I sometimes get emails asking me about the purity of our products.  This is usually because of names like ‘Green Tea extract (standardized for 90% EGCG)’ or ‘Resveratrol 98%.’

There appears to be some confusion with these percentages and it appears that some people believe that our products use ‘fillers’ and are therefore no good.

Let me explain this

If someone emails me and asks “Are your products pure?” then the answer is “YES.”

They are pure, because we do not add any fillers.  So, that means when you buy our Grapeseed extract, it is 100% Grapeseed extract, NOT 60% Grapeseed extract and 40% red colored flour.

What about those percentages?

The percentages indicate the amount of the active ingredient in the powder.  For example, the active ingredient we want in Grapeseed extract are the Proanthocyanidins.

So, when you see the name Grapeseed extract 95% Proanthocyanidins, then you know that the active is 100% pure Grapeseed extract and that it has been standardized for 95% Proanthocyanidins.

The term used to show you this is the assay (http://en.wikipedia.org/wiki/Assay), we list the assay for all our products on each product’s page.

Why do we sell products that are standardized for 70% or 95%, why not 100%

Well, the more a plant extract is standardized, the more expensive the manufacturing process.  This REALLY makes a big difference.  For example, White Willow Bark extract is standardized for 25.23% Salicin, it costs hundreds of dollars per KG. It is also possible to buy the same product standardized for 95% Salicin, but that will cost THOUSAND of dollars per KG.

So, sometimes it is prohibitively expensive to buy plant extracts that are standardized at a high percentage.

We therefore buy products that are standardized at as high a percentage as possible, while at the same time keeping the price reasonable.

I really do not think you would be willing to spend US$80 for a gram of White Willow Bark 95%, especially when it is easier, a lot cheaper, and just as effective to use Salicylic acid (BHA).

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.

I sometimes get asked how L-ascorbic acid, also know as Vitamin C, ( CAS# 50-81-7) is made and, more often, what the source material is in the manufacturing and production of  l-ascorbic acid.

Here is the process, as I understand it.

First,  cornstarch is used to make Glucose.

Then, using a multi-step method called ‘The Reichstein process‘ , L-ascorbic acid is produced.

Short and sweet, L-ascorbic acid is made from corn.

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.