Dimethyl Isosorbide (DMI) is a high purity solvent and carrier which offers a safe, effective delivery enhancement mechanism for active ingredients in personal care products. Sunless tanners, facial and eye-zone treatments, skin serums, anti-acne formulations and make-up removers are just some of the products whose performance can be improved with the use of Dimethyl Isosorbide (DMI) in formulation. In addition to improving performance, its use as an epidermal penetration enhancer can allow formulators to reduce the amount of actives required to achieve effects, resulting in reduced formulation costs, and lower skin irritation with aggressive active ingredients.

Active ingredients for skin care formulations are only as effective as the delivery system. The more efficient the delivery system, the more likely it is that the active ingredient will perform as intended. Consider all of the benefits made possible by Dimethyl Isosorbide delivery enhancer, a safe carrier ingredient proven to place active ingredients where they are needed most on skin. A water-white liquid with excellent solvent properties,Dimethyl Isosorbide offers formulators the option to boost the penetration of actives in the epidermis layer of skin, enabling targeted delivery for products such as self-tanners, anti-acne treatments and more.

Consumers of skin care products will notice the difference in products formulated with a delivery enhancement agent. Test results show that Dimethyl Isosorbide contributes to fast color development of sunless tanner, with less streaking and longer lasting tan as compared with self-tanner products without the carrier ingredient. In other specialty products, such as eye-zone treatments, skin serums, scalp treatments, Dimethyl Isosorbide may be used to enhance skin penetration. The unique solvency properties of Dimethyl Isosorbide boosts performance of formulations such as make-up removers.

The skin care formulators’ performance booster

Ask consumers why they use a skin care product and chances are good they will purchase one they perceive to be effective. Formulators can improve the odds that an active ingredient will work to the benefit of the consumer in products designed for skin treatment. With Dimethyl Isosorbide, the formulator can enhance the delivery of active ingredients without having to add more active. Effective delivery of actives such as salicylic acid, Vitamin C, lactic acid, hydrocortisone and hyaluronic acid can even reduce the active ingredient concentration requirement, serving to reduce the formulation cost of finished products.

Other benefits of Dimethyl Isosorbide:

• Dimethyl Isosorbide offers enhanced penetration of actives to the epidermis, enabling targeted delivery.
• Dimethyl Isosorbide provides a lower level of skin irritation with a reduction in the required concentration level of aggressive actives.
• Dimethyl Isosorbide gives improved formulation shelf stability, including those susceptible to hydrolysis and transesterfication.
• Dimethyl Isosorbide has miscibility with most organic solvents and non-ionic surfactants.
• Dimethyl Isosorbide allows incorporation within many product forms, including clear gels.
• Dimethyl Isosorbide has a long history of safe usage.
• Dimethyl Isosorbide has the ability to transport water soluble actives into skin, without recrystallization of the active.
• Dimethyl Isosorbide has the ability to produce formulations with standard equipment, without the need for flammable materials handling.

Buy Arlasolve DMI / Dimethyl Isosorbide

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

Active ingredients for skin care formulations are only as effective as the delivery system. The more efficient the delivery system, the more likely it is that the active ingredient will perform as intended. Consider all of the benefits made possible by Arlasolve DMI delivery enhancer, a safe carrier ingredient proven to place active ingredients where they are needed most on skin. A water-white liquid with excellent solvent properties, Arlasolve DMI offers formulators the option to boost the penetration of actives in the epidermis layer of skin, enabling targeted delivery for products such as self-tanners, anti-acne treatments and more.

Consumers of skin care products will notice the difference in products formulated with a delivery enhancement agent. Test results show that Arlasolve DMI contributes to fast color development of sunless tanner, with less streaking and longer lasting tan as compared with self-tanner products without the carrier ingredient. In other specialty products, such as eye-zone treatments, skin serums, scalp treatments, Arlasolve DMI may be used to enhance skin penetration. The unique solvency properties of Arlasolve DMI boosts performance of formulations such as make-up removers.

The skin care formulators’ performance booster

Ask consumers why they use a skin care product and chances are good they will purchase one they perceive to be effective. Formulators can improve the odds that an active ingredient will work to the benefit of the consumer in products designed for skin treatment. With Arlasolve DMI, the formulator can enhance the delivery of active ingredients without having to add more active. Effective delivery of actives such as salicylic acid, Vitamin C, lactic acid, hydrocortisone and hyaluronic acid can even reduce the active ingredient concentration requirement, serving to reduce the formulation cost of finished products.

Other benefits of Arlasolve DMI include:

• Enhanced penetration of actives to the epidermis, enabling targeted delivery
• A lower level of skin irritation with a reduction in the required concentration level of aggressive actives
• Improved formulation shelf stability, including those susceptible to hydrolysis and transesterfication
• Miscibility with most organic solvents and non-ionic surfactants
• Incorporation within many product forms, including clear gels
• A long history of safe usage
• Ability to transport water soluble actives into skin, without recrystallization of the active
• Ability to produce formulations with standard equipment, without the need for flammable materials handling

Arlasolve DMI / Dimethyl Isosorbide

Preservatives are chemicals that kill bacteria, fungi and molds. They are commonly present in ANY product that contains water. For this reason, oil-based skin care products and anhydrous (water free) skin care products, do not need preservatives.

However, creams, lotions and any other product where water is present, require adding a preservative.

If you do NOT use a preservative, or if you decide to believe the hype and try out a ‘natural’ preservative (such as grapefruit seed extracts), then you are putting yourself, and your skin, at RISK.

The only way you can avoid using preservatives is if you make your products FRESH every week, and store them in the refrigerator. This is what we, at BulkActives, do.

We have now started carrying three preservative systems. None are formaldehyde releasing, but they do contain other chemicals that have been getting a bad name (phenoxyethanol and the paraben family).

Let me repeat, if you make your products FRESH every week, and store them in the refrigerator, then, and ONLY then, can you avoid using preservatives.

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.