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.

Lipofuscin will not respond to IPL because the chromophore is in fact not melanin.

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.

Lipofuscins are often confused with solar lentigines because they also has a UVR exposure element in their formation

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

Vitamin E under an electron microscope

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.

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 in active mode

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.

Summary
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.

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