Recent posts on various DIY skin care forums have discussed the issue of the penetration of L-ascorbic acid suspended in a silicone base into the skin.

More precisely, a few posters have started promoting the idea that L-ascorbic acid cannot penetrate into the skin, because silicone forms a barrier on the skin.

I would like to address this issue in more detail.

Background: Stable L-ascorbic acid products for skin care

The DIY skin care community has long struggled with the formulation of a stable L-ascorbic acid skin care product. In fact, professional skin care companies and formulators have also struggled with the same problem.

Some attempts have been made by professionals to develop a stable vitamin C skin care product.  The best example of this is the Skinceuticals C+E+Ferulic product.  This is based on the 2006 study “Ferulic acid stabilizes a solution of vitamins C and E and doubles its photoprotection of skin” by Pinnel and others.

This study claimed that

“Ferulic acid is a potent ubiquitous plant antioxidant. Its incorporation into a topical solution of 15% L-ascorbic acid and 1% tocopherol improved chemical stability of the vitamins (C+E) and doubled photoprotection to solar-simulated irradiation of skin from 4-fold to approximately 8-fold as measured by both erythema and sunburn cell formation.” http://www.nature.com/jid/journal/v125/n4/full/5603565a.html

However, consumers have found that skinceuticals C E ferulic product is often orange tinted.  This color usually indicates that the L ascorbic acid has oxidized, thus making it pro-oxidant.  So, even though Ferulic acid may stabilize l ascorbic acid in the lab, in practicality there appear to be some serious issues that have not been addressed.

DIY skin care formulators are able to work around this.  By making a CE Ferulic product at home, it is possible to have a fresh supply every week, thus reducing (but not eliminating) the amount of vitamin C oxidization.

Solution: The Fitzpatrick study

Another study of interest is the 2002 “Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage” by Fitzpatrick.

Even though this study predates the CE+Ferulic study, it did not start getting discussed on the DIY skin care forums until quite recently.

Fitzpatrick’s method was as follows:

“Ten patients having facial photodamage were recruited for a double-blind pilot study of a newly formulated vitamin C complex having 10% ascorbic acid, a water soluble acid, and 7% tetrahexyldecyl ascorbate, a lipid soluble analog.

Both of these are combined in an anhydrous polysilicone gel base, which acts as a ‘dermal patch,’ releasing the water soluble acid slowly and the lipid soluble analog rapidly. The active vitamin C complex was applied to one side of the face and the inactive placebo base was applied to the opposite side of the face once a day.” http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11896774&query_hl=7&itool=pubmed_ExternalLink

Now, this is where a very few posters start having some issues.  The base used is an anhydrous silicone gel, and the doubt seems to be in the fact that a very few posters believe that silicone forms a barrier and therefore hinders the absorption of active ingredients.

However, let’s look at the next part of Fitzpatrick’s study:

“Biopsies showed increased Grenz zone collagen, as well as increased staining for mRNA for type I collagen. This formulation of vitamin C results in clinically visible and statistically significant improvement in wrinkling when used topically for 12 weeks. This clinical improvement correlates with biopsy evidence of new collagen formation.”

Now, if silicone prevents the absorption of active ingredients, than there would not have been an increase collagen.

So, this should put to rest the claims that using silicone as a base prevents the absorption of active ingredients.

Flawed study

There is one troubling aspect about the Fitzpatrick study.  The study did not test the use of each key ingredient separately.

The two key ingredients in the anhydrous C product are L-ascorbic acid (which is water soluble), and Ascorbyl Tetraisopalmitate (also known as Tetrahexyldecyl Ascorbate ) which is oil soluble.

So, even though the study shows that the combination the two active ingredients in a silicone base led to an increase of collagen, we do not know if this was caused by the Tetrahexyldecyl Ascorbate, the Vitamin C, or the combination of the two.

This brings us back full circle to the original problem! We do not know which active is responsible for the increase in collagen. So it is possible to claim that the L-ascorbic acid is in fact not absorbed by the skin, and that the increase of collagen is cause by the Tetrahexyldecyl Ascorbate.

The blame for this confusion can be put purely with Fitzpatrick. It seems a simple matter to have tested the activity of both l-ascorbic and Tetrahexyldecyl Ascorbate in anhydrous silicone, separately. However, he chose not to do this.

So, we remain with his original statement.

“Both of these are combined in an anhydrous polysilicone gel base, which acts as a ‘dermal patch,’ releasing the water soluble acid slowly and the lipid soluble analog rapidly.”

To me the dermal patch idea makes sense, and I personally put more trust in this than the doubt caused by a very few (but very ‘vocal’) posters on skin care forums.

In the end the choice is yours.

I will continue to use the anhydrous C product as my number one weapon in anti aging skin care.  Why? Because no matter which active did the job, somehow this product has improved my skin and that is ultimately what I want.

http://www.bulkactives.com/siliconegel.htm

http://www.bulkactives.com/ascorbicacid.htm

http://www.bulkactives.com/ascorbyltetraisopalmitate.htm

It is a well-known fact of life that exposure to UV light, especially the UVA component, festers skin disorders like melanoma and non-melanoma skin cancers. Superficial remedies such as sunscreens are effective only to a limited extent. This realization has led to investigation of new methods to protect the skin from photo-damaging effects of solar UV radiation, or “photo-carcinogenesis” as it is called. Recent years have seen considerable interest in identifying naturally-occurring botanicals with anti-oxidant and anti-inflammatory properties, and which exhibit anti-carcinogenic and anti-mutagenic functionality.

It is in this light that the medicinal benefits of milk thistle have been a subject of intense research by scientists. Though its value as a medicine for a host of health conditions, including dermatological, has been known for over 2,000 years, it is only now that science has seriously begun looking at the role played by milk thistle and “Silymarin”, its active compound, in treating skin damage.

In an experiment conducted at Palacky University in Czechoslovakia (1), researchers studied the impact of two components of Silybum marianum (technical name for milk thistle) as both a preventative as well as treatment intervention for skin damage against UVA exposure. Their findings were positive, in that it was discovered that these two components – collectively known as “flavonolignans” – perform a host of functions, such as increasing the viability of keratinocytes in irradiated cells, inhibiting the production of ROS, stopping further depletion of ATP and GSH taking place at intracellular level, and halting the peroxidation of membrane lipids. Further, the activation of caspases-3 process that UVA exposure initiates gets halted and reversed when the two components of Silybum marianum are applied. The overall picture that emerges, therefore, is that Silybum marianum is a good candidate to be considered for inhibiting UV damage.

An interesting experiment conducted on mice at the University of Alabama in Birmingham has been reported in the March-April 2008 issue of Photochem Photobiology journal (2). Two observations from this research are of special relevance to us here. One, it is the CD11b+ cells, which are the major source of oxidative stress in UV-irradiated skin, were inhibited by Silymarin. The flavonoid also suppresses the infiltration of leukocytes that UV exposure had induced. The second important observation is that Silymarin not only halts UV damage, it also acts as a preventive measure. Another researcher has gone one step ahead with the identification of yet another reversal that this chemical performs to UV action: it reduces the volume of H2O2-producing and cytokine interleukin-10 producing cells, both of whose generation is activated by UV (6).

Nearly the same conclusion has been arrived at by researchers working in the Department of Pharmaceutical Sciences at the University of Colorado (3). Their research has shown a positive effect of Silibinin on the repair of UVB-induced DNA damage. Another experiment conducted at the Department of Dermatology of the University of Alabama has observed the inhibition affect that the flavonoid has on tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate, mezerein, benzoyal peroxide and okadaic acid (4).

Topical application of Silibinin prior to, or immediately after, UV irradiation has been found to inhibit thymine dimer positive cell generation that UV induces in the epidermis (5). This research has also shown that terminal sunburn cell formation that is again induced by UV is inhibited too, when Silibinin is applied.

A strong case for Silymarin being a very effective agent in inhibiting and reversing carcinogen and tumor-promoter-induced cancers is made by two independent researches. In both the experiments (7), (8), it has been reported that Silibinin inhibits cancer-causing cells (ERK1/2 activation) and promotes benign cells (JNK1/2, p38), making it an effective cancer-intervention agent for cancer.

A paper published in the journal “Cancer Research” details yet another in-depth investigation carried out on the efficacy of Silymarin as a possible intervention agent against Stage I and Stage II tumors (9). The paper reports that the milk thistle extract has been found to be especially useful in Stage I tumor suppression, and inhibits edema, hyperplasia, proliferation index and oxidant state which take place due to UV irradiation. This same result has been arrived by an independent group of researchers, who used a different chemical to induce skin edema in mice (10).

From the above researches being conducted around the world, it may safely be concluded that Silymarin is proving to be very effective in inhibiting UV-induced skin damage, and the day may not be far when milk thistle becomes one of the major ingredients in sunscreen lotions.

References

Svobodová A, Zdarilová A, Walterová D, and Vostálová J. Flavonolignans from Silybum marianum moderate UVA-induced oxidative damage to HaCaT keratinocytes. J Dermatol Sci. 2007 Dec;48(3):213-24. Epub 2007 Aug 3.

Katiyar SK, Meleth S, and Sharma SD. Silymarin, a flavonoid from milk thistle (Silybum marianum L.) inhibits UV-induced oxidative stress through targeting infiltrating CD11b+ cells in mouse skin. Photochem Photobiol. 2008 Mar-Apr;84(2):266-71. Epub 2007 Nov 28.

Singh RP, and Agarwal R. Mechanisms and preclinical efficacy of silibinin in preventing skin cancer. Eur J Cancer. 2005 Sep;41(13):1969-79.

Katiyar SK. Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects. Int J Oncol. 2005 Jan;26(1):169-76.

Dhanalakshmi S, Mallikarjuna GU, Singh RP, and Agarwal R. Silibinin prevents ultraviolet radiation-caused skin damages in SKH-1 hairless mice via a decrease in thymine dimer positive cells and an up-regulation of p53-p21/Cip1 in epidermis. Carcinogenesis. 2004 Aug;25(8):1459-65. Epub 2004 Mar 19.

Katiyar SK. Treatment of Silymarin, a plant flavonoid, prevents ultraviolet light-induced immune suppression and oxidative stress in mouse skin. Int J Oncol. 2002 Dec;21(6):1213-22.

Singh RP, Tyagi AK, Zhao J, and Agarwal R. Silymarin inhibits growth and causes regression of established skin tumors in SENCAR mice via modulation of mitogen-activated protein kinases and induction of apoptosis. Carcinogenesis. 2002 Mar;23(3):499-510.

Jifu Zhao, Moushumi Lahiri-Chatterjee, Yogesh Sharma and Rajesh Agarwal. Inhibitory effect of a flavonoid antioxidant Silymarin on benzoyl peroxide-induced tumor promotion, oxidative stress and inflammatory responses in SENCAR mouse skin. Carcinogenesis, Vol. 21, No. 4, 811-816, April 2000.

Lahiri-Chatterjee M, Katiyar SK, Mohan RR, and Agarwal R. A flavonoid antioxidant, Silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model. Cancer Res. 1999 Feb 1;59(3):622-32.

Zhao J, Sharma Y, and Agarwal R. Significant inhibition by the flavonoid antioxidant Silymarin against 12-O-tetradecanoylphorbol 13-acetate-caused modulation of antioxidant and inflammatory enzymes, and cyclo-oxygenase-2 and interleukin-1-alpha expression in SENCAR mouse epidermis: implications in the prevention of Stage I tumor production. Mol Carcinog. 1999 Dec;26(4):321-33.

In the last two articles we have covered the types of UV damage, and looked at the current range of common ingredients. With that out of the way, it is time to cover botanical sun care.

The simple truth is that, with the issues surrounding some of the chemical UV protection ingredients, you may not always want to lather up. When it comes to those days that you will spend hours out in the sun, the benefits outweigh the risks, and you should protect yourself from the suns damage.

For the days that you won’t be in the sun for long periods of time, though, it is better to use botanical products. Many botanical ingredients provide anti-oxidant protection, have anti-inflammatory properties, and have been shown to be able to repair the suns effects.

The advantage to using botanical sun products is that you aren’t covering your body in harmful chemicals. For the times that you are using the chemical products, a good botanical antioxidant can also provide protection against the damaging effects of the sunscreen itself.

Botanical Sun Care Ingredients

Studies are currently being done into botanical ingredients that provide UV protection. Some of the ingredients that I have listed do provide mild UVB protection, but they aren’t adequate for long term exposure. What you really want when you start to make a sun care product, from botanicals, are ingredients that provide antioxidant protection, and ingredients that help to repair the suns damage.

With that let’s look at some botanical ingredients that work well for sun care. The idea that some ingredients are better than others does hold true here, and I have tried to indicate the best ingredients for the job.

Botanical Antioxidants and Sun Care Ingredients

Conclusion – Protect Yourself

With the last three article we have covered UV damage, and how to protect yourself. You should now have a good knowledge of ingredients that can be harmful, and those that work for you. With this last article you also have a good guide to ingredients to use in your botanical sun care products.  When it comes to sun protection and to DIY skin care, choosing the right ingredients for the job is important to ensuring your skin’s health!

This is BulkActives’ current list of active ingredients, cosmeceuticals, or skin actives for DIY and make your own, homemade skin care products:

Allantoin

Alpha Lipoic Acid (Thioctic acid, RS-ALA)

L-ascorbic Acid (Ascorbic Acid, L- , Vitamin C)

Ascorbyl Tetraisopalmitate (Tetrahexyldecyl Ascorbate)

Beta 1-3 Glucan YEAST (70%)

Beta 1-3,1-4 Glucan OAT(90%)

Beta Hydroxy acid (Salicylic Acid)

Bisabolol,Alpha (Natural)

Boswellia serrata

Centella Asiatica

CoEnzyme Q10 (CoQ10, Ubiquinone)

Dipotassium Glycyrrhizinate

DMAE Bitartrate

D-Panthenol USP (liquid)

Ellagic Acid

Ferulic Acid (Natural)

GABA

Gamma oryzanol

Ginkgo Biloba

Glucosamine (N-acetyl-D)

Glycyrrhizinic acid

Grape seed proanthocyanidins

Green Tea EGCG (90%) – white

Gynostemma

Hyaluronic Acid (NaH)

ultra low weight Hyaluronic Acid (ULMW NaH)

Idebenone

Jiaogulan

L-carnitine

L(+) Lactic acid

Magnesium Ascorbyl Phosphate (MAP)

Niacinamide

Pantothenic acid

Pine Bark Proanthocyanidins (95%)

Pomegranate Extract (Ellagic acid 40%)

Quercetin

Resveratrol (98%) – white

Saw Palmetto

Silymarin

Soy isoflavones

White Willow – bark extract

Wild Yam

It is fairly common knowledge that the sun has damaging effects on the skin. Anyone who has spent anytime soaking up the sun’s rays can likely tell you all about sunburns, and anyone who has ever read a newspaper or watched the evening news will likely be able to tell you that the sun is responsible for many types of skin cancer. What most of us aren’t aware of, however, are the different types of UV light and the effects that they can have on our skin.

In this article we will look at the different types of UV radiation, and how they affect us. In a world where skin cancer is now the leading cause of cancer-related deaths, understanding the sun is more important than ever.

UVA, UVB, and UVC Rays

To begin our look at the sun’s damaging rays let’s first begin with a look at the different types of UV radiation. When we generalize, without getting extremely scientific, there are three basic types of UV radiation. They can be divided into categories according to wavelength:

• UVC: 100-290nm
• UVB: 290-320nm
• UVA: 320-400nm

The two types of UV rays that have damaging effects on the skin are UVB, and UVA rays. The other type, UVC, is absorbed by the atmosphere and has no damaging effects.

UVB Rays

The most well known type of UV ray is UVB. These rays vary throughout the day, and are at their highest from 10am to 2pm. The summer months tend to be the worst for UVB damage, accounting for 70% of most people’s exposure.

UVB rays are responsible for tanning, sunburns, and in general cause the most immediately visible damage.UVB is generally considered to be the most potent and damaging type of UV light. It directly affects the epidermis (upper layer of skin), and causes damage quickly.

This is what most sunscreens protect against. In fact, that Sun Protection Factor (SPF), which is listed on your commercially bought sunscreen, directly correlates to UVB protection.

UVA Rays

The other type of UV light that causes harm is UVA. There are actually two types of UVA rays: shortwave UVA (also known as UVA II), and long-wave UVA (UVA I). The second type (UVA I) is the one that is most damaging to the skin.

Until recently UVA light was thought to have little effect on the skin. Recent studies have altered that perception.

UVA light is different than UVB in that it has some unique qualities. Firstly, it isn’t more prevalent at any time of the day. Whenever the sun is up, UVA light remains constant. It is also different in that it cannot be filtered by common glass. Window glass and automobile glass cannot stop UVA rays from passing through.

UVA has the ability to penetrate deep within the skin to affect the dermis. Its effects are more long term, and exposure to UVA light can build with time. Most sunscreens do not protect against UVA light, and until recently actually, none of them did.

Understanding the Effects of UVA and UVB Exposure

With a basic understanding of UV light, let’s begin to discuss how sunlight really affects the skin. Exposure to the sun has both short and long term effects, and understanding those dangers is the first step in being able to protect yourself.

Short-term Effects of UV Exposure

UVB light is responsible for most of the shorter term effects of sun damage. These include: sunburn, discoloration, tanning (yes a tan is damage to), and skin hyperplasia, as well as other short term effects. Too much exposure to UVB light leads to a thickening of the outer layer of skin. This is the body’s natural defense but can also cause more damage, since it also causes the epidermis to absorb and scatter more of the UVB light.

The most damaging effects of UVB light come with sunburn. Acute sunburn can lead to even more damage. The most danger occurs when the skin peels.

Peeling occurs when the body kills its cells as a last ditch effort to repair the outer layer of skin, this process is called Apoptosis. The problem is that when this occurs, under certain conditions that come with UV exposure, the body is unable to properly kill the cell. This can lead to a damaged cell that divides and turns into a tumor, and even becomes cancerous.

Some of the other short term effects of exposure to both UVB and UVA light include:

1. A reduction in  collagen production
2. An increase in free radicals which prevent normal cell function
3. Damage to enzymes  that repair DNA
4. Negative effects on your immune system as a whole.
5. Free Radical Production that causes damage to the cells, and also causes serious long term effects.

Long Term Effects of UV Exposure

The long term effects are where things begin to get even scarier. Both UVA and UVB light have long term effects.

One thing that should be noted is that exposure to UVA light builds over time. Unlike UVB exposure where the epidermis is damaged and the body then repairs it, UVA exposure adds upon itself. In other words – 5 minutes today, 1 hour in the sun tomorrow, 3 hours on the beach last Friday, and tomorrows trip to the zoo – all combine and add to the damage that has already been done.

This leads to a few common long term problems. These include free radical damage, photo-aging, and photocarcinogenisis.

Free Radical Production: One of the long term effects of UV exposure is free radical production. Free radicals are chemical particles that have at least one malfunctioning or missing electron. In the skin the most common free radicals are oxygen molecules. These tiny particles have the ability to chip away at a cell, causing it damage. After a cell is damaged the free radicals can further damage DNA and RNA that actually make the cell. Free radicals contribute to both photo-aging, and photocarcinogenesis.

Photo-Aging: UVA light is the type of ray mostly responsible for photo-aging. UVB exposure can add to this by repeatedly damaging the skin, but most UVB light is absorbed by the epidermal layer. UVA gets right under the epidermis.

Photocarcinogenesis: Both UVA and UVB light can cause skin cancer. UVB light does so by causing damage, and promoting free radicals that can alter DNA. Recent studies are beginning to show that UVA light is capable of directly altering DNA through the production of free radicals as well, which can lead to malignant tumors and even cancer.

The simple truth is that a basic understanding of UV light and the damage it can cause is the first step in protecting yourself from the negative effects of the sun.

References

Negishi, K; Higashi, S; Nakamura, T; Otsuka, C; Watanbe , M; Negishi, T. (2007) Oxidative DNA Damage Induced by 364-nm UVA Laser in Yeast Cells. Originally published by the Japanese Environmental Mutagen Society. Accessed online July 16^th 2008 from http://www.jstage.jst.go.jp/article/jemsge/28/2/74/_pdf

Brannon, Heather MD. (March 23, 2008). Effects of Sun on the Skin: Cellular Skin Changes Caused by UV Radiation. Article hosted on about.com. Accessed July 16^th, 2008 from http://dermatology.about.com/cs/beauty/a/suneffect.htm

Hugget, J. (June 28, 2005) Less Than Full Protection: Most Sunscreens Do Only Half the Job, Blocking Unsafe UVB Rays But Not Skin-Damaging UVA. Can We Get Better Cover. Washington Post. Accessed July 16^th 2008 from http://www.washingtonpost.com/wp-dyn/content/article/2005/06/27/AR2005062701099.html

Eldich, R Dr. and Various other Authors (2004) Photoprotection by Sunscreens with Topical Antioxidants and Systemic Antioxidants to Reduce Sun Exposure.  Journal of Long-Term Effects of Medical Implants. Begal House Inc. Accessed July 16^th 2008 from http://www.pacificcenterplasticsurgery.com/articles/Photoprotection-by-Sunscreens.pdf

Reinheckel, Thomas,  Bohne, Marisela,  Halangk, Walter,  Augustin, Wolfgang,  Gollnick, Harald. Evaluation of UVA-mediated oxidative damage to proteins and lipids in extracorporeal photoimmunotherapy. A Study hosted on findarticles.com Accessed July 16^th 2008 from http://findarticles.com/p/articles/mi_qa3931/is_199905/ai_n8838478

Columbia-Presbyterian Medical Center, no author listed. Two Cancer Studies: Tomatoes, Green Tea, and Cancer. Originally published in the P&S Journal: Fall 1997, Vol.17, No.3 Research Reports. Accessed July 16^th 2008 from http://cpmcnet.columbia.edu/news/journal/journal-o/archives/jour_v17n03_0009.html