Are the high profile department store brands better than those used by beauty therapists or are they just well marketed with pseudo-science?
The skin care product market is huge: annual sales exceed $3 billion in the UK alone, however professional beauty therapists, aestheticians and skin treatment practitioners see only a very small portion of this revenue.
Why? You may ask. It is not that the products sold by department store chains and direct marketing is any better than the products the therapists sell, it is simply the mass marketing and accessibility that the cosmetic brands provides gives the perception they are.
The reality is in most cases that the department store brands are no more (and in many cases, less) effective than the products sold by salons, its just your customers dont believe it to be the case.
This makes it harder to convince them that the same amount of
money spent on a series of corrective clinic facials as on a flashy department store or direct sales product will give a better and lasting effect.
For most women today, beauty is less about vanity and more about self-confidence, and cosmetics are less about the science and more about emotions. This is why with the millions spent on advertising campaigns and celebrity endorsements you would be forgiven for believing all of the statements of how product X will make your wrinkles disappear virtually overnight are true.
The reality is however that in many countries there are insufficient consumer protection controls in place to force manufacturers and marketers to tell the truth. In many countries, the logic that if it cant harm you, then you dont need to know seems to be the norm.
With formulations for anti-ageing products becoming increasingly sophisticated, the boundaries of product efficacy are being constantly stretched. You would think that when promoting these products, there should be complete transparency and no room for ambiguity when it comes to efficacy claims.
The reality of course is much different.
Cosmetic Vs Therapeutic
Lets think about some of the statements made by some cosmetic companies regarding the efficacy of their products.
If you have products that are indeed making physiological changes to the metabolism of skin cells, restructuring DNA, and regenerating collagen to make wrinkles disappear, then we are talking about therapeutic formulations that could be considered drugs.
(Aestheticians and skin treatment practitioners undertake treatments on their clients that provide these physiological actions every day, however the therapist providing the treatments is appropriately qualified, trained and skilled.)
Therapeutic skin care products are generally not available from retailers, but logically limited to skin treatment therapists as professional products, with the prescription and use of them based
on the findings of a skin analysis consultation.
In fact, any product that has physiological altering properties should be only be used when the outcome is predictable. A typical example is retinoid reactions when too stronger concentration of vitamin A is used on a particular skin type and condition.
This therapeutic class of products in some countries also falls under the administration of some form of therapeutic goods legislation, where false and misleading efficacy statements are considered illegal and punished with reprimands and the kind of publicity that cosmetic companies try to avoid at all costs.
An example of enthusiastic marketing claims catching up with cosmetic companies was played out in Australia in early May 2007, where an astounding five top cosmetics manufacturers were ordered to withdraw advertisements after complaints to Australia's Therapeutic Goods Administration. (TGA)
Brands included in the complaints were Lancome, Clinique, Estee Lauder, L'Oreal and Payot.
The TGA's complaints panel established that the advertised creams, peels and serums were only cosmetics, however the companies were making claims that led consumers to believe that they were therapeutic formulations that would make a physiological difference.
Claims Vs Reality
In the case of Estee Lauder, the company argued that because they were known as a cosmetics company and their product Perfectionist Correcting Serum was being advertised in a fashion magazine "readers could not reasonably expect the product to have a therapeutic use".
They also testified to the TGA that the product used optical technology among other methods to blur the effect of wrinkles. This revelation was despite advertising promising that their AUD $160 product could fill in and smooth out expression lines instantly and "helps the skin amplify its natural collagen production".
The TGA complaints panel concluded it was unable to accept the claim was merely cosmetic and had "no doubt" it was intended as a therapeutic claim. This was due to the fact that consumers would reasonably believe that the expression lines would be instantly removed by biological means.
In the case of Payot, the TGA panel said it was concerned about the comparison they had made between its AUD$175 Payot Rides Relax to injections of the wrinkle-relieving toxin Botox.
The panel subsequently ordered Payot to withdraw its claims that the serum was "wrinkle correcting".
In Europe, cosmetic manufacturers and marketers have been facing similar scrutiny over advertising claims, with direct selling leader Avon being reprimanded in early 2007 by the UK Advertising Standards Agency (ASA) over a misleading advertising campaign for an anti-aging face cream that claimed to be a face lift in a jar.
In a ruling published by the ASA, they stated that the claims were unfounded and the company did not have (or could not provide) any comprehensive scientific evidence to support the claim, despite carrying out a consumer study.
In another case, cosmetics giant Clinique was investigated by the ASA for displaying misleading content regarding their anti-ageing treatment, Repairwear. In the advert, Clinique stated that the cream enabled the skin to steer hearty cells to the base of wrinkles, thus triggering the skins own natural collagen production.
An expert at the ASA testified that Clinique had not tested the product on consumer's skin and therefore the accuracy of the claim was not valid. The tests had been in fact undertaken in a laboratory environment.
The reprimanding of cosmetics giants for misleading claims is not new. Back in 2005, L'Oreal had a number of complaints against a series of adverts featuring celebrity model Claudia Schaffer promoting anti wrinkle and anti cellulite products upheld by the UK Advertising Standards Agency (ASA).
In the wrinkle cream advert, it was claimed that 76% of users had reported a visible reduction in expression lines over a three week period and that wrinkles could be reduced in the space of just one hour, an assertion that was considered by the panel to be extreme because the product could be reasonably understood to have a 'physiological action with a cumulative effect'.
Claims about the product's inclusion of Boswelox to counteract micro contractions was also investigated, and after consulting its own experts in the field, the ASA concluded that L'Oreal's specific reference to the product's effects on expression lines were unsubstantiated - a key point that was emphasised by Schaffer pulling a variety of different faces in the advert.
With the anti-cellulite product, the agency upheld complaints made against a product called Perfect Slim specifically claims that 71 % of women in a study had said it had visibly reduced the appearance of cellulite.
In upholding the complaint about the study, an ASA expert had examined the results of the trial but had found no evidence to support the claims, as it had been open and used no control or blind testing. Further details also proved that half of the individuals taking part in the study had not registered the improvement claimed.
Its all a matter of interpretation
It would appear that in some cases, cosmetics companies somehow confuse product popularity and customer satisfaction with efficacy and actual documented results. It is well known that product popularity and satisfaction is directly associated with customer self-assessment, (which at best is subjective) and this is in no way scientific evidence to support efficacy claims.
Unperturbed, they are encouraged to continue to make claims that make good marketing copy rather than provide factual information.
Despite all the diversional tactics of the marketers, independent experts such as consultant dermatologists believe that most of the research carried out by the cosmetic companies is indeed legitimate, with all of the cosmetics giants having good scientific grounding. The problem is however, that the science within the products is not so much in dispute as the techniques employed by some of these companies to cloud the science and therefore mislead consumers.
Why you ask go to all the bother if the product works so well? Why not simply tell the truth?
Thankfully, the action taken by the Australian and British authorities points to mounting pressure on the cosmetic companies to substantiate claims for cosmetics products that are said to make physical improvements to the skins appearance.
Interestingly, professional skin care companies will rarely make claims of how well a particular product will work, only point out the potential for success if used appropriately. This is because they are well aware that the ultimate success will only come from the therapists knowledge and skill in performing the treatments and the clients willingness to follow up with their prescribed home care. This is something that consumers with high expectations also need to understand.
What you can do
There is fierce competition between cosmetics companies to continue to innovate new products, and this is good for all of us. Much of the research and experimentation for department store brands is used by professional skin care manufacturers, and with hundreds of millions of dollars and thousands of researchers worldwide looking for the next big thing in a skin care breakthrough, it ultimately means that we have access to high-tech skin care products at affordable prices.
Perhaps it is time to start marketing your own treatments using cues from the mainstream cosmetics companies.
Start compiling case histories of your most positive client outcomes, and use them to promote the real differences you can make. Ensure every client is prescribed appropriate take-home care products with detailed instructions on their use. More importantly, don't give them a reason to go elsewhere to buy department store skin care.
Its time for you to take your bigger slice of the multi-billion dollar skin care pie.
© 2007 Virtual Beauty Corporation
Have you observed at the end of a long treatment program for pigmentation that some pigment just does not respond to treatment? The frustration, disappointment and dashed expectation experienced by both client and therapist cannot be described.
The pigmented anomalies you are observing are not pigmented lesions caused by melanin, but a colored anomaly that has a similar appearance: Lipofuscins.
Initial analysis is not easy; they will however, not always follow the normal pattern of pigmentation. They are often linked to trauma like surgery, over use of sun beds and chemical burns, and will be found in most Fitzpatrick skin tones, with a greater predominance in the Fitzpatrick 3 & 4 category.
The lesion will not respond to IPL because the chromophore is in fact not melanin.
I have observed this type of pigmented lesion for many years not fully understanding what it was, but I had however linked part of the cells & systems involved and affected to other similar skin conditions.
An example is the type of pigment that occurs from bruising or damage involving the vascular system, and I think the best example of this pigmentation is the lesion often seen after scelotherapy or the removal of varicose veins. To see this pigment at a cellular level will help you choose a more appropriate treatment option.
Cells and systems involved with the formation of Lipofuscins
Lipofuscin is a yellow-brown pigmented waste material deposited in many nerve and skin cells, where it
is believed to interfere with cellular metabolism. Lipofuscin is made up of cross-linked, peroxidized lipids and cross-linked proteins (Glycation). Lipofuscin deposits in skin are easily misdiagnosed as solar lentigines.
Lipofuscin remains after the breakdown and absorption of damaged blood cells and understandably, these deposits of lipofuscin debris increase with aging. They can be found in deep organ tissues as well as in skin tissue. Lipofuscin is merely a sign that other deleterious reactions have already taken place.
For example; free radicals and toxic aldehydes may react with the cross-linked proteins, causing damage and leaving lipofuscin as a superfluous by-product.
I believe the terminology peroxidized lipids also requires further discussion because Lipofuscins can begin at this point also.
Lipid peroxidation refers to the oxidative degradation of lipids. It is the process whereby free radicals `steal' electrons from the lipids in cell membranes, resulting in cell damage.
This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturated fatty acids like phospholipids, because they contain multiple double bonds in between which lie methylene -CH2- groups that are especially reactive hydrogen.
Living organisms have evolved different molecules that catch free radicals and protect the cell membrane, one of which is alpha-tochopherol also known as vitamin E.
What must be remembered is that Vitamin E is not a very efficient anti-oxidant and can only neutralise small amounts of free radicals before it becomes inactive.
For this vital resident antioxidant to be continually effective within a cell membrane Vitamin C must be available, because Vitamin C will reactivate Vitamin E
so it may continue the antioxidant process.
I think this really reinforces the synergy of cells and systems and one must always be aware of what works with what, so that the complete story is understood.
Understanding that the health of a cell membrane is imperative to skin health may seem a little fundamental, however a cell can only perform and make what it was genetically designed to do, if it itself is in good health.
A cell membrane is a complicated and intricate eco system that requires better understanding if one is to embark on treatment programs that may improve skin appearance.
Cell health has to always be part of the preparatrory phase of the treatment program otherwise very limited results will occur.
Now that you have a better understanding of the cause and effect of Lipofuscin, let us turn our minds to treatment.
Cell preparation will be a basic part of dispersing this anomaly, and the client will have to make a commitment to cell nutrition to obtain the best result. The daily topical application of actives and weekly salon treatments will be the basis of this treatment program.
It has been proven that some remedies and actives do exist. They will not be prevalent in products just yet, but some innovative formulators have sourced and include these actives into modern skin lightening ranges. In doing so they have covered their bases in the treatment of all pigmented anomalies. This has come about from the understanding that Lipofuscins are not easily discernable from melanin based pigmented lesions like solar lentigines, and the Lipofuscin lesion does have a UVR exposure element in its formation.
Lipofuscin treatment actives
You will be seeking formulations with the following active ingredients:
DMaE, or dimethylaminoethanol. This naturally occurring substance has been shown to help cells rid themselves of lipofuscin, while allowing them to retain useful nutrients. DMaE also helps strengthen cell walls, resulting in better skin tone and elasticity.
Alpha Lipoic Acid: another naturally occurring antioxidant that has the benefit of being both water and oil soluble. This enables the antioxidant to have a effect both inside & outside the cell and the cell membrane. From a formulators point of view this is an added advantage. If something can applied to skin that the cells and systems already recognise there is less chance of an adverse inflammatory response occurring within skin.
Retinyl palmitate, of the vitamin A family is now well known to have nothing but positive effects on skin cells. This vitamin works in synergy with Vit C & Vit E so is part of the triangle of antioxidants that will benefit lipofuscin lesions. Of course even the simple beta carotene that is so undermined as an antioxidant would have to be considered of benefit to this condition, my main reason for this is that an antioxidant it can quench vast numbers of free radicals, is stable in formulations and will sit happily alongside most other actives.
Vitamin E (Tocopherols): Due to its multifunctional abilities and roles in skincare, Vit E is one of the most valuable of all the vitamins. Naturally occurring vitamin E is responsible for the protection and maintenance of the lipids and lipoproteins in the cell membranes of the heart, muscles and blood vessels. It also assists the skins water binding ability. These properties help maintain healthy connective tissue and epidermis. The vitamin has shown proven biological activity as an anti-oxidant, anti-inflammatory and free radical scavenger, making Vitamin E a necessary part of any anti-ageing formula.
It is important to remember that the effects of Vitamin E is assisted by Vitamin C: When Vit E has had a neutralising effect on a free radical it becomes inactive. Vitamin C reactivates Vit E to continue working as an antioxidant, completing the triangle of these cellular antioxidants.
Essential Fatty Acids: EFA's are often referred to as Vitamin F, and consist principally of unsaturated linoleic, linolenic and arachidonic acids. Deficiency of essential fatty acids lead to abnormally enhanced transdermal water transport in addition to dryness, scaly skin.Essential fatty acids (EFA's) form the basic building blocks of body fats, biological membranes and prostaglandins. Any deficiency of the essential fatty acids will lead to a reduction in the formation of prostaglandins, eventually resulting in compromised cell membranes.
Correctly identifying Lipofuscin before treating with conventional pigment modalities will mean the chances of making a difference will be greater.
The quest for the achievement of the perfect skin goes on, repair of damaged proteins being the greatest challenge. The race is on and with every year that passes more and more weapons to treat the damaged ageing skin are being developed.
I do however believe that prevention is easier than cure; and you the skin treatment therapist can easily achieve this by giving preventative protocols and products to young clients and by raising early awareness of the effects that nutrition, environment and genetics can have on skin cells.
By offering anti-ageing treatments clients during their 20's, and by continuing your own education you will be in a position to offer effective long term solutions to clients and keep them for a longer period of time.
2006 Virtual Beauty Corporation
The skin has various regeneration and repair mechanisms. These are employed to eliminate any damage caused by external influences and to restore lost function
Reactions of the horny layer
The action of external mechanical, physical or chemical irritants causes the horny layer to thicken. Typical examples are the thickening found after intensive UV radiation and the formation of calluses on areas subject to mechanical stress (palms of the hands and soles of the feet).
Regeneration following UV-related damage
Intense UV-exposure causes primary damage to the genetic material. Secondary damage is inflicted on the cell proteins and membranes by UV-induced free radicals.
The skin is known to have many mechanisms for the repair of damaged DNA. In humans the most important are the excision repair and post-replication repair mechanisms: The excision repair mechanism is based on recognition, removal and replacement of the damaged DNA segment.
This way mutations are prevented as long as the repair mechanism is not overburdened or defective.
The post-replication repair mechanism, on the other hand, works around the damaged DNA segment, meaning that it is ignored when the genetic code is read. Only later is the damage repaired. This mechanism is so faulty however, that often more mutations are caused by the repair than by the original radiation damage.
Regeneration following ablative skin injury
The epidermis does not scar
The layer of epidermal mother cells - the basal layer - ensures a steady renewal of the epidermis, through continual cell division (proliferation). If an injury is confined to the uppermost skin layer, this damage, known as erosion, can heal without scarring. It can however pigment.
The dermis does scar
If the damage reaches the dermis (e.g. an ulcer) and thus involves the basal membrane (dermal epidermal junction), then healing is usually accompanied by scar formation. When this happens, destroyed epidermal cells are replaced by connective tissue.
Ablative wound-healing in several consecutive stages:
1. Inflammatory Response (1 to 5 days)
On initial damage the Mast Cells in the tissue release Histamine.
Which triggers the inflammatory response, the local capillaries & arterioles dilate to improve blood circulation to the area.
The capillary walls open up slightly to allow fluid, Inflammatory Exudate (IE), to pass into the tissue. The IE contains antibodies to neutralise any foreign material and precursors to fibrin which gets laid down in a mesh to prevent the spread of any foreign material. IE will also contain leucocytes, which move through the capillary walls, to remove foreign material and dead tissue by phagocytosis.
If bleeding has taken place, Haemostasis occurs soon after the injury. Platelets in the area of the wound build up a plug over the damage and release Serotonin. Serotonin cause the blood vessels to contract and reduce the blood flow. If this is insufficient to stop the bleeding then a series of chemical messengers starts the Clotting Mechanism. This results in large quantities of fibrin being laid down in the area to bind everything together. Hence a scab contains, dried blood cells, dried inflammatory exudate (and its white blood cells), platelets and any foreign matter not washed away by the flow of blood and exudate.
After the initial rush of the Inflammatory Response. It is the period when the leucocytes and the later arriving macrophages remove the dead tissue and foreign material and the fibrin net (blood clot) laid down in the tissues is dissolved.
The mighty macrophage is the key player, these white cells have both scavenger and non-scavenger functions. With no slight intended to the other inflammatory cells, without macrophages there is no healing or what healing occurs is poor.
Macrophages release tissue destroying enzymes to rid the wound of debris, leaving room for healthy cells to fill the void.
The macrophage is critical to the inflammatory stage of wound healing and also essential to new tissue development through macrophage derived growth factors (MDGF).
It will take 3-5days for the macrophages to stimulate the differentiation of fibroblasts, this next phase of wound healing is called the fibroplastic stage. The fibroplastic phase is usually established within 5 days of wounding and last for up to 4 weeks.
2. Fibroplastic stage (5 days to 4 weeks)
Fibroblasts that are normally found in low numbers in the dermis, proliferate in the wound and migrate with the help of the growth factors (MDGF) and a very important glycoprotein called fibronectin. Fibronectin acts as a conduit for fibroblasts. It binds to both the wound matrix and the fibroblast, allowing the fibroblast to march down it (the fibronectin), move along the chemotactic gradient of growth factors, and take up residence in the wound.
Once in the wound, fibroblasts begin to synthesize wound collagen (type 3) fibres and produce proteoglycans, structural proteins, and adhesive proteins -- connective tissue ground substances. Other fibrous protein in the wound include elastin and reticulin.
Vitamin C, iron, and copper are essential to the synthesis of collagen, which constitutes 50% of the protein found in scar tissue.
New blood vessels start to infiltrate the wound (Granulation Tissue)
Collagen, however, cannot be synthesized in the absence of adequate oxygen supply, and the wound has derailed blood flow. Angiogenesis is required. Through their enzymatic actions, growth factors break down the vascular membrane of the venules. Endothelial cells that migrate through the defect aggregate to form vascular buds. Buds connect with contiguous buds to form loops. Loops develop a basal membrane from extracellular matrix components and then develop their own vascular buds.
This process continues until contact is made with an intact blood vessel and a capillary loop forms with directed blood flow. The wound is now adequately re-perfused and this has all been accomplished within days of the trauma. New highly vascularized tissue has a granular appearance (which may be why it's called granulated tissue), and is recognizable by its visible pinhead-size rounded nodules. Nodules that are dark red in color and appear moist and shiny indicate good healing. Poor healing is indicated by a bluish color and a smeary fibrin appearance.
The type 3 (wound) collagen initially laid down by the fibroblasts, has been temporarily holding the wound together while healing. The wound collagen is haphazard in its layout and not very strong.
The type 3 collagen will now begin to change to type1 collagen, giving strength and structural integrity back to the wounded area by being reorganized into regularly aligned bundles oriented along the lines of stress in the healing wound. This is done by the enzyme collagenase. (Green packman looking object in picture (left).
Having formed abundant collagen fibres, the fibroblasts transform either into fibrocytes or myo-fibroblasts.
Myo-fibroblasts in the wound area are responsible for wound contraction; the normal process where the edges of the wound migrate toward the wound centre.
Epithelial cells divide and migrate over the basal layers to regenerate the epithelium.
Basal cells continue to divide until the epithelial stratification is restored. When the coverage of the wound surface beneath the scab is complete the scab sloughs off and the epidermis begins to keratinise. Remodelling of the collagen matrix may continue for years with the extent varying among individuals and with age. The scar is rarely as strong as the tissue it replaced.
© 2003 Virtual Beauty Corporation