 414-8.

(24.) Cimino F, Cristani M, Saija A, et al. Protective effects of a red orange extract on UVB-induced damage in human keratinocytes. Biofactors. 2007;30(2):129-38.

(25.) Frasca G, Panico AM, Bonina F, et al. Involvement of inducible nitric oxide synthase and cyclooxygenase-2 in the anti-inflammatory effects of a red orange extract in human chondrocytes. Nat Prod Res. 2010;24(15):1469-80.

(26.) Saija A, Tomaino A, Lo Cascio R, et al. In vitro antioxidant activity and in vivo photoprotective effect of a red orange extract. Int J Cosmet Sci. 1998;20(6):331-42.

(27.) Bonina F, Puglia C. Effect of the supplementation with Red Orange Complex[R] on ultraviolet-induced skin damage in human volunteers. Italy: BIONAP Report.

(28.) Calzavara-Pinton P, Ortel B, Venturini M. Non-melanoma skin cancer, sun exposure and sun protection. G Ital Dermatol Venereol. 2015;150(4):369-78.

(29.) Tornaletti S, Pfeifer GP. Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer. Science. 1994;263(5152):1436-8.

(30.) Ha G-H, Breuer E-KY. Mitotic Kinases and p53 Signaling. Biochemistry Research International. 2012;2012:14.

(31.) Boiteux S, Jinks-Robertson S. DNA repair mechanisms and the bypass of DNA damage in Saccharomyces cerevisiae. Genetics. 2013;193(4):1025-64.

(32.) Rastogi RP, Richa, Kumar A, et al. Molecular mechanisms of ultraviolet radiation-induced DNA damage and repair. J Nucleic Acids. 2010;2010:592-980.
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Author:Downey, Michael
Publication:Life Extension
Article Type:Report
Date:Jul 1, 2018
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