Rovectin Barrier Repair Complex (RBC)™

Expertly Formulated to Repair Skin Barrier Dysfunction

Dry, cracked and irritated skin is caused by a weakened skin barrier. Even the most healthy skin barrier can break down due to environmental stress, hormonal changes, nutritional deficiencies, common cleansers, illness and age. [1,2]. When the skin barrier weakens, irritants easily penetrate your skin and lead to uncomfortable and embarrassing skin disorders like Atopic Dermatitis (Eczema)[1,3]. A broken skin barrier results in severe dryness, cracking, redness, itching and inflammation.

Trans-Epidermal Water Loss (TEWL) & Free Radical Activity

A weak skin barrier can’t hold in essential moisture. This results in what scientists refer to as trans-epidermal water loss (TEWL). Excessive TEWL leads to a compromised skin barrier that is more porous, allowing irritating compounds to penetrate your skin. The result is red, itchy, dry, sensitized skin. Another problem is that the inflammatory cascade that occurs in sensitive skin leads to free radical activity. Free radicals encourage your body’s own enzymes to break down precious collagen and elastin. This leads to wrinkles, sagging and slackened skin. Even if you are not bothered by painfully dry skin, it’s important to maintain a healthy skin barrier so you can prevent signs of premature aging like wrinkles.

Protective Lipids

A weak skin barrier lacks protective lipids, or fats. These protective lipids are known specifically as ceramides, fatty acids, cholesterol, cholesteryl esters and phospholipids. Dermatologists report dramatic healing of dry skin disorders through topical application of lipids to the skin. [1,4,5]. RBC™ was designed base on this technology.

RBC™ replenishes lost lipids in your skin using bio-identical, natural, plant-derived ingredients. These ingredients are structurally identical to the healthy fats in your skin. This reduces moisture loss (TEWL) and strengthens your skin barrier. BRC™ is made with Linoleic Acid, Beta Sitosterol, and 97% pure Phospholipids. This nourishing blend helps replace essential lipids, encouraging a strong and healthy skin barrier free from redness, itching, dryness or premature wrinkles.

Because RBC™ is so effective at restoring your skin barrier, it does more than just restore lost moisture. It’s also effective for protecting your skin from damaging and irritating toxins. This prevents allergic, inflammatory reactions to environmental elements, also known as eczema or atopic dermatitis.

Source: Data on file, ROVECTIN Laboratories 2012; Lampe MA, Burlingame AL, Whitney J, et al. Human stratum corneum lipids: Characterization and regional differences.

Rovectin Barrier Repair Complex (RBC)™ Clinical Data

Rovectin Barrier Repair Complex™ Clinical Data
Decreases Trans-Epidermal Water Loss, even ceasing product usage after 6 weeks, meaning Rovectin BRC™ strengthens skin’s natural power to hold moisture

Reference

1. Berra, B., Veggetti, E., The Role of Epidermal Ceramides in Barrier Function, J. Applied Cosmetol. 14, pp. 51-57 (a/j96)
2. Ghadially, R., Brown, B. E., et al., The aged Epidermal Permeability Barrier: Structural, Functional, and Lipid Biochemical Abnormalities in Humans and a Senescent Murine Model, J Clin Invest., Volume 95(5), May 1995, pp. 2281-90.
3. Imokawa, G., Yada, Y., et al., Pseudo-acylceramide with Linoleic Acid Produces Selective Recovery of Cutaneous Barrier Function in Essential Fatty Acid- deficient Rats and has an Inhibitory Effect on Epidermal Hyperplasia, J. Clin Invest., Volume 94(1). July 1994, pp. 89-96.
4. Man, M., et al., Exogenous Lipids Influence Permeability Barrier Recovery in Acetone-treated Murine Skin, Arch, Dermatol. Vol 129(June 93), pp. 728-38.
5. Thornfeldt, C., et al., Optimization of Physiological Lipid Mixtures for Barrier Repair, J. Invest. Dermatol., Vol 106, pp. 1096-101, 1996.

Rovectin Anti-irritant Technology- Asta Cell Fortifier™

UV rays, pollution and even stress all cause oxidation, damaging your skin barrier over time. Asta Cell Fortifier™ (ACF) is rich in Astaxanthin, a powerful antioxidant extracted from microalgae that is naturally bright orange in color. Astaxanthin neutralizes reactive oxygen species (ROS), preventing the enzymatic breakdown of collagen and hyaluronic acid that leads to premature aging.

What are Free Radicals?
Free radicals are unpaired (free) electrons. They desperately search for another electron to pair with, and end up stealing electrons from the lipids in your skin. This creates a domino effect, and eventually damages your cell membranes, mitochondria and cellular DNA. This cascade damages precious skin lipids and weakens your skin barrier.

Powerful Antioxidant Astaxanthin
A potent antioxidant, Astaxanthin inhibits ROS to preserve your healthy skin barrier.

Astaxanthin facts:
• Antioxidant activity is 550 times stronger than Vitamin E
• Antioxidant activity is 550 times stronger than Green tea (catechin)
• Antioxidant activity is 850 times stronger than Coenzyme Q10
• Antioxidant activity is 6,000 times stronger than Vitamin C

Rovectin Anti-irritant Technology- Asta Cell Fortifier™ Clinical Data

Astaxanthin Cell Protection
Astaxanthin protected fibroblasts from damage by singlet oxygen

*Study Method: Human fibroblasts** were pre-incubated with Astaxanthin and then exposed to singlet oxygen. Protection was evaluated by cell viability by MTT method.
**Fibroblasts: Cells that constitute dermis and produce collagen and hyaluronic acid.

Age Spot Treatment
The age spot visibly reduced after 8 weeks treatment

*Study Method: 29 Healthy female subjects applied Astaxanthin topical product for 8 weeks. Comparison of age spots between 0 and 8 weeks were determined by image analysis.

Astaxanthin Repairs Wrinkles (By Analysis Methods with Replicas)
Wrinkle topography of the subject’s crow’s feet was evaluated with replica by image analysis before and after treatment

Reference:

1. Tominaga et al., (2009). Cosmetic effects of astaxanthin for all layers of skin. Food Style 21, 13(10):25-29.
2. Tominaga et al., (2009). Protective effects of astaxanthin against singlet oxygen induced damage in human dermal fibroblasts in-vitro. Food Style 21, 13(1):84-86.
3. Cui Hang; Kong Yahui; Zhang Hong (2011). "Oxidative Stress, Mitochondrial Dysfunction, and Aging”
4. Further Reading
5. Camera et al., (2009). Astaxanthin, canthaxanthin and ß-carotene differently affect UVA-induced oxidative damage and expression of oxidative stress-responsive enzymes. Exp Dermatol., 18(3):222-231.
6. Nishida et al., (2007). Quenching activities of common hydrophilic and lipophilic antioxidants against singlet oxygen using chemiluminescence detection system. Carotenoid Sci., 11:16-20.
7. Yamashita (2006). The effects of a dietary supplement containing astaxanthin on skin condition. Carotenoid Sci., 10:91-95.
8. Lee et al., (2003). Astaxanthin inhibits nitric oxide production and inflammatory gene expression by suppressing IκB Kinase-dependent NF-κB activation. Molecules and Cells, 16(1):97-105.
9. Arakane (2002). Superior skin protection via astaxanthin. Carotenoid Sci., 5:21-24.
10. Lyons & O’Brien (2002). Modulatory effects of an algal extract containing astaxanthin on UVA-irradiated cells in culture. J. Derma. Sci., 30(1):73-84.
11. Yamashita (2002). Cosmetic benefit of the supplement health food combined astaxanthin and tocotrienol on human skin. Food Style 21, 6(6):112-117.
12. Seki et al., (2001). Effects of astaxanthin from Haematococcus pluvialis on human skin. Fragrance J., 12:98-103.
13. Black (1998). Radical Interception by carotenoids and effects on UV carcinogenesis. Nutrition Cancer., 31(3):212-217.
14. O’Connor & O’Brien (1998). Modulation of UVA light induced oxidative stress by beta-carotene, lutein and astaxanthin in cultured fibroblasts. J. Derma. Sci., 16(3):226-230.
15. Savoure et al., (1995). Vitamin A status and metabolism of cutaneous polyamines in the hairless mouse after UV irradiation: action of beta-carotene and astaxanthin. Int. J. Vit. and Nutr. Res., 65(2):79-86.
16. Yamashita (1995). Suppression of post UVB hyperpigmentation by topical astaxanthin from krill. Fragrance J., 14:180-185.