| HLB explained in detail. The linked book in pdf is an excellent explanation of the HLB system. SEA has created an online HLB calculator that will allow a DIY or other to easily and rapidly calculate the HLB for their system as well as create their own emulsifier suitable to their purpose. |
Sunday, September 30, 2012
HLB Calculator
Friday, September 21, 2012
Skin Lightening: Of Natural Derivation
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To beautify the skin, i.e. reduce evidence of age spots, darkened areas of pigmentation, is of great concern to many. An even skin tone is considered by most cultures to be beautiful. How to safely achieve even skin tone for sun damaged skin is more difficult. Skin beauty is a personal journey and the stigma attached to skin lightening is often not considered. The experts on what constitute beautiful skin are the ones in the mirror's reflection. Healthy skin, is generally considered to be even in tone, of smooth texture, unlined and without acne. Many of the natural skin lightening ingredients also contain cross over action in other mechanism due to the complexity of the chemical composition inherent to several of the known plant extract lighteners. While they are effective at skin lightening, they remain effective antioxidants. Whether dark skinned or light skinned, even skin tone remains a desirable aspect of beauty. While many wish to lighten their skin tone, others are trying to go darker. That which constitutes beauty, lies in the eyes of the beholder, even if that remains the self.
As the end user of any lotion, milk , serum, cream, it is the individual experience that determines the efficacy or not thereof. DIY / homemade lotions, bath body wash and serums are made with the goal to lighten the skin, in hopes that pigment will disappear or old age spots likewise. Can this be done safely and without irritation or allergic reactions? Drugstores and big name labels sell lotions that claim to lighten the skin, however the concentrations of the active components are unknown. They may also be in a base that causes allergic reaction, where as the active itself may not. Some actives are inherently unstable, and by the time they reach the consumer, they are of little use. Safest and most effective are not necessarily mutually exclusive when it comes to skin lightening. Safest generally requires longer treatment time.
To improve the efficacy of a skin whitening treatment or regime, it is prudent not to play games with chemicals that are proven to cause permanent damage when it can readily be avoided. Several plant extracts contain effective chemicals for lightening pigmentation and the research has greatly refined the understanding of the mechanisms of action over the years. It remains prudent to keep in mind that not each individual will have the same success,. It would be nice to guarantee the efficacy of a product however far too many variables come into play. The type of oil used to make a homemade/ DIY lotion due to the palmitic acid content can undo the positive effect of the lightening chemical component/ extract. As the consumer knowledge base continues to increase, producers are forced to meet the demand. Unfortunately due to restrictions in various jurisdictions for health and safety concerns, truly effective formulas are not necessarily readily available.
Understanding the pigmentation pathway as currently known is useful prior to examining the various skin-lightening compounds and the assosciated mechanisms of action. Skin color is determined by both the type and quantity of melanin synthesized by the melanocyte and its distribution pattern in the epidermis. The formation of melanin is through a series of oxidative reactions involving the amino acid tyrosine and the enzyme tyrosinase.
Most critical is the first reaction as the reaction sequence that follows proceeds spontaneously at physiological pH. At this point in the sequence, tyrosinase converts tyrosine to dihydroxyphenylalanine (DOPA) and subsequently to dopaquinone. Thereafter, dopaquinone is converted to dopachrome through auto-oxidation, and, finally, to dihydroxyindole or dihydroxyindole-2-carboxylic acid (DHICA) to form eumelanin (black-brown pigment= darken the skin). The latter reaction occurs in the presence of dopachrome tautomerase and DHICA oxidase. In the presence of cysteine or glutathione, dopaquinone is converted to cysteinyl DOPA or glutathione DOPA. The latter results in the formation of pheomelanin, a yellow-red pigment. ( influences skin tone )
Tyrosinase regulates melanin synthesis in melanocytic cells. It is a membrane-bound copper containing glycoprotein, and the critical rate-limiting enzyme of melanin production. Tyrosinase is produced only by melanocytic cells, post its synthesis it is further processed in the ER and Golgi. After processing it is transported to melanosomes, where the pigment is synthesized and deposited. Melanosomes are transferred from melanocytes to neighboring keratinocytes and are distributed in the skin and hair to produce visible color. An excess of melanin or abnormal distribution can cause irregular pigementation and hyperpigmentation of the skin. Developing effective therapies to treat disorders of pigementation, disruption of tyrosinase activity is the usual target. Several approaches exist to decreases tyrosinase activity i.e. competitive or non-competitive inhibition of tyrosinase catalytic activity, disruption of tyrosinase maturation or by reduce its stability. Manipulation of tyrosinase levels include modulating of tyrosinase messenger RNA (mRNA) transcription and its post-transcriptional stability or reducing its potential for synthesis at the gene expression level.
Before treating hyperigmentation the etiology must first be elucidated. It is not always clear as there are many factors that influence hyperpigmentation: 1) photo sensitizing agents, 2) hormone imbalance, 3) UV exposure, 4) Systemic disease, 5) drug interactions. etc.
Hydroquinone:
A variety of topical treatments have been developed and some with exceptional effect. The current Gold Standard is the use of Hydroquinone (HQ) . HQ is considered to be one of the most effective in vivo and in vitro inhbitors of melanogensis which causes a reversible inhibition by affecting both DNA and RNA synthesis. The unfortunate aspect is that while it is effective at inhibiting melanocytes it remains cytotoxic to the surrounding cellular structures and leads to degeneration of both collagen and elastin fibers. Inappropriate usage may lead to darkening of the skin. Care must be taken when using potent lightening agents.
Tyrosinase Inhibitors:
There are a variety of effective inhibitors however they are not true inhibitors of tryosinase, rather they act to interfere with the production of melanin. L ascorbic acid is one such molecule. It acts to to reduce o-dopaquinone to dopa, avoiding dopachrome and melanin formation. AA2G is also shown to be particularly effective for those that cannot tolerate the low pH requirement of LAA.
Phenolic compounds are another broad category of which many have been isolated and found to be effective. These enzyme substrates show good affinity for the binding site on tyrosinase and result in a reduction in the formation of dopachrome. Some act as cheltors of copper which also acts to inhibit enzymatic activity via destabilization of tyrosinase.
Acids or bases also act as inactivators of tyrosinase. These act to denature the enzyme, leaving it non functional and as such, inhibit activity.
Suicide substrates are another class of inhibitors and more correctly true inhibitors. These act to bind tyrosinase irreversibly. These inhibitors are catalyzed by tyrosinase forming covalent bonds and inducing the enzyme catalyzing "suicide reaction."
True inhibitors are of four types. 1) competitive inhibitors, 2) noncompetitive inhibitors, 3) mixed (competitive/non-competitive) inhibitors, and 4) non-competitive inhibitors.
1. Competitive inhibitor: a substance that combines with a free enzyme in a manner that prevents substrate binding. That is, the inhibitor and the substrate are mutually exclusive, often because of true competition for the same site.
2. Non competitive inhibitors: can bind only to the enzyme-substrate complex.
3. Mixed (Competitive/ Non competitive) inhibitors: can bind with a free enzyme and with the enzyme-substrate complex.
4. Non-competitive inhibitors: bind to a free enzyme and an enzyme-substrate complex with the same equilibrium constant.
The science of skin lightening/ depigmentation is growing as each year more compounds are isolated and their mechanism of effect studied. As knowledge of melanocyte biology and underlying processes of melanin synthesis are understood, new approaches to the treatment of skin hyperpigmentation become available. Not only is tyrosinase inhibition of catalytic activity an option, other alternatives include: 1) inhibition of tyrosinase mRNA transcription, 2) aberration of tyrosinase glycosylation and maturation, 3) acceleration of tyrosinase degradation, 4) interference with melanosome maturation and transfer, 5) inhibition of inflammation-induced melanogenic response, and 6) acceleration of skin turnover.
Kojic acid is one of the most commonly used depigmenting agents and a natural agent with few side effects. It is well tolerated by most but skin sensitivity can occur in some individuals and the potential for irritation increase with the concentration. Kojic acid is a fungal metabolite produced by many species of Aspergillus, Acetobacter, and Penicillium. It is know to act as a competitive and reversible inhibitor of tyrosinase which catalyzes the conversion of tyrosine to melanin via 3,4-dihydroxyphenylalanine and dopaquinone. Kojic acid remains the standard against which new de- pigementing agents are measured. As it is a completely natural product its popularity has grown, albeit it is not the most effective.
Arbutin (ß) ( Uva Ursi and bearberry extract, hydroquinone-beta-D-glucopyranoside) is a botanical extract in which the active component hydrolyzes readily into hydroquinone. Researchers shows it inhibits the oxidation of L-DOPA catalysed by mushroom tyrosinase and is effective in the topical treatment of various cutaneous hyperpigmentations characterized by hyperactive melanocyte function. A another study indicated that arbutin inhibits melanin synthesis by inhibition of tyrosinase activity apparently due to the inhibition of melanosomal tyrosinase activity rather than the suppression of this enzyme’s synthesis and expression. Arbutin itself is oxidized at an extremely slow rate, but accelerates when dihydroxyphenylalanine (L-DOPA) becomes available as co factor.
Morus alba, Mulberry extract is a composite of polyphenols which have shown to have 32 fold the inhibitory activity of Kojic acid. It acts non-competitively on both monophenolase and diphenolase activity of mushroom tyrosinase. The inhibtion mechanism of the compound directly inhibits enzyme activity but does not affect gene expression. Aside from its more potent effect than Kojic acid for melanin inhibition, Morus alba extract has also shown superoxide scavenging activity.
Licorice extract, extracts from the roots and seeds of Glycyrrhiza species are commonly used in Asia as a lightening compound. Glabridin and glabrene are the two components of Licorice extract that act in a non competitive manner to inhibit melanogenesis. Glabridine has 15 times the activity of kojic acid and exhibited higher depigmenting activity than arbutin. Glycyrrhizic acid another compound within Morus alba is renowned for it's anti inflammatory and anti oxidant effects.
Raspberry ketone from Rheum officinale, one of the major aromatic compounds of raspberry, is widely used in perfumery, cosmetics, and as a flavoring agent in foodstuffs has shown strong inhibitory effects. Currently it is marketed primarily as a weight loss aid, however it is also known for anti-androgenic activity and anti inflammatory activity. It has also been shown to be an extremely potent tyrosinase inhibitor on par with hydroquinone. The exact mechanism is not completely understood however it is suggested that RK inhibits melanogenesis through a post-transcriptional regulation of tyrosinase gene expression, which results in down regulation of both cellular tyrosinase activity and the amount of tyrosinase protein, while the level of tyrosinase mRNA transcription is not affected. Rk hold particular promise as it is a safe compound and effective on mammalian tyrosinase. RK is also multifunctional as in other research it has shown to reduce the signs of dermal laxity and exhibits some promise in hair loss reduction.
Each compound has quantifiable capacity to affect melanogenesis via specific mechanisms. None are permanent. The complete eradication of pigment from the skin remains dangerous. Melanin is the first line of defense from the ravages of UV damage. When using lightening compounds one must also use a high SPF sunscreen. Sensible precautions must be employed. Endangering one's health for the sake of change of skin color is not worth the long term side effects. When using any homemade creams or lotions, test for sensitivity and observe the reactions. Adjust accordingly or discontinue if necessary.
1. Ando, H.; Kondoh, H.; Ichihashi, M.; Hearing, V.J. Approaches to identify inhibitors of melanin biosynthesis via the quality control of tyrosinase. J. Invest. Dermatol 2007, 127, 751-761.
2. Briganti, S.; Camera, E.; Picardo, M. Chemical and instrumental approaches to treat hyperpigmentation. Pigment Cell Res 2003, 16, 101-110.
3. Draelos, Z.D. Skin lightening preparations and the hydroquinone controversy. Dermatol. Ther 2007, 20, 308-313.
4. Halaban, R.; Patton, R.S.; Cheng, E.; Svedine, S.; Trombetta, E.S.; Wahl, M.L.; Ariyan, S.; Hebert, D.N. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway. J. Biol. Chem 2002, 277, 14821-14828.
5. Harada N, Okajima K, Narimatsu N, Kurihara H, Nakagata N. Effect of topical application of raspberry ketone on dermal production of insulin-like growth factor-I in mice and on hair growth and skin elasticity in humans. Growth Horm IGF Res. 2008 Aug;18(4):335-44
6. Kim, Y.M.; Yun, J.; Lee, C.K.; Lee, H.; Min, K.R.; Kim, Y. Oxyresveratrol and hydroxystilbene compounds. Inhibitory effect on tyrosinase and mechanism of action. J. Biol. Chem 2002, 277, 16340-16344
7. Parvez, S.; Kang, M.; Chung, H.S.; Cho, C.; Hong, M.C.; Shin, M.K.; Bae, H. Survey and mechanism of skin depigmenting and lightening agents. Phytother. Res 2006, 20, 921-934.
8. Rendon, M.I.; Gaviria, J.I. Review of skin-lightening agents. Dermatol. Surg 2005, 31, 886-889.
9. Sang Hee LEE,a Sang Yoon CHOI,a Hocheol KIM,a Jae Sung HWANG,b Byeong Gon LEE,b
Jian Jun GAO,c and Sun Yeou KIM, Mulberroside F Isolated from the Leaves of Morus alba Inhibits Melanin Biosynthesis. Biol. Pharm. Bull. 2002 25(8) 1045—1048
10. Solano, F.; Briganti, S.; Picardo, M.; Ghanem, G. Hypopigmenting agents: an updated review on biological, chemical and clinical aspects. Pigment Cell Res 2006, 19, 550-571.
11. Victor Chia-Hsiang Lin , Hsiou-Yu Ding , Shiou-Yi Kuo , Ling-Wei Chin , Jiumn-Yih Wu
and Te-Sheng Chang , Evaluation of in Vitro and in Vivo Depigmenting Activity of Raspberry Ketone from Rheum officinale. Int. J. Mol. Sci. 2011, 12, 4819-4835;
12. Wang, N.; Hebert, D.N. Tyrosinase maturation through the mammalian secretory pathway: bringing color to life. Pigment Cell Res 2006, 19, 3-18.
13. Zhu, W.; Gao, J. The use of botanical extracts as topical skin-lightening agents for the improvement of skin pigmentation disorders. J. Investig. Dermatol. Symp. Proc 2008, 13, 20-24.
Skin lightening, de pigmentation of the skin is of growing interest
amongst the aging population as well as those choosing to lighten their
skin for cosmetic or cultural reasons. In some countries there remains a
stigma attached if a person is known to be actively lightening their
skin. Skin lightening / whitening may utilize ingredients with various
associated hazards when used inappropriately, while others have a less
toxic effect. Skin lightening, naturally has been explored to varying
degrees of success. Many choose to DIY skin lightening lotions, body
wash, creams, due to the cost as well as the fear of steroids
potentially being included. Lemon juice, lime juice, citric acid and
various other components are used as a simple and moderately effective
methods to lighten the skin. People around the globe of many ethnicity
are looking to lighten skin for personal reasons. Hyper pigmentation due
to UV exposure over a life time has become a common theme. Do It
Yourself methods meet with varying degrees of success. Not all skin
lightening products are created equal, nor do they work along the same
mechanisms. Some are next to useless. To whiten or bleach the skin is
not a simple matter, nor is it permanent. Effective treatment requires
several months before the effects are noticed and are quickly lost due
to sun exposure. Maintaining a consistent regime will play an important
role in the efficacy of any treatment, whether you make it yourself or
purchase from a drugstore.
To beautify the skin, i.e. reduce evidence of age spots, darkened areas of pigmentation, is of great concern to many. An even skin tone is considered by most cultures to be beautiful. How to safely achieve even skin tone for sun damaged skin is more difficult. Skin beauty is a personal journey and the stigma attached to skin lightening is often not considered. The experts on what constitute beautiful skin are the ones in the mirror's reflection. Healthy skin, is generally considered to be even in tone, of smooth texture, unlined and without acne. Many of the natural skin lightening ingredients also contain cross over action in other mechanism due to the complexity of the chemical composition inherent to several of the known plant extract lighteners. While they are effective at skin lightening, they remain effective antioxidants. Whether dark skinned or light skinned, even skin tone remains a desirable aspect of beauty. While many wish to lighten their skin tone, others are trying to go darker. That which constitutes beauty, lies in the eyes of the beholder, even if that remains the self.
As the end user of any lotion, milk , serum, cream, it is the individual experience that determines the efficacy or not thereof. DIY / homemade lotions, bath body wash and serums are made with the goal to lighten the skin, in hopes that pigment will disappear or old age spots likewise. Can this be done safely and without irritation or allergic reactions? Drugstores and big name labels sell lotions that claim to lighten the skin, however the concentrations of the active components are unknown. They may also be in a base that causes allergic reaction, where as the active itself may not. Some actives are inherently unstable, and by the time they reach the consumer, they are of little use. Safest and most effective are not necessarily mutually exclusive when it comes to skin lightening. Safest generally requires longer treatment time.
To improve the efficacy of a skin whitening treatment or regime, it is prudent not to play games with chemicals that are proven to cause permanent damage when it can readily be avoided. Several plant extracts contain effective chemicals for lightening pigmentation and the research has greatly refined the understanding of the mechanisms of action over the years. It remains prudent to keep in mind that not each individual will have the same success,. It would be nice to guarantee the efficacy of a product however far too many variables come into play. The type of oil used to make a homemade/ DIY lotion due to the palmitic acid content can undo the positive effect of the lightening chemical component/ extract. As the consumer knowledge base continues to increase, producers are forced to meet the demand. Unfortunately due to restrictions in various jurisdictions for health and safety concerns, truly effective formulas are not necessarily readily available.
Understanding the pigmentation pathway as currently known is useful prior to examining the various skin-lightening compounds and the assosciated mechanisms of action. Skin color is determined by both the type and quantity of melanin synthesized by the melanocyte and its distribution pattern in the epidermis. The formation of melanin is through a series of oxidative reactions involving the amino acid tyrosine and the enzyme tyrosinase.
Most critical is the first reaction as the reaction sequence that follows proceeds spontaneously at physiological pH. At this point in the sequence, tyrosinase converts tyrosine to dihydroxyphenylalanine (DOPA) and subsequently to dopaquinone. Thereafter, dopaquinone is converted to dopachrome through auto-oxidation, and, finally, to dihydroxyindole or dihydroxyindole-2-carboxylic acid (DHICA) to form eumelanin (black-brown pigment= darken the skin). The latter reaction occurs in the presence of dopachrome tautomerase and DHICA oxidase. In the presence of cysteine or glutathione, dopaquinone is converted to cysteinyl DOPA or glutathione DOPA. The latter results in the formation of pheomelanin, a yellow-red pigment. ( influences skin tone )
Tyrosinase regulates melanin synthesis in melanocytic cells. It is a membrane-bound copper containing glycoprotein, and the critical rate-limiting enzyme of melanin production. Tyrosinase is produced only by melanocytic cells, post its synthesis it is further processed in the ER and Golgi. After processing it is transported to melanosomes, where the pigment is synthesized and deposited. Melanosomes are transferred from melanocytes to neighboring keratinocytes and are distributed in the skin and hair to produce visible color. An excess of melanin or abnormal distribution can cause irregular pigementation and hyperpigmentation of the skin. Developing effective therapies to treat disorders of pigementation, disruption of tyrosinase activity is the usual target. Several approaches exist to decreases tyrosinase activity i.e. competitive or non-competitive inhibition of tyrosinase catalytic activity, disruption of tyrosinase maturation or by reduce its stability. Manipulation of tyrosinase levels include modulating of tyrosinase messenger RNA (mRNA) transcription and its post-transcriptional stability or reducing its potential for synthesis at the gene expression level.
Before treating hyperigmentation the etiology must first be elucidated. It is not always clear as there are many factors that influence hyperpigmentation: 1) photo sensitizing agents, 2) hormone imbalance, 3) UV exposure, 4) Systemic disease, 5) drug interactions. etc.
Hydroquinone:
A variety of topical treatments have been developed and some with exceptional effect. The current Gold Standard is the use of Hydroquinone (HQ) . HQ is considered to be one of the most effective in vivo and in vitro inhbitors of melanogensis which causes a reversible inhibition by affecting both DNA and RNA synthesis. The unfortunate aspect is that while it is effective at inhibiting melanocytes it remains cytotoxic to the surrounding cellular structures and leads to degeneration of both collagen and elastin fibers. Inappropriate usage may lead to darkening of the skin. Care must be taken when using potent lightening agents.
Tyrosinase Inhibitors:
There are a variety of effective inhibitors however they are not true inhibitors of tryosinase, rather they act to interfere with the production of melanin. L ascorbic acid is one such molecule. It acts to to reduce o-dopaquinone to dopa, avoiding dopachrome and melanin formation. AA2G is also shown to be particularly effective for those that cannot tolerate the low pH requirement of LAA.
Phenolic compounds are another broad category of which many have been isolated and found to be effective. These enzyme substrates show good affinity for the binding site on tyrosinase and result in a reduction in the formation of dopachrome. Some act as cheltors of copper which also acts to inhibit enzymatic activity via destabilization of tyrosinase.
Acids or bases also act as inactivators of tyrosinase. These act to denature the enzyme, leaving it non functional and as such, inhibit activity.
Suicide substrates are another class of inhibitors and more correctly true inhibitors. These act to bind tyrosinase irreversibly. These inhibitors are catalyzed by tyrosinase forming covalent bonds and inducing the enzyme catalyzing "suicide reaction."
True inhibitors are of four types. 1) competitive inhibitors, 2) noncompetitive inhibitors, 3) mixed (competitive/non-competitive) inhibitors, and 4) non-competitive inhibitors.
1. Competitive inhibitor: a substance that combines with a free enzyme in a manner that prevents substrate binding. That is, the inhibitor and the substrate are mutually exclusive, often because of true competition for the same site.
2. Non competitive inhibitors: can bind only to the enzyme-substrate complex.
3. Mixed (Competitive/ Non competitive) inhibitors: can bind with a free enzyme and with the enzyme-substrate complex.
4. Non-competitive inhibitors: bind to a free enzyme and an enzyme-substrate complex with the same equilibrium constant.
The science of skin lightening/ depigmentation is growing as each year more compounds are isolated and their mechanism of effect studied. As knowledge of melanocyte biology and underlying processes of melanin synthesis are understood, new approaches to the treatment of skin hyperpigmentation become available. Not only is tyrosinase inhibition of catalytic activity an option, other alternatives include: 1) inhibition of tyrosinase mRNA transcription, 2) aberration of tyrosinase glycosylation and maturation, 3) acceleration of tyrosinase degradation, 4) interference with melanosome maturation and transfer, 5) inhibition of inflammation-induced melanogenic response, and 6) acceleration of skin turnover.
Kojic acid is one of the most commonly used depigmenting agents and a natural agent with few side effects. It is well tolerated by most but skin sensitivity can occur in some individuals and the potential for irritation increase with the concentration. Kojic acid is a fungal metabolite produced by many species of Aspergillus, Acetobacter, and Penicillium. It is know to act as a competitive and reversible inhibitor of tyrosinase which catalyzes the conversion of tyrosine to melanin via 3,4-dihydroxyphenylalanine and dopaquinone. Kojic acid remains the standard against which new de- pigementing agents are measured. As it is a completely natural product its popularity has grown, albeit it is not the most effective.
Arbutin (ß) ( Uva Ursi and bearberry extract, hydroquinone-beta-D-glucopyranoside) is a botanical extract in which the active component hydrolyzes readily into hydroquinone. Researchers shows it inhibits the oxidation of L-DOPA catalysed by mushroom tyrosinase and is effective in the topical treatment of various cutaneous hyperpigmentations characterized by hyperactive melanocyte function. A another study indicated that arbutin inhibits melanin synthesis by inhibition of tyrosinase activity apparently due to the inhibition of melanosomal tyrosinase activity rather than the suppression of this enzyme’s synthesis and expression. Arbutin itself is oxidized at an extremely slow rate, but accelerates when dihydroxyphenylalanine (L-DOPA) becomes available as co factor.
Morus alba, Mulberry extract is a composite of polyphenols which have shown to have 32 fold the inhibitory activity of Kojic acid. It acts non-competitively on both monophenolase and diphenolase activity of mushroom tyrosinase. The inhibtion mechanism of the compound directly inhibits enzyme activity but does not affect gene expression. Aside from its more potent effect than Kojic acid for melanin inhibition, Morus alba extract has also shown superoxide scavenging activity.
Licorice extract, extracts from the roots and seeds of Glycyrrhiza species are commonly used in Asia as a lightening compound. Glabridin and glabrene are the two components of Licorice extract that act in a non competitive manner to inhibit melanogenesis. Glabridine has 15 times the activity of kojic acid and exhibited higher depigmenting activity than arbutin. Glycyrrhizic acid another compound within Morus alba is renowned for it's anti inflammatory and anti oxidant effects.
Raspberry ketone from Rheum officinale, one of the major aromatic compounds of raspberry, is widely used in perfumery, cosmetics, and as a flavoring agent in foodstuffs has shown strong inhibitory effects. Currently it is marketed primarily as a weight loss aid, however it is also known for anti-androgenic activity and anti inflammatory activity. It has also been shown to be an extremely potent tyrosinase inhibitor on par with hydroquinone. The exact mechanism is not completely understood however it is suggested that RK inhibits melanogenesis through a post-transcriptional regulation of tyrosinase gene expression, which results in down regulation of both cellular tyrosinase activity and the amount of tyrosinase protein, while the level of tyrosinase mRNA transcription is not affected. Rk hold particular promise as it is a safe compound and effective on mammalian tyrosinase. RK is also multifunctional as in other research it has shown to reduce the signs of dermal laxity and exhibits some promise in hair loss reduction.
Each compound has quantifiable capacity to affect melanogenesis via specific mechanisms. None are permanent. The complete eradication of pigment from the skin remains dangerous. Melanin is the first line of defense from the ravages of UV damage. When using lightening compounds one must also use a high SPF sunscreen. Sensible precautions must be employed. Endangering one's health for the sake of change of skin color is not worth the long term side effects. When using any homemade creams or lotions, test for sensitivity and observe the reactions. Adjust accordingly or discontinue if necessary.
1. Ando, H.; Kondoh, H.; Ichihashi, M.; Hearing, V.J. Approaches to identify inhibitors of melanin biosynthesis via the quality control of tyrosinase. J. Invest. Dermatol 2007, 127, 751-761.
2. Briganti, S.; Camera, E.; Picardo, M. Chemical and instrumental approaches to treat hyperpigmentation. Pigment Cell Res 2003, 16, 101-110.
3. Draelos, Z.D. Skin lightening preparations and the hydroquinone controversy. Dermatol. Ther 2007, 20, 308-313.
4. Halaban, R.; Patton, R.S.; Cheng, E.; Svedine, S.; Trombetta, E.S.; Wahl, M.L.; Ariyan, S.; Hebert, D.N. Abnormal acidification of melanoma cells induces tyrosinase retention in the early secretory pathway. J. Biol. Chem 2002, 277, 14821-14828.
5. Harada N, Okajima K, Narimatsu N, Kurihara H, Nakagata N. Effect of topical application of raspberry ketone on dermal production of insulin-like growth factor-I in mice and on hair growth and skin elasticity in humans. Growth Horm IGF Res. 2008 Aug;18(4):335-44
6. Kim, Y.M.; Yun, J.; Lee, C.K.; Lee, H.; Min, K.R.; Kim, Y. Oxyresveratrol and hydroxystilbene compounds. Inhibitory effect on tyrosinase and mechanism of action. J. Biol. Chem 2002, 277, 16340-16344
7. Parvez, S.; Kang, M.; Chung, H.S.; Cho, C.; Hong, M.C.; Shin, M.K.; Bae, H. Survey and mechanism of skin depigmenting and lightening agents. Phytother. Res 2006, 20, 921-934.
8. Rendon, M.I.; Gaviria, J.I. Review of skin-lightening agents. Dermatol. Surg 2005, 31, 886-889.
9. Sang Hee LEE,a Sang Yoon CHOI,a Hocheol KIM,a Jae Sung HWANG,b Byeong Gon LEE,b
Jian Jun GAO,c and Sun Yeou KIM, Mulberroside F Isolated from the Leaves of Morus alba Inhibits Melanin Biosynthesis. Biol. Pharm. Bull. 2002 25(8) 1045—1048
10. Solano, F.; Briganti, S.; Picardo, M.; Ghanem, G. Hypopigmenting agents: an updated review on biological, chemical and clinical aspects. Pigment Cell Res 2006, 19, 550-571.
11. Victor Chia-Hsiang Lin , Hsiou-Yu Ding , Shiou-Yi Kuo , Ling-Wei Chin , Jiumn-Yih Wu
and Te-Sheng Chang , Evaluation of in Vitro and in Vivo Depigmenting Activity of Raspberry Ketone from Rheum officinale. Int. J. Mol. Sci. 2011, 12, 4819-4835;
12. Wang, N.; Hebert, D.N. Tyrosinase maturation through the mammalian secretory pathway: bringing color to life. Pigment Cell Res 2006, 19, 3-18.
13. Zhu, W.; Gao, J. The use of botanical extracts as topical skin-lightening agents for the improvement of skin pigmentation disorders. J. Investig. Dermatol. Symp. Proc 2008, 13, 20-24.
Sunday, September 16, 2012
Labeling Claims
Not much is more confusing to consumers than product claims regulations. Let's not mention how it may confuse some formulators.
Questions with respect to the rules :
1. What level of proof is required?
2. What claims can be made and who decides?
3. What are the penalties for making a false claim?
4. Who/ what is responsible for regulating the claims?
Plenty of regulations are in place, however with the lack of enforcement behind them, it makes precious little difference. How does it occur ? Without uniform consistent enforcement, companies can claim to not be aware of which rules to follow or what they can legally state. As the regulations are not enforced, self regulation goes out the window while they chase their nearest competitor's latest wild claim.
Let's take a look at what actually goes into the product's ingredients list: Only INCI names are allowed on cosmetic product labels. That should not be a mystery. It's also what a DIY'er will exploit should they choose to. Due to the ball dropping act of lack of enforcement of the rules, companies are free to list all sorts of claims in their ingredient statements though. The tricky question at the end of the day, are consumers reading the ingredients or only the cosmetic chemists? Apparently both.
Of these horrific errors in labeling, purified water , deionized water, natural spring water, is the most common. Purified water is the drug name for water, as defined in the US Pharmacopoeia, and is reserved for use on the labels of drugs that do not make cosmetic claims. Calling water anything but water, is an infraction, but we see it all the time. Using 'vitamin' is another illegal advertising claim on cosmetic ingredient labels. And where have we seen that? Vitamins are categorized separately from cosmetic ingredients as they are not recognized as providing benefits in a cosmetic product according to the FDA. Oddly enough and with some strange lack of reason the FDA does not object to stating the product contains vitamins outside of the ingredient listing. ( if you do this does it make it outside? )
Terms like vegetable, natural, organic, or of even greater emotional impact,(*) certified organic, is another label marketing twisted trend that is intended to highlight the "natural" origins of ingredients. Some marketers further emphasize this delight by inserting an asterisk (*) within the ingredients list to call attention to materials in the product that are of this highly pedigreed origin. Whether of natural or synthetic origin, they are still chemicals.
Juice Beauty The Organic Solution.
Juice Beauty Stem Cellular Repair Booster Serum
Scientific Technology, Organic Innovation, Ultimate Results
An ultra-light gel serum power packed with an optimum dose of our proprietary blend of fruit stem cells and a potent dose of Vitamin C infused boosts the skin's ability to repair and renew cellular turnover. Formulated to enhance the performance of the Stem Cellular Repair Moisturizer by improving its ability to penetrate the skin and maximize the results at a cellular level to increase dermal firmness and eliminate deep wrinkles.
Those are some fancy claims based on this ingredients list for that bit of merchanise. And this list, is repleat with every marketing trick in the book, including those that ride the razor's edge of the rules. They make great use of images and stories of wonder about the organic ingredients, what they supposedly contain, the reality is quite different. If one were to quantify it, it would add up to subclinical levels.
Juice Beauty proprietary blend of fruit stem cells: apple buds, grape buds & lemon bark. Ingredients: Organic juices of pyrus malus (organic apple juice)*, vitis vinifera (organic white grape juice)*, citrus medica limonum (organic lemon juice)*, aloe barbadensis (organic aloe leaf juice)*, vegetable glycerin, organic plant oils of helianthus annus (organic sunflower seed oil)*, simmondsia chinensis (organic jojoba seed)*, butyrospermum parkii (organic shea butter)*, octyl palmitate, caprylic/capric triglyceride, glyceryl stearate, magnesium ascorbyl phosphate (Vitamin C), stearic acid, cetearyl alcohol, malus sylvestris (apple buds), vitis vinifera (grape buds) & citrus limonum (lemon bark), organic essential fatty acids of oenothera biennis (organic evening primrose oil)*, linum usitatissimum (organic linseed oil)*, borago officinalis (organic borage seed oil)*, xanthan gum, panthenol (Vitamin B5), allantoin, sodium hyaluronate (hyaluronic acid), tocopherol (Vitamin E), sodium benzoate, potassium sorbate, ethylhexylglycerin, citrus reticulata (mandarin), litsea cubeba (may chang) and cinnamomum camphora (ho wood) pure essential oils *certified organic by a USDA approved agency
Optimum does of Vitamin C for DNA repair. Prepares the skin for the Stem Cellular Repair Moisturizer.
And a new mechanism of DNA repair has arrived in the form of MAP. I do like MAP, but not for that reason.
There is no difference in chemicals from 'natural' or synthetic origins. Hyaluronic acid from which origin? It's found in animals, cocks combs and animal hooves is a primary source. Not popular. Call it bioengineered, bacterial production method, and all is well. Preferable to many. Glycerin shares the same strange story. (*) certified organic glycerin is chemcially no different, nor preferentially treated by the skin, than is synthetic. Albeit of the two, I will defineitly err on the side of the bioengineered HA.
Clinically Validated instrument measured Stem Cellular Repair Results
100% improved hydration
96% improved dark circles and puffiness around eyes
88% reduction in 3D visual analysis of fine lines and wrinkles
88% improved skin tone and luminosity
75% improved elasticity of the skin
Really? Where are these clinical validations? Non existent. Claim. Unfortunately, it seems that the "natural/ organic" crowd are the some of the worst offenders with regards to labels and claims. Much as I prefer natural, they give natural cosmetics a bad name. The list above includes several "non natural" and non organic ingredients, but call it all organic anyways. Doesn't matter, it sells. Don't forget "proprietary blend of fruit stem cells", perhaps they didn't want to go so far as labeling "Patent Pending" because there is nothing there. Utter bunk.
Slather On Your Vegetables
Juice Beauty, they seem to have nice products. It is only an example of what pops up in google with labeling and claims when hitting "true organic aging labels." Deep wrinkle eliminating? No.
The distinction between drugs and cosmetics is based principally by the promoted intent of effect of the product . If the claim suggests a product to have drug-like effects, that product will be regulated as a drug. This ruling based on intent is subjective as is more than clear by the outrageous claims that usher in the new latest and greatest actives and products. Drug vs. Cosmetic Claims in the USA, ought to keep the FDA busy for the next century.
"Elimination of Deep Wrinkles" ?? Would that not qualify? That's more of a plastic surgery claim. It's not explicitly covered in the FDA labeling requirements, and as is obvious, self regulation went out the proverbial window.
Cosmetics that are also Drugs
Products that are cosmetics but are also intended to treat or prevent disease, or otherwise affect the structure or functions of the human body, are considered also drugs and must comply with both the drug and cosmetic provisions of the law. Examples of products which are drugs as well as cosmetics are anticaries toothpastes (e.g., "fluoride" toothpastes), hormone creams, suntanning preparations intended to protect against sunburn, antiperspirants that are also deodorants, and antidandruff shampoos.
Most currently marketed cosmetics which are also drugs are over-the-counter drugs. Several are new drugs for which safety and effectiveness had to be proved to the agency before they could be marketed. A new drug is a drug which is not generally recognized by experts as safe and effective under the conditions of intended use or which has become so recognized but has not been used to a material extent or for a material time under such conditions.
To further complicate the matter, different jurisdictions allow different types of claims. Health Canada is known for being rather strict, but minimum they provide a list of what constitutes acceptable claims for cosmetics. The claims must be accurate, true and verifiable.
Guidelines for Cosmetic Advertising and Labeling Claims
The European Union takes this a step farther and states that a company must have proof of the effect claimed for the product. If claims exist the company then most also make available on the packaging an EU address that the Competent Authorities may contact in order to inspect evidence of the claims made. One would be erroneous in assuming that the competent authority is the consumer.
Cosmetic products (until 2013)
Proof of Claims is expensive, most companies prefer to make claims without doing the work or shouldering the cost. Cuts into the bottom line rather deeply. Unfortunately they rely almost solely upon the ingredient suppliers claims. The National Advertising Division of the Council of Better Business Bureaus, in the USA acts as big brother for all advertising claims. In theory they do not accept ingredient claims as a base for finished goods claims. But you would be forced to accept quite the contrary when reading the plethora of advertisements that are clearly in opposition . In the EU, ingredient suppliers’ claims are being accepted as long as the cosmetics company use the exact same ingredient at the exact same dosage in a formulation. In future, this is most unlikely, but who knows?
Reading through EU legalese is a migraine inducing activity. The FDA is light reading by comparison. Health Canada, simple. DIY, total freedom, where none of the above applies.
Saturday, September 15, 2012
Cosmetic Science : The Religion
Cosmetic science without biology is lame, biology without cosmetic science is useless.
Cosmetic science is supposedly at a point where it can identify the optimum ingredients that can help reverse the merciless hands of time. Not, really. Minimum, not cosmetic products as we see them marketed.
If you are just starting out or are unsure whether DIY skin care is for you, rest assured, it's not for many skin care companies either. You have to decide for yourself if your skin is important enough. Decided? Yes, my skin is important enough. Therefore, I agree that beauty is more than skin deep and that something to do with biology/ science is important. Education in the fundamental biological mechanisms is what it takes to stay at the forefront with every cosmetic formulation and personal care product. But what if you don't have a degree in science? Don't worry, most cosmetic scientists don't either! No college degree, no university degree is required! You have the same chance of success at creating the Fountain of Youth in a Cheap Plastic Bottle as they do. It may require a bit of trial and error correcting your method, but you'll create something nice. Some basic tools, become familiar with your equipment and the basic technology of creating a lotion and you are standing rather well more advanced then many give themselves credit for. Are you motivated?
i.e. Water + Oil + Emulsifier = Lotion/ serum/ body butter
[ensure against micro-flora/ fauna, add a preservative]
Active ingredients.
Cosmetic science is a sophisticated field of study that applies the principles of chemistry and pharmaceutics to the development of all types of body and personal care products, hair care, skin care products and makeup. Cosmetic science is developing and evolving daily, with the constant introduction of new active ingredients that presumably assist in the optimal functioning of our skin, rejuvenating those aging adult stem cells and mitigating the damage of exposure to the sun. Or so the story goes.
From DIY face lifting masks, desperate wishing and daydreaming it would seem that cosmetic science is the most relevant of them all. Formulators can make any lotion feel like anything they want. Sensorial appeal is of utmost importance, fragranced or unfragranced. Cosmetic science is now relatively well developed and can be used to minimize the risk of substance irritation, reduce chance of contamination or maximize the efficacy of cosmetic ingredients. Or so we are led to believe. The reality is glaringly the opposite with respect to the latter.
Cosmetic science is devoted to the enhancement of perceived physical beauty. Stimulating those fibroblasts to produce more collagen and elastin is the Holy Grail of cosmetic science. The world of cosmetic science is growing fast and furious and it is helping cosmetic companies fatten up the bottom line. The latest breakthrough in cosmetic science is that of the miraculous age defying ability of "name that fantastic flotsam" and the marketing story, repleat with celebrity endorsement. Cosmetic science as it appears to function from the consumer point of view, is purely a guide as to what is likely to not cause irritation, preserve from contamination nor separate in the bottle. Not much comfort. This is not true for all products, just the vast majority. For those that are potentially effective, keep reading...
Modern cosmetic science promises to gently yet effectively produce products to unveil the youthful vitality lurking within each aging consumer. One of the latest innovations now in the cosmetic science is the use of serum products. Reduced the amount of fillers? Science, especially cosmetic science is purely a guide, as to what is supposedly likely to be beneficial. However given the current marketing conundrum, the FDA and the 7% -15% maximum expenditure allowed to a cosmetic scientist to formulate an effective product with a 1000% + profit margin. We're out of luck for the most part. Most are utterly useless as anything but moisturizers. To be fair one can't blame the formulator for that. It's h/is/er job to formulate what ever the client requests.
One would have to have faith in cosmetic science, sculpt a belief around technologies of the psychologies and desires of the consumer. Charge outrageous amounts of money for the story behind the mystical byproduct of bacterial metabolism on a substrate of sacred parameters and market it accordingly. That category falls under Marketing Science. This acts to increase the price, ramps up the emotional sore points, tweaks on one's desires and promises to deliver results with out plastic surgery. We are to have confidence in the cosmetic science and training of the forumlator/s to improve our appearance. Professional marketing takes no prisoners and from what is apparent, with all the free shipping world wide, the mark up is truly beyond substantial. It's a dream.
The medical industry offering various surgical procedures is far more reluctant to make such fantastic claims. But the cosmetic industry shows no such hesitance.
Cosmetic companies, their promises and marketing are an advanced technology in the manipulation of the psychological parameters that motivate people to buy their cosmetic products. Cosmetic is precisely what they are. For were they not, they are to be classified as drugs. And this is where the FDA spins into itself and its own definitions. Fortunately there exist several escape clauses. This affords signficant marketing power to companies. From the DIY stand point, none of that is relevant. We are at liberty to formulate for maximum effectiveness. Step out of the realm of "cosmetic" and into the beauty where nature is science. Increase the probablity of positive effect. It remains similar, but fundamentally different.
"Nature hides her secret because of her essential loftiness, but not by means of ruse." Einstein
Nature is Science.
Friday, September 14, 2012
Vitamin C: Derivatives and Anti Aging
Lancome is promising : "Boosts the activity of genes and stimulates the production of youth proteins," and "A powerful combination of unique ingredients—Reconstruction Complex and Pro-Xylane™, a patented scientific innovation—has been shown to improve the condition around the stem cells and stimulate cell regeneration to reconstruct skin to a denser quality."
FDA said "Your products are not generally recognized among qualified experts as safe and effective for the above referenced uses and, therefore, the products are new drugs." The agency went on to say its letter is not exhaustive of all the violations associated with the company's products.
Sending Out An SOS: FDA's Warning Letter to Lancome
Alissa Marrapodi Copyright 2012 by Virgo Publishing.
http://cosmetics.supplysideinsights.com/
The "patented scientific innovation" without a shred of evidence to be found anywhere. There is no Fountain of Youth in a Cheap Plastic Bottle, but marketing would have us believe otherwise. Are there effective anti aging ingredients? Yes, however, one must check one's expectations against reality. There is not a cream/ serum on the market that is going to make a 60 year old look like s /he's 20. There is no subsititute for a life time of regular exercise, healthy diet and the use of an effective SPF. Supplements, antioxidants, well formulated creams cannot change the chronological age, but minimum, one doesn't have to look it. There are always choices and thereby one can make a significant difference in the final outcome.
Due to the Baby boomers ongoing quest for effective products that may actually meet the claims, countless products are swamping the market. Endless types of treatments are made available, promoted via websites and beauty blogs. Invasive and potentially harmful treatements, Laser to botox, you name it. Topical treatments, repleat with Apple stem cell extract, and if that wasn't bad enough, the latest, Green Tea Stem Cell extract. Let's not forget Lancome's foray into botanical stem cell science with the Absolue hilarity of Rose Stem cell extract. All of which are bunk. Let's not discuss the price for that either.
Vitamin C serums are almost synonymous with Anti aging. Where you see anti aging as a focus of skin care, invariably, Vitamin C or its derivatives come up in discussion. That Vitamin C is an extremely useful active in skin care is proven. It is an effective anti oxidant, up regulates collagen synthesis, exfoliates and is a mild lightening agent. L ascorbic acid is an inexpensive ingredient and very easy to source. The question then becomes, why are cosmetic companies selling this extremely useful and cheap ingredient for over $100.00 for 30 ml? Relatively simple answer, it works and most people are unaware of the multiples in the profit margin. The main problem with LAA, is that due to its excellent antioxidative effect in the skin, it oxidizes quite readily. It is fundamentally unstable. The effective use is limited by the pH requirement, generally under 3.2- 3.5. That low pH is problematic for many. Over time it may cause irritation and flaky skin due to over exfoliation. Not quite the "glowy" look one is going for.
To better deal with the short shelf of LAA and irritation due to pH, several vitamin C derivatives have been developed. They are not LAA, however when applied to the skin and through enzymatic processess, ascorbic acid is released. Unfortunately not all Vitamin C derivatives are created equal, nor do they share the same capacity for positive dermal/ cosmetic effect.
MAP, VC-PMG, Magnesium Ascorbyl Phosphate is the more gentle version of Vitamin C. pH is closer to neutral and requires 7.2 in solution/ serum / cream at higher use levels to avoid hydrolyzing and giving off a potent stench. MAP was shown in clinical trial to have the same capacity as LAA with respect to collagen up regulation. This makes it quite a good substitute for LAA if that is the focus of the end user. As a lightening agent, is not as effective as LAA, however LAA is not particularly effective to begin with. It's been incorrectly labled as a tyrosinase inhibitor by some, it is not, it acts to to reduce o-dopaquinone to dopa, avoiding dopachrome and melanin formation. Quite different mechanism. MAP has also been shown to improve moisture content in the skin, where as LAA did not. One study suggests that MAP at 10% was useful for treatment of melasma.
Tetra C, ATIP, VC-IP, Ascorbyl Tetra-Isopalmitate, Tetrahexadecyl Ascorbate. A lipophillic Vitamin C derivative. The majority of the data behind the use of Tetra C comes from the makers of the derivative. Another study promoting its use had 7% LAA in the vehicle from which they drew astoundingly glowing conclusions regarding its efficacy. To be fair, in other research it was shown to be more effective at protecting from UVA induced oxidative stress than LAA. One may hypothesize that it may be due to the depot effect in the skin and the slow release. Whether that is the case invivo is not clear.
As far as antioxidative effect, LAA is more effective than either. MAP is more effective than TetraC in a water based formula, however that reverses in favor of TetraC in an oil base.
Ascorbyl Acid 2 Glucoside stacks up quite nicely next to MAP, if not better for it's ease of formulation and stability but also for it's effect on collagen synthesis. Slow release is also part of the stated mechanism for it's effect. Ascorbic Acid 2-glucoside has been shown to maintain prolonged biological activity of ascorbic acid longer than SAP [sodium L-ascorbic acid 2-phosphate], another conventional ascorbic acid derivative .
SAP, Asc 2-P, Sodium Ascorbyl Phosphate, this one doesn't stack up too well. It's sold as being equal to MAP, but it is 1/10 as effective as MAP or LAA at its ability to stimulate collagen synthesis. It is stable by comparison to LAA. Non irritating, and not particularly effective at increasing collagen synthesis when compare to MAP or LAA.
AP, Ascorbyl Palmitate, ascorbic acid-6-palmitate , is unfortunately not the solution to the problem either. It may be stable, however when applied to the skin and exposed to UVB, which occurs every day, AP was found to strongly promote ultraviolet-B-induced lipid peroxidation, c-Jun N-terminal kinase activation, and cytotoxicity. Not a good choice as, despite the selling point being that it is lipid soluble, it is the lipid component of ascorbic acid-6-palmitate that contributes to the generation of oxidized lipid metabolites that are toxic to epidermal cells.The data suggested that, despite its antioxidant properties, ascorbic acid-6-palmitate may intensify skin damage following physiologic doses of ultraviolet radiation. It may be convenient to work with, however it is certainly not worth using.
Clearly there are differences in the concept of what consititutes an effective choice even for a simple C serum. Who wants to waste their time or money on the wrong ingredients? Wrinkles don't 'go away' with wishful thinking. Defying the hands of time requires proven modalities. Fighting the effects of aging , cumulative sun damage, years of free radicals, it helps to choose the correct products. Whether one is looking to prevent or to reverse the signs of aging, a Vitamin C serum is a good place to start. It's something anyone is able to DIY and incorporate into their current skin care system. Beautiful skin is not a brand, it's not a right either, it's something one must work at to maintain.
Due to the marketing stories and the plethora of new ingredients, it can be very confusing for the vast majority. Is SAP better than MAP? No. Is Tetra C better than MAP? No. Is LAA better than MAP? No, but if your skin can not tolerate LAA, than the answer is Yes. Same answer for Tetra C, but personally, I wouldn't bother as the data on AA2G is more compelling. Which is the most effective lightener? None of them. There are other actives that are more effective. Used in conjunction, it won't hurt and may help. When it comes to purchasing skin care, it's caveat emptor. When it comes to DIYing it, you increase the odds several fold.
Long story short with regards to the efficacy of the C derivatives.
LAA ≥MAP ≥ AA2G> TetracC >SAP>;
If one is hoping to remove wrinkles, that most probably isn't going to happen. Reduction in fine lines, is a reasonable possibility. Damaged skin took many years to accumulate. To suggest that any topical product is going to undo years of damage is more than a leap of faith. It is an out right lie. Marketing takes no prisoners. There are many useful functional ingredients available. They are the boring, non patented type without the fanfare, but have a great deal in the way of solid clinical trials to suggest that their use may be of some benefit. Each is responsible for their choices in skin care whether to DIY or purchase. Hopefully over time, the average baby boomer skin care consumer will take the initiative to become more selective and demanding of the products they purchase.
1.Campos PM, Gonçalves GM, Gaspar LR. In vitro antioxidant activity and in vivo efficacy of topical formulations containing vitamin C and its derivatives studied by non-invasive methods.Skin Res Technol. 2008 Aug;14(3):376-80.
2. Hitoshi Mitsuzumi. Properties of a Novel Vitamin C Supplement, L-Ascorbic Acid 2-Glucoside, and Its Uses in the Field of Foods. Foods Food Ingredients J. Jpn., Vol. 211, No.5, 2006
3. Kameyama, K.; Sakai, C.; Kondoh, S.; Yonemoto, K.; Nishiyama, S.; Tagawa, M.; Murata, T.; Ohnuma, T.; Quigley, J.; Dorsky, A.; Bucks, D.; Blanock, K. Inhibitory effect of magnesium L-ascorbyl-2-phosphate (VC-PMG) on melanogenesis in vitro and in vivo. J. Am. Acad. Dermatol. 1996, 34, 29-33.
4. Kumano, Y.; Sakamoto, T.; Egawa, M.; Iwai, I.; Tanaka, M.; Yamamoto, I. In vitro and in vivo prolonged biological activities of novel vitamin C derivative, 2-O- -D-glucopyranosyl-L-ascorbic acid (AA-2G), in cosmetic fields. J. Nutr. Sci. Vitaminol. 1998, 44, 345-359.
5. Kunikazu Moribe,Waree Limwikrant, Kenjirou Higashi, and Keiji Yamamoto. Drug Nanoparticle Formulation Using Ascorbic Acid Derivatives. Journal of Drug Delivery Volume 2011, Article ID 138929, 9 pages
6. Lee SC, Yuk HG, Lee DH, Lee KE, Hwang YI, Ludescher RD.Vitamin C derivative ascorbyl palmitate promotes ultraviolet-B-induced lipid peroxidation and cytotoxicity in keratinocytes.J Invest Dermatol. 2002 Nov;119(5):1103-8.
7. Miyai E.; Yanagida M. ; Akiyama J.-I. ; Yamamoto I. ; Ascorbic acid 2-O-α-glucoside-induced redox modulation in human keratinocyte cell line, SCC : Mechanisms of photoprotective effect against ultraviolet light B. Biological & pharmaceutical bulletin ,1997, vol. 20, no6, pp. 632-636 (36 ref.)
8. Xiao L, Kaneyasu K, Saitoh Y, Terashima Y, Kowata Y, Miwa N.Cytoprotective effects of the lipoidic-liquiform pro-vitamin C tetra-isopalmitoyl-ascorbate (VC-IP) against ultraviolet-A ray-induced injuries in human skin cells together with collagen retention, MMP inhibition and p53 gene repression. J Cell Biochem. 2009 Mar 1;106(4):589-98.
Friday, August 31, 2012
The Science of Anti Aging and We the Consumers:
Does any cosmetic company truly have the Fountain of Youth in a bottle? Apparently, not. As each and every day a new "wonder ingredient" is promoted with or without a shred of evidence of efficacy. The latest essential ingredient to bombard can be any thing from a rare botanical milk to magical drops, mystical water or fermented eye of newt. In truth, were the eyes of newt fermented in Sake, you may actually benefit. That being said, the newt eyes wouldn't be the reason. Does anything actually erase wrinkles? Are homemade recipes / formulas as effective as the $300.00 US / 30 ml advertised to rid us of our wrinkles and age spots or money back? Can age spots be removed? Can age spots be bleached? Can they really be made to fade? What are they really? Sagging SKIN!! Now what?
Like becoming middle aged wasn't hard enough! Do any of these products really work? Or are they just another hyped moisturizer? Is night cream more important than day cream? What is the best time to apply lotions for maximum effect? Which ingredients are essential? How to know the difference? Which lotions are safe, which ones aren't. What does 'safe' mean? Will it cause an allergic reaction? There are many methods and ideas about what consititutes a solid skin care regime,
Which one is the best?
Are low cost beauty products of any value? Some are, some aren't.
Natural vs. Chemical? Which one is better? Or does it matter? Which one gives the best results? Perhaps both.Why are natural products so much more expensive? What does Ecocert really mean, and what is the difference between organic vs a not organic natural product? Why when I look at a product touted as 'natural organic', does the ingredients list have a '*' with "certified organic", what about the other ingredients? Does it really make a difference?
When did "The Science of Anti Aging and the Consumer" become a cosmetics company's marketers money making dream child? It's easy to press the emotional buttons. You are middle aged, the fatal 40 has just passed by and an 18 year old model in full makeup, advertising the latest new lotion / potion with the magical ingredient is informing us of that fact. This product will make you look just like her! No, it won't. But many will spend thousands of dollars chasing that pipe dream.
Wading through the marketing morass of false promises, email anti aging SPAM is a daily exericise in
hilarity. Every once in a while a gem arrives, but it's usually an old ingredient dolled up with a new trade
name and host of claims to go with it. Dragosine for example, L carnosine. Excellent active, but didn't require a name change to make it any more effective. Another one, Effineo, coffeeberry extract, but an unknown amount of the active component chlorogenic acid and it was kindly diluted for me in propylene glycol. Really not necessary to do that.
All sorts of treatments are being dreamed up. Some even have scientific basis, most others, not so much. But they have a great deal in the way of "secret" data. "Secret Data" ingredients or treatments are round file worthy.
This is a "secret": Vast majority of the cosmetic preparations available on the market are next to useless. Why is that? Multiple reasons. Regulations for one, the other, the end product wasn't designed with cell physiology in mind. It was designed with "what ever sells" in mind.
DIY SEA style, is a very different species of 'cosmetic'. The focus is beyond 'cosmetic'. That's just the visible end result and can not be washed off. Unfortunately, such treatments as those made by DIY'ers are rarely available, and if they are on the market, they are well over $150.00 / 30 ml. Some, are just simply ludicrous.
Deep Hydration Serum (1fl oz.)
by Bakel
Price: $140.00
Ingredients:Aqua/Water, Sodium Hyaluronate.
To DIY that, is $0.71 and 5 minutes. That is a very expensive bottle.
This particular post should more correctly be titled:
The Science of Ripping Off the Aging Consumer.
Sunday, June 3, 2012
Lemon Peel Bioferment Skin Brightening Serum
Lemon Peel Bioferment is touted as being as effective as hydroquinone for lightening the skin and overall brightening. The research supporting such a claim is scant at best. It is known that citral and myrcene have inhibitory effect of tyrosinase. Citric acid itself has a long history of efficacy. Niacinamide and N-acetyl D glucosamine are proven lightening agents.
SkinCare forum is available to ask and answer questions. SEA has been invited to participate at that venue.
SkinCare forum is available to ask and answer questions. SEA has been invited to participate at that venue.
| Ingredients | Percentage % |
| Niacinamide | 5 % |
| N-acetyl D glucosamine | 5% |
| Distilled Water | 37 % |
| Lemon Peel Bioferment | 5% |
| Sea Kelp Bioferment | 5% |
| Sea Emollient | 5% |
| Vitamin E acetate | 1% |
| Sclerotium gum 2% base | 20% |
| Hyaluronic Acid Hi wt.1% | 7.5% |
| Chamomille Extract | 5% |
| Glycerin | 2% |
| Polysorbate 20 | 2% |
| Phenoxyethanol | 0.5 % |
1. Weigh all ingredients.
2. B3 and NAG into water, stir until dissolved. Add Vitamin E acetate. Stir
3. Add LPB to water phase, HA 1% and Sclerotium gum. Blend
4. Add Chamomille extract, Polysorbate 20 , glycerin and Oil. Blend.
5. Add phenoxyethanol.
6. Bottle serum in a sterilized container.
Creates a white colored light and silky serum.
To create a thicker serum with similar silky spreading, increase water by 18% and use sclerotium powder at 2% of total formulation.
Saturday, June 2, 2012
Oil Cleansing Method, Emulsified OCM
Oil cleansing method that rinses easily and cleanly. Readily tailored to your skin type and needs.
Oils of choice based on skin type and needs ~ 70-80%
Castor 0il ~10-20%
Polysorbate 20 or polysorbate 80. ~ 8-10%
Essential oils chosen on same basis = Less than 1%
Combine the oils and polysorbate in a sterilized bottle. Shake and ready to use.
For further information: The Oil Cleansing Method.
Chrysalis Eye Serum
Vit K1, Chrysin and Retinol have been shown to aid in the fight against
time and this is most prominent in the eye area. Dark circles due to RBC
by products often appear and are bothersome. Chrysin has been shown to
up regulate the expression UGT1A1 which leads to the breakdown of
bilirubin and it's eventual removal via the bloodstream.
Primarily developed for the eye area. It has a very light, almost a mousse like texture. Tingly but not irritating, however everyone is different. The serum is based on a few studies.
Chrysin protects epidermal keratinocytes from UVA- and UVB-induced damage.The induction of human UDP-glucuronosyltransferase 1A1 mediated through a distal enhancer module by flavonoids and xenobiotics.
Application of Retinol to Human Skin In Vivo Induces Epidermal Hyperplasia and Cellular Retinoid Binding Proteins Characteristic of Retinoic Acid but Without Measurable Retinoic Acid Levels or Irritation.
Levels of retinyl palmitate and retinol in the stratum corneum, epidermis, and dermis of female SKH-1 mice topically treated with retinyl palmitate.
Effects of topical vitamin K and retinol on laser-induced purpura on nonlesional skin.
Human vitamin K 2,3-epoxide reductase complex subunit 1-like 1 (VKORC1L1) mediates vitamin K-dependent intracellular antioxidant function.
Destabilization of egg lecithin liposomes on the skin after topical application measured by perturbed gamma gamma angular correlation spectroscopy (PAC) with 111In.
The role of topical vitamin K oxide gel in the resolution of postprocedural purpura.
Formulation optimization of prostaglandin E(1)-loaded lipid emulsion: Enhanced stability and reduced biodegradation.
Citric acid to adjust pH.
2. Place the water soluble actives[water phase, H20, Sea Emollient, B5 , Vit E acetate, Vit A acetate.] together and blend thoroughly.
3.a. Chrysin needs to go into solution with only just enough 1 N NaOH then is quickly added to the water phase.
3.b. Adjust pH to 6.3.
4. Place the water mix into the ultrasound cleaner. Slowly sprinkle in the egg lecithin while blending.
5. Warm the oils to 40 C and then combine in the beaker in the ultrasound cleaner.
6. Allow to cool, add Vitamin K and Phenoxyethanol.
This method will allow for the creation of liposomes. Egg lecithin allows for a stable emulsion and is exquisite for facial and eye care. It however does have a scent that is readily masked with various essential oils. Neroli and Frankincense are useful.
TEST the serum prior to use, or reduce the key potentially irritating actives. Retinol and Vitamin K and increase with tolerance.
*n.b. Lecithin may clump, this can be most readily avoided by sprinkling the powder into the water phase while blending at the same time. Should clumps occur, filtering the emulsion will result in the removal.
Primarily developed for the eye area. It has a very light, almost a mousse like texture. Tingly but not irritating, however everyone is different. The serum is based on a few studies.
Chrysin protects epidermal keratinocytes from UVA- and UVB-induced damage.The induction of human UDP-glucuronosyltransferase 1A1 mediated through a distal enhancer module by flavonoids and xenobiotics.
Application of Retinol to Human Skin In Vivo Induces Epidermal Hyperplasia and Cellular Retinoid Binding Proteins Characteristic of Retinoic Acid but Without Measurable Retinoic Acid Levels or Irritation.
Levels of retinyl palmitate and retinol in the stratum corneum, epidermis, and dermis of female SKH-1 mice topically treated with retinyl palmitate.
Effects of topical vitamin K and retinol on laser-induced purpura on nonlesional skin.
Human vitamin K 2,3-epoxide reductase complex subunit 1-like 1 (VKORC1L1) mediates vitamin K-dependent intracellular antioxidant function.
Destabilization of egg lecithin liposomes on the skin after topical application measured by perturbed gamma gamma angular correlation spectroscopy (PAC) with 111In.
The role of topical vitamin K oxide gel in the resolution of postprocedural purpura.
Formulation optimization of prostaglandin E(1)-loaded lipid emulsion: Enhanced stability and reduced biodegradation.
| Ingredients | Percent % |
| Chrysin | 1 % |
| Retinol | 2% |
| Vit E acetate/ oil | 1% |
| Egg Lecithin | 5 % |
| Polysorbate 80 | 2% |
| Borage oil | 30% |
| Distilled H20 | 21.75% |
| Dex Panthenol | 3% |
| Vitamin K | 2% |
| Sea Emollient | 29. 5 % |
| 1 N NaOH | 2.25 % |
| Phenoxyethanol | 0.5 % |
1. Set up equipment and weigh all actives first. Calibrate your pH meter.
3.a. Chrysin needs to go into solution with only just enough 1 N NaOH then is quickly added to the water phase.
3.b. Adjust pH to 6.3.
4. Place the water mix into the ultrasound cleaner. Slowly sprinkle in the egg lecithin while blending.
5. Warm the oils to 40 C and then combine in the beaker in the ultrasound cleaner.
6. Allow to cool, add Vitamin K and Phenoxyethanol.
This method will allow for the creation of liposomes. Egg lecithin allows for a stable emulsion and is exquisite for facial and eye care. It however does have a scent that is readily masked with various essential oils. Neroli and Frankincense are useful.
TEST the serum prior to use, or reduce the key potentially irritating actives. Retinol and Vitamin K and increase with tolerance.
*n.b. Lecithin may clump, this can be most readily avoided by sprinkling the powder into the water phase while blending at the same time. Should clumps occur, filtering the emulsion will result in the removal.
Chrysalis lends itself nicely to the addition of AHYP, as well as sclerotium gum. Using a sclerotium gum 1-2 % base , same can be done using hyaluronic acid , one can easily sub out up to half the Sea Emollient and create an even more silky serum. Make the appropriate adjustments using the batch size calculator.
DIY C Serum ~ SEA T Honey
15% LAA, 0.5% Ferulic acid, 1.0 Vitamin E , EGCG 90% @ 5%
Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG.
Green tea polyphenol (-)-epigallocatechin-3-gallate treatment of human skin inhibits ultraviolet radiation-induced oxidative stress.
Protective effects of EGCG on UVB-induced damage in living skin equivalents.
Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin.
Fucoidan inhibits UVB-induced MMP-1 promoter expression and down regulation of type I procollagen synthesis in human skin fibroblasts
Sclerotium rolfsii scleroglucan: the promising behavior of a natural polysaccharide as a drug delivery vehicle, suspension stabilizer and emulsifier.
Ferulic Acid Stabilizes a Solution of Vitamins C and E and Doubles its Photoprotection of Skin
Topical ascorbic acid on photoaged skin. Clinical, topographical and ultrastructural evaluation: double-blind study vs. placebo.
Scleroglucan: A Versatile Polysaccharide for Modified Drug Delivery
1. Weigh and measure your ingredients.
In combination of free radical
scavenger and metal chelator, the chelator decreases the oxidation rates
by inhibiting metal-catalyzed oxidation; resulting in, fewer free
radicals generated in the system. Inactivation of antioxidants via
termination reaction or participation in autoxidation occurs to a lesser
extent in such situations. The concentration of antioxidant, available
to scavenge free radicals, will always be greater at a given time than
when no metal chelator is present. The combination of chelator and
radical scavenger decreases free radical generation and increases
radical scavenging potential . Synergistic activity has been observed in
the mixtures of natural tocopherols and citric acid. The synergistic
effect of this mixture is caused by the chain-breaking ability of
tocopherols and metal chelation of citric acid .
E. N. Frankel, Lipid Oxidation, The Oily Press, West Ferry, Dundee, 1998, pp. 13, 79, 115, 129, and 167.
E. A. Decker, in C. C. Akoh and D. B. Min, eds., Food Lipids: Chemistry, Nutrition and Biotechnology, 2nd ed., Marcel Dekker, Inc., New York, 2002, p. 517.
E. N. Frankel, Lipid Oxidation, The Oily Press, West Ferry, Dundee, 1998, pp. 13, 79, 115, 129, and 167.
E. A. Decker, in C. C. Akoh and D. B. Min, eds., Food Lipids: Chemistry, Nutrition and Biotechnology, 2nd ed., Marcel Dekker, Inc., New York, 2002, p. 517.
Green tea polyphenol (-)-epigallocatechin-3-gallate treatment of human skin inhibits ultraviolet radiation-induced oxidative stress.
Protective effects of EGCG on UVB-induced damage in living skin equivalents.
Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin.
Fucoidan inhibits UVB-induced MMP-1 promoter expression and down regulation of type I procollagen synthesis in human skin fibroblasts
Sclerotium rolfsii scleroglucan: the promising behavior of a natural polysaccharide as a drug delivery vehicle, suspension stabilizer and emulsifier.
Ferulic Acid Stabilizes a Solution of Vitamins C and E and Doubles its Photoprotection of Skin
Topical ascorbic acid on photoaged skin. Clinical, topographical and ultrastructural evaluation: double-blind study vs. placebo.
Scleroglucan: A Versatile Polysaccharide for Modified Drug Delivery
| Ingredients | % required |
| L Ascorbic acid | 15 % |
| Vitamin E Oil | 1% |
| Ferulic acid | 0.5 % |
| Sea Emollient | 28% |
| EGCG /Green Tea Extract | 5% |
| Sclerotium Gum | 2% |
| Distilled Water | 40.5% |
| 1 N NaOH | 2% |
| Citric Acid | 0.5% |
| Oil of Choice | 5 % |
| Phenoxyethanol | 0.5% |
1. Weigh and measure your ingredients.
2. Ferulic acid into solution with NaOH or ETOH, stir till dissolved = white
3. LAA into water, stir till dissolved, may have some light dust, don't panic.
4. EGCG into LAA and Water Stir, Will turn a honey color tan/ brown
5. Citric acid into mix, stir/ blend
6. Sclerotium gum , mix and blend
7. Sea emollient, blend
8. Vit E oil, Oil of choice + Phenoxy
9. Adjust pH to 3.2 or under.
Creates an ultra light and silky serum.
Tuesday, May 22, 2012
AA2G Serum
AA2G Serum: AA2G is the stable C form which allows for a great deal of flexibility when formulating. It is proven in clinical trials to be effective antioxidant as well as up regulate collagen production. Proline is included as it has been shown to be an effective quencher of photoexcited states ( QPES.) L carnosine, is the most effective anti glycation active. The serum is elegant, light and silky. Ideal for day time wear under a sunscreen.
If you wish to simply purchase the AA2G serum, please contact MyFawnie
SkinCare forum is available to ask and answer questions. SEA has been invited to participate at that venue.
pH 5.5
1. AA2G into solution
2. Ferulic acid into solution using 1N NaOH add to AA2G adjust pH to @ 5.5
3. Proline, Carnosine, Vit E acetate. Blend.
4. Sclerotium gum, blend. Will thicken.
5.While blending slowly add ALA to oil at room temp.
6.Combine oil and water phase + phenoxy.
7. Leave over night, next day will be a thick gel and spreads like silk.
*n.b. AA2G is very acidic in solution. Adding small amounts of solid NaOH into the solution and testing is more effective,.mix a 3 to 4 N NaOH solution.
If you wish to simply purchase the AA2G serum, please contact MyFawnie
SkinCare forum is available to ask and answer questions. SEA has been invited to participate at that venue.
| Ingredients | Percentage |
| AA2G | 2 % |
| Alpha Lipoic Acid | 1% |
| Oil of preference | 10 % |
| L-Proline | 1% |
| L- Carnosine | 1 % |
| Sclerotium gum | 2 % |
| Vitamin E oil or acetate | 1 % |
| Glycerin | 2 % |
| Distilled water | 76 % |
| Ferulic acid | 0.5 % |
| 1N NaOH | 2 % |
| Phenoxyethanol | 0.5 % |
| Adjustments | 1 % |
pH 5.5
1. AA2G into solution
2. Ferulic acid into solution using 1N NaOH add to AA2G adjust pH to @ 5.5
3. Proline, Carnosine, Vit E acetate. Blend.
4. Sclerotium gum, blend. Will thicken.
5.While blending slowly add ALA to oil at room temp.
6.Combine oil and water phase + phenoxy.
7. Leave over night, next day will be a thick gel and spreads like silk.
*n.b. AA2G is very acidic in solution. Adding small amounts of solid NaOH into the solution and testing is more effective,.mix a 3 to 4 N NaOH solution.
AA2G- Ascorbyl Glucoside
AA2G is the stable C form which allows for a great deal of flexibility
when formulating. It is proven in clinical trials to be effective
antioxidant as well as up regulate collagen production.
L-Ascorbic acid functions in many biological processes i.e. anti-oxidation, collagen synthesis, intestinal absorption of iron and amino acid metabolization . L-ascorbic acid is essential as a cofactor for the hydroxylation of proline and lysine residues in collagen, a major protein component of the body. LAA also increases transcription rate of procollagen genes and stabilizes procollagen mRNA. AA2G has proven to be effective at percentages as low as 2% . It is the extremely stable form of vitamin C LAA is unstable and prone to oxidation in solution and only functional at pH below 3.5. AA2G is not limited by these requirements while delivering the same postive results as LAA. AA2G is stable to air, heat , light and metal ions. It's range of formulation is greater than MAP and delivers greater dermal benefits than any other C derivative at present. It is convenient to formulate with.
The hydroxyl group of the second carbon in ascorbic acid is highly reactive and plays an important role in the natural biologic activity, however, it can also be the site of inactivation and decomposition.
Ascorbyl Glucoside is produced from vitamin C and starch by using a natural enzymes which result in binding glucose to the hydroxyl group of the same reactive carbon of the ascorbic acid.
An enzyme releases vitamin C at the cellular surface and provides benefits over a sustained period of time. Ascorbyl Glucoside is hydrolyzed by glucosidase, an enzyme present in the membrane of skin cells.
This process releases vitamin C in its natural active form. When vitamin C enters cells it results in significant well-documented biological responses.
Ascorbyl Glucoside has been demonstrated to be hydrolyzed over a prolonged period giving its beneficial physiological effects to the cells and tissues in a constant and sustained manner.
Suppression of melanin synthesis:
When Ascorbyl Glucoside is converted to vitamin C and enters the cells it significantly reduces the production of melanin by inhibiting tyrosinase activity. This results in a reduction of Dopaquinone, an intermediate of melanin synthesis. Additionally it converts existing Dopaquinone to L-Dopa.
Ascorbyl Glucoside bleaching of extant melanin:
When Ascorbyl Glucoside is converted to vitamin C and enters the cells it can significantly lighten existing black melanin by a reduction reaction.
Reduction in hyperpigmentation via AA2G topical application:
Creams containing Ascorbyl Glucoside are beneficial for lightening skin pigmentation.
Sixteen female volunteers (37 to 55 years old) applied a face cream containing 2% of AA2G™ twice a day to a hyperpigmented area of their face for a total of 90 days.The areas were matched against pantone color samples and the brightness (L* value) of the areas were measured by a colorimeter on day 0, 45 and 90. (*Significantly different from day 0 at <0.01)
Ascorbyl Glucoside suppresses cellular damage due to UV irradiation:
When Ascorbyl Glucoside is converted to vitamin C it can dramatically reduce the free radicals that result from UV irradiation of the skin, and significantly reduce cell damage. Human skin fibroblasts were cultured for 1 day. Fibroblast samples were cultured a second day with or without 1mM AA2G™. The cells were irradiated with 20mJ/cm2 UVA and B radiation, and then cultured for 2 additional days.
The number of viable cells were determined. (*Significantly different from UV irradiated cells without AA2G™ at <0.05)
Ascorbyl Glucoside promotes collagen synthesis:
After cultivation of normal human skin fibroblasts for 1 day, the cells were cultured in the presence of vitamin C 0.2mM) or AA2G™ (0.2mM) for 2-4 days. The percentage of collagen to total protein was determined. (*Significantly different from control at p<0.05, and significantly different from vitamin C at p<0.05).
Ascorbyl Glucoside reduces wrinkles and roughness:
L-Ascorbic acid functions in many biological processes i.e. anti-oxidation, collagen synthesis, intestinal absorption of iron and amino acid metabolization . L-ascorbic acid is essential as a cofactor for the hydroxylation of proline and lysine residues in collagen, a major protein component of the body. LAA also increases transcription rate of procollagen genes and stabilizes procollagen mRNA. AA2G has proven to be effective at percentages as low as 2% . It is the extremely stable form of vitamin C LAA is unstable and prone to oxidation in solution and only functional at pH below 3.5. AA2G is not limited by these requirements while delivering the same postive results as LAA. AA2G is stable to air, heat , light and metal ions. It's range of formulation is greater than MAP and delivers greater dermal benefits than any other C derivative at present. It is convenient to formulate with.
Ascorbyl Glucoside is produced from vitamin C and starch by using a natural enzymes which result in binding glucose to the hydroxyl group of the same reactive carbon of the ascorbic acid.
This process releases vitamin C in its natural active form. When vitamin C enters cells it results in significant well-documented biological responses.
Ascorbyl Glucoside has been demonstrated to be hydrolyzed over a prolonged period giving its beneficial physiological effects to the cells and tissues in a constant and sustained manner.
Suppression of melanin synthesis:
When Ascorbyl Glucoside is converted to vitamin C and enters the cells it significantly reduces the production of melanin by inhibiting tyrosinase activity. This results in a reduction of Dopaquinone, an intermediate of melanin synthesis. Additionally it converts existing Dopaquinone to L-Dopa.
Ascorbyl Glucoside bleaching of extant melanin:
When Ascorbyl Glucoside is converted to vitamin C and enters the cells it can significantly lighten existing black melanin by a reduction reaction.
Reduction in hyperpigmentation via AA2G topical application:
Creams containing Ascorbyl Glucoside are beneficial for lightening skin pigmentation.
Sixteen female volunteers (37 to 55 years old) applied a face cream containing 2% of AA2G™ twice a day to a hyperpigmented area of their face for a total of 90 days.The areas were matched against pantone color samples and the brightness (L* value) of the areas were measured by a colorimeter on day 0, 45 and 90. (*Significantly different from day 0 at <0.01)
When Ascorbyl Glucoside is converted to vitamin C it can dramatically reduce the free radicals that result from UV irradiation of the skin, and significantly reduce cell damage. Human skin fibroblasts were cultured for 1 day. Fibroblast samples were cultured a second day with or without 1mM AA2G™. The cells were irradiated with 20mJ/cm2 UVA and B radiation, and then cultured for 2 additional days.
The number of viable cells were determined. (*Significantly different from UV irradiated cells without AA2G™ at <0.05)
Ascorbyl Glucoside promotes collagen synthesis:
Collagen plays an important role in the structure and firmness of skin. Ascorbyl Glucoside is converted to vitamin C and promotes collagen synthesis of skin fibroblasts. Ascorbyl Glucoside maintains its effects for a sustained period of time, resulting in increasing benefits.
After cultivation of normal human skin fibroblasts for 1 day, the cells were cultured in the presence of vitamin C 0.2mM) or AA2G™ (0.2mM) for 2-4 days. The percentage of collagen to total protein was determined. (*Significantly different from control at p<0.05, and significantly different from vitamin C at p<0.05).
Products containing Ascorbyl Glucoside are highly beneficial for improving wrinkles and roughness of skin. Sixteen female volunteers (37 to 55 years old) applied a face cream containing 2% of AA2G™ twice a day for a total of 90 days to the outer corners of their eyes and cheek area. Silicone replicas of the corner of the eyes and the other treated areas were taken on days 0, 45 and 90 and wrinkle depth and skin roughness were measured by profilometry. (*Significantly different from day 0 at p<0.01)
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