WO2001082878A1

WO2001082878A1 - Treatment of skin damage using acetyl carnitine and phosphatidylcholine and/or ascorbyl fatty acid esters

Info

Publication number: WO2001082878A1
Application number: PCT/US2001/013401
Authority: WO
Inventors: Nicholas V. Perricone
Original assignee: Perricone Nicholas V
Priority date: 2000-05-02
Filing date: 2001-04-25
Publication date: 2001-11-08
Also published as: AU2001259158A1

Abstract

Acetyl carnitine and phosphatidylcholine and/or ascorbyl fatty acid esters are topically applied to treat skin damage, such as contact dermatitis, atopic dermatitis, xerosis, eczema, rosacea, seborrhea, psoriasis, thermal and radiation burns, other types of skin inflammation, and aging. Typical compositions contain from about 0.025 % to about 5 %, more narrowly from about 0.5 % to about 2% acetyl carnitine. Where employed, ascorbyl fatty acid ester concentrations range from about 0.5 % to about 7 %, more narrowly from about 1 % to about 5 %, by weight, and the esters are preferably fat-soluble and saturated. A preferred embodiment contains L-acetyl carnitine, ascorbyl palmitate, and food grade lecithin.

Description

TITLE OF THE INVENTION

TREATMENT OF SKIN DAMAGE USING ACETYL CARNITINE AND PHOSPHATIDYLCHOLINE AND/OR ASCORBYL FATTY ACID ESTERS

CROSS-REFERENCES TO RELATED APPLICATIONS

This application claims priority benefit of U.S. application serial number 09/563,108, filed 2 May 2000.

BACKGROUND OF THE INVENTION

Field of the Invention. This invention relates to the topical application of acetyl-carnitine and phosphatidylcholine and/or fatty acid esters of ascorbic acid for the treatment of acute and chronic skin damage. Therapies according to the invention are particularly efficacious for treating a variety of skin conditions including contact dermatitis, atopic dermatitis, xerosis, eczema, rosacea, sebor- rhea, psoriasis, thermal and radiation burns, other types of skin inflammation, and the tissue degerative effects of aging.

Description of Related Art. Skin inflammation and aging are closely related phenomena. So similar are the processes involved with both, that aging is sometimes described dermatologically as a chronic low grade inflammatory condition. In acute inflammation, there is typically a respiratory burst of neutro- phil activity that initiates cascades that typically involve a change in the oxidation state of the cell. Acute inflammation is also characterized by mast cell degranula- tion wherein serotonin is produced, which acts as a signal transduction factor. Following that, excited oxygen species are generated, e.g. , superoxide anion, and these damage the lipid-rich membranes and activate the chemical mediators of proinflammation and mflammation.

Alteration in the redox state of the cell activates transcription factors such as NFKB as well as API, which then causes production of proiriflammation mediators. These mediators, such as TFα and various interleukins, cause a burst of cytokines. Arachadonic acid is released, which is oxidized to biologically active mediators. When arachadonic acid is oxidized via the cyclooxygenase or lipoxygenase pathways, for example, prostaglandins, leukotrines, and hyroxyeicosatetraenoic acid (HETE) are produced, which cause erythma, edema, and free radical production. Transcription factors such as NF/cB and API alter DNA expression in the cell and produce cytokines and proteinases such as collagenase.

Similar metabolic events are observed in skin aging. Cell age is due in part to free radical damage, which takes place mostly within the cell membrane. The cell membrane is most susceptible to attack by free radicals because of its dense molecular structure largely comprising lipids and lipoproteins, which are easily oxidized by reactive oxygen species. In skin, reactive oxygen species such as singlet oxygen, the superoxide anion, and hydroxyl radicals, as well as other free radicals, are generated in normal metabolism, as well as through ultraviolet sun exposure, other forms of radiation, other environmental factors such as pollution or exposure to chemicals in the home or workplace, and the like, active in the arachidonic acid cascade. As in inflammation, free radicals activate chemical mediators that produce prostaglandins and/or leukotrines.

The body contains an endogenous antioxidant defense system made up of antioxidants such as vitamins C and E, glutathione, and enzymes, e.g., superoxide dismutase. When metabolism increases or the body is subjected to other stress such as infection, extreme exercise, radiation (ionizing and non-ionizing), or chemicals, the endogenous antioxidant systems are overwhelmed, and free radical damage takes place. Over the years, the cell membrane continually receives damage from reactive oxygen species and other free radicals, resulting in cross-linkage or cleavage or proteins and lipoprotins, and oxidation of membrane lipids and lipoproteins. Damage to the cell membrane can result in myriad changes including loss of cell permeability, increased intercellular ionic concentration, and decreased cellular capacity to excrete or detoxify waste products. As the intercellular ionic concentration of potassium increases, colloid density increases and m-RNA and protein synthesis are hampered, resulting in decreased cellular repair. Some cells become so dehydrated they cannot function at all.

In skin aging, the regularity of tissue structure is lost. Individual cells enlarge, but the total number of cells decreases approximately 30%. Intercellular collagen increases, and the proportion of soluble collagen decreases. Cross-linking between long-chain collagen macromolecules occurs. Elastin loses its discrete structure and elasticity, and has an increased calcium content. The dermis microscars and diminishes.

Sunlight and chemical exposure wreaks far greater destruction on the skin than time itself, and intensifies and augments the aging process. There is substantial evidence that ultraviolet radiation induces the formation of reactive oxygen species which are implicated as toxic intermediates in the pathogenesis of photoaging (Ibbot- son, S.H., et al, J. Investig. Derm. 112: 933-938 (1999)). Activation of transcrip- tion factors such as API causes gene expression of coUagenases which cause further damage. Free radical damage to the surface of the skin from sun and chemical exposure is manifested as lines, mottling, discoloration, precancers and cancers. Aging of both skin and other tissues is, in part, the result of constant free radical damage to cell membranes, leading to decreased cell function. This results in accumulation of waste products in the cells, such as lipofuscin; increase in the potassium content of the cells, which results in dehydration of the cells; and decreased production of messenger RNA and proteins. Early suggestions for dealing with aging effects in skin were predominantly aimed at lubrications and emollients through use of topical compositions containing soothing agents, e.g., as exemplified by commercial hand lotion products and the like. More recently, attention has been directed to agents which address the underlying pro- cesses involved in skin damage, such as the free radical generation processes (N.N. Perricone, The Wrinkle Cure, Rodale Press, Emmaus, PA, 2000). In this regard, investigations have been made with respect to the antioxidants vitamin E and vitamin C to quench free radicals on the surface of the skin and to protect lipid membranes intracellularly (Wilson, R., Drug and Cosmetic Industry, 32-34, 38, and 68, August 1992).

Acetyl carnitine has been shown to have a scavenging effect on free superoxide anions. This antioxidant activity, coupled by acetyl carnitine 's effect of reducing an increase in reduced glutathione and reduced ubiquinone levels, provides a stabilizing effect on membranes by decreasing membrane lipid peroxidation. Carnitine is a molecule that can be derived from the diet or, in the presence of ascorbic acid, be synthesized in the human body. L-carnitine, 3-carboxy-2-hydroxy- Ν,Ν,Ν-trimethyl-l-propanaminium hydroxide (see the Merck Index, 11th ed. , 1989, entry 1856), more commonly known as jS-hydroxy-γ-trimethyl amino butyric acid, is a molecule that is essential for the transportation of fatty acids across the mitochon- drial membrane to be oxidized. If L-carnitine is not present in adequate amounts, fatty acid metabolism is impaired, and there is a marked decrease in energy production. The fatigue associated with scurvy may be associated with carnitine deficiency.

It is known that carnitine enhances mitochondrial energy production, probably by increasing cytochrome oxidase activity, the final enzyme in the cellular respiratory chain. This results in a more efficient cellular maintenance and repair. There is some evidence that carnitine given as an oral supplement may enhance muscular and cellular function and increase energy levels and repair. Carnitine does not pass the blood-brain barrier. However, biologically equivalent derivatives such as acetyl carnitine, can pass the barrier. Acetyl carnitine has been used in cognitive enhancement and has been shown to slow damage to the mitochondria with age, as well as to enhance mitochondrial function.

Acetyl carnitine has been suggested for the treatment of viral infections, including skin infections such as those caused by Herpes, including lesions that occur after sunlight or UN exposure (U.S. Pat. No. 5,314,689 to Scandurra and Aurelian). Acetyl carnitine was suggested as an optional ingredient in a composition containing glutathione and selenoamino acid for reducing and repairing x-ray radiation-induced skin damage (U.S. Pat. No. 5,667,791 to Hersh and Warshaw). Oral administration of acetyl carnitine has also been suggested for the treatment of AIDS symptoms, including skin inflammation (U.S. Pat. No. 5,667,791 to Weil and Scandurra). Oral or parenteral acetyl carnitine has also been disclosed as useful in stimulating the immune system of patients with an impaired immune system (U.S. Pat. No. 4,415,588 to Cavazza), and in the therapeutical treatment of impaired cardiac function, myocardial anoxia and cardiac arrhythmias {ibid.).

It would be desirable to utilize the properties of acetyl carnitine more efficiently in alternative topical compositions for skin damage, particularly compositions that are efficient in free radical scavenging intracellularly and in membranes.

BRIEF SUMMARY OF THE INVENTION

It is an objective of the invention to provide new methods for the treatment of skin damage, such as atopic dermatitis, contact dermatitis, xerosis, eczema, rosacea, seborrhea, psoriasis, thermal and radiation burns, other types of skin inflammation, and aging. These and other objectives of the invention are accomplished by the present invention, which provides methods for topically applying acetyl carnitine and phos- phatidylcholine and/or fatty acid esters of ascorbic acid to exposed or affected skin areas, primarily for the treatment but also for the prevention of skin damage, often in association with a dermatologically acceptable carrier. The amount of acetyl carnitine and phosphatidylcholine and/or fatty acid esters of ascorbic acid necessary to treat damaged skin is not fixed per se, and necessarily is dependent upon the acetyl carnitine preparation employed, the amount of acetyl carnitine, the amount and identity of the ascorbyl esters where employed, the amount and type of any adjunct ingredients employed in the composition, the user's skin type, and the severity, extent, and nature of the dermatological problem treated. In some typical embodiments, the composition contains from about 0.025% to about 5 weight %, more narrowly from about 0.5% to about 2%, by weight acetyl carnitine, and, where employed, from about 0.5% to about 7%, more narrowly from about 1 % to about 5% by weight saturated fatty acid esters of ascorbic acid such as ascorbyl palmitate.

Adjunct ingredients such as an α-hydroxy acid may be added to compositions of the invention in some embodiments.

DETAILED DESCRIPTION OF THE INVENTION

In the practice of the invention, acetyl carnitine and phosphatidylcholine are used and/or fatty acid esters of ascorbic acid to treat skin damage when topically applied in effective amounts.

Thus, in the practice of the invention, L-acetyl carnitine and/or biologically equivalent derivatives of acetyl carnitine such as D-acetyl cartinine, DL-acetyl carnitine, DL-acetyl cartinine hydrochloride, DL-acetyl carnitine chloride, acetyl D,L carnitine hydrochloride, acetyl L-carnitine hydrochloride can, when administered with phosphatidylcholine and/or ascorbyl fatty acid esters, penetrate skin and cause enhanced function of skin cells and skin structures such as keratinocytes and fibro- blasts. Advantageous embodiments deliver carnitine directly into skin cells through the use of acetyl carnitine and/or a biologically active derivative, to enhance mito- chondrial function. This, in turn, leads to high energy production in the cell, which then can maintain the integrity of cellular membranes and increase exchange of nutrients and wastes across these membranes. Use of effective amounts of acetyl carnitine gives skin a softer, smoother appearance, and decreases epidermal age pigments.

Any synthetic or natural acetyl carnitine preparation may be employed in compositions of the invention. Acetyl carnitine,

+ (CH₃)₃N— CH₂— CH— CH₂COO OCOCH₃

is a known compound that can be purchased, prepared, or isolated from natural sources. As illustrated above, it contains an asymmetric carbon atom, and thus exists in the racemic form and in the optically active dextrorotary and levorotary forms. As used herein, the term "acetyl carnitine" encompasses D-, L-, or DL- acetyl carnitine, and biologically active derivatives such as those listed above. L-acetyl cartine is preferred because it is the most active form. Preferred concentrations of acetyl carnitine in compositions of the invention vary from about 0.025% to about 5%, more narrowly from about 0.5% to about 2%, by weight.

Phosphatidylcholine (sometimes hereafter abbreviated "PC"), commonly called lecithin, is a mixture of diglycerides of stearic, palmitic, and oleic acids, linked to the choline ester of phosphoric acid. It can be isolated from eggs, soybeans, and other biological materials rich in PC, chemically synthesized, or obtained commercially from many sources. Food grade lecithin is preferred. Some commercial grades, for example, contain about 2.2% PC. It is an advantage of the invention that both acetyl carnitine and phosphatidylcholine are natural products that have been shown to have no toxicity to mammals, and ascorbyl fatty acid esters are similarly nontoxic. Indeed, phosphatidylcholine is edible and digestible, and used in margarine, chocolate, and the food industry in general. Moreover, since acetyl carnitine penetrates poorly when topically administered, it is a particular advantage of the invention that combining it with phosphatidyl choline considerably enhances penetration of this active ingredient.

Alternatively, or in addition to PC, fatty acid esters of ascorbic acid are employed with acetyl carnitine in the practice of the invention. Fat-soluble fatty acid esters of ascorbic acid (vitamin C) is employed as an adjunct ingredient in other embodiments, alone or in combination with c -hydroxy acids. The more oxidation-resistant saturated fatty acid esters of ascorbic acid are preferred, including, but not limited to, ascorbyl laurate, ascorbyl myristate, ascorbyl palmitate, ascorbyl stearate, and ascorbyl behenate. Ascorbyl palmitate is used in one embodiment. As denoted herein, where fatty acid esters are described, e.g. , ascorbyl stearate, compositions having predominantly that ester, e.g. , predominantly stearate, are included. The esters may be prepared using hydrogenated oils or fats, or fractions thereof, and contain small amounts of another ester. Ascorbyl stearate prepared using canola, for example, commonly contain about 4% ascorbyl palmitate. Typical concentrations of ascorbyl esters in compositions of the invention are from about 0.5% to about 7% by weight, more narrowly from about 1 % to about 7% to 10% by weight. It is an advantage of the invention that where fatty acid esters of ascorbic acid are employed in compositions of the invention, they help stabilize the compositions of the invention and enhance the radical scavenging properties of acetyl carnitine.

As described more fully below, the active ingredient combination is topically applied to exposed or affected skin areas in amounts effective to treat skin damage. By "effective amount" is meant an amount of both active ingredients sufficient to stabilize the cell plasma membrane by scavenging and neutralizing free radicals and exhibiting antioxidant activity, thereby inhibiting the arachidonic acid cascade which leads to the activation of transcription factors that direct the cell nucleus into producing pro-inflammatory chemicals such as arachidonic acid. In the practice of the invention, active ingredients are typically delivered to lipid-rich layers of the skin in amounts effective to prevent inflammation and accelerate collagen synthesis.

Acetyl carnitine, fatty acid esters of ascorbic acid, and PC are fat-soluble. Therefore, compositions of the invention can be applied neat to skin tissue, and this is preferred in some embodiments. One embodiment comprises acetyl carnitine in food grade lecithin; another comprises acetyl carnitine and ascorbyl palmitate in food grade lecithin. It is an advantage of the invention that PC is fatty so that compositions of the invention physically contribute to the lubrication of affected skin areas to which it is applied.

Active ingredients may also be administered in association with a carrier, which is particularly useful where lower amounts are needed to treat skin damage

(including either inflammation or aging or both), or adjunct ingredients not effectively solubilized in PC are added to compositions of the invention. Where employed, the carrier is inert in the sense of not bringing about a deactivation or oxidation of the acetyl carnitine or ascorbyl fatty acid esters and in the sense of not bringing about any adverse effect on the skin areas to which it is applied. Where carriers or vehicles (e.g. , lotions, creams, ointments, soaps, sticks, or the like) are employed, they are formulated as to facilitate topical application and, in some cases, provide additional therapeutic effects as might be brought about, e.g. , by moisturizing of the affected skin or mucosal areas. While the carrier for dermatological compositions can consist of a relatively simple solvent or dispersant such as water, it is generally preferred that the carrier comprise a composition more conducive to topical application, and particularly one which will form a film or layer on the skin to which it is applied so as to localize the application and provide some resistance to washing off by immer- sion in water or by perspiration and/or aid in the percutaneous delivery of the active agent. Many preparations are known in the art, and include lotions containing oils and/or alcohols and emollients such as hydrocarbon oils and waxes, silicone oils, vegetable, animal or marine fats or oils, glyceride derivatives, fatty acids or fatty acid esters or alcohols or alcohol ethers, lanolin and derivatives, polyhydric alcohols or esters, wax esters, sterols, phospholipids and the like, as well as lecithin, and generally also emulsifiers (nonionic, cationic or anionic), although some such as lecithini inherently possess emulsifying properties. These same general ingredients can be formulated into a cream rather than a lotion, or into gels, or into solid sticks by utilization of different proportions of the ingredients and/or by inclusion of thickening agents such as gums or other forms of hydrophilic colloids. Such compositions are referred to herein as dermally or dermatologically acceptable carriers.

Suitable carriers include water, alcohols, oils and the like, chosen for their ability to dissolve or disperse acetyl carnitine and any other ingredients used in the treatment. Generally, even low concentrations of active ingredients in a carrier are suitable, depending upon the application regimen and adjunct ingredients employed. Chronic conditions typically require a lower concentration of active acetyl carnitine ingredient than to acute conditions. As a practical matter, however, to avoid the need for repeated application, it is desirable that the topically applied composition (i.e. , acetyl carnitine plus PC and/or ascorbyl esters, and, in some cases, carrier) be formulated to contain at least about 0.01 % by weight, preferably at least about 0.025% acetyl carnitine. Similarly, where ascorbyl esters comprise part of the composition, these are present in concentrations of at least about 0.25%, preferably at least about 0.5% . As summarized above, typical compositions of the invention contain from about 0.5% to about 2% acetyl carnitine and about 1 % to about 5% ascorbyl palmitate or other saturated ester.

Generally in the practice of methods of the invention, the composition is topically applied to the affected skin areas in a predetermined or as-needed regimen either at intervals by application of a lotion or the like, it generally being the case that gradual improvement is noted with each successive application. Insofar as has been determined based upon clinical studies to date, no adverse side effects are encountered.

Some embodiments of this invention contain at least one other adjunct ingredient such as α-hydroxy acids in addition to acetyl carnitine. As used herein, the term "α-hydroxy acid" has reference to and encompasses the general class of organic compounds containing at least one hydroxy group and at least one carboxyl group, and wherein at least one hydroxyl group is located on the α-carbon atom. Typically, the compounds are organic acids having at least one carboxylic acid group and at least one hydroxyl group on the α-carbon atom, and may contain other functional groups including additional hydroxyl and carboxylic acid moieties. Preferred α-hydroxy acids and/or α-hydroxy acid derivatives are less bulky structurally so that they penetrate the skin well, and thus have a backbone of from one to three carbon atoms such as those set out in U.S. Pat. No. 5,965,618 at column 6 lines 4 to 29. Where employed, glycolic and/or lactic acid or their derivatives are preferred; glycolic acid is especially efficacious.

While not wishing to be bound to any theory, it is possible that acetyl carnitine in PC and/or ascorbyl fatty acid esters is efficacious in the treatment of skin damage because it is fat-soluble and readily disperses in cell membranes and other cellular components. In the presence of PC and/or ascorbyl fatty acid esters, acetyl carnitine readily penetrates skin. As mentioned above, it also is an active antioxidant that has been shown to protect against lipid peroxidation. Acetyl carnitine acts as a free radical scavenger and neutralizer, and prevents the cross-linking of cell membranes that is often seen in its post-inflammatory phases. By the same token, acetyl carnitine modulation of free radicals and other oxidative species appears to affect gene expression, including expression of nuclear factor κ-B (NF-κB), nitric oxide synthe- tase and other mediators at all stages of proinflammation and inflammation. Acetyl carnitine's alteration of lipid peroxidation, protein cross-linking, growth factor stimulation, and membrane permeability may explain its negative effect on the symptoms of damaged skin. And the effects of acetyl carnitine are enhanced by using it in combination with ascorbyl fatty acid esters such as ascorbyl palmitate, because these compounds also act as antioxidants and scavenge free radicals.

When skin is inflamed from ultraviolet radiation, irritants, trauma, and other reasons, phospholipase-A-2 produces arachidonic acid from the phospholipid- rich membranes of the cell, resulting in the production of metabolites. We now know that stabilization of the cell membrane can inhibit the inflammatory cascade, therefore preventing the inflammatory response. It is also now known that arachidonic acid has a direct toxic effect on the mitochondria, resulting in the uncoupling of oxidative phosphorylation, resulting in free radical damage to the mitochondrial membrane. Acetyl carnitine with PC and/or fatty acid esters of ascorbic acid appear to intersperse in the cell membrane, stabilizing the membrane, and, at the same time, providing antioxidant capability. In addition, the delivery of acetyl carnitine into the cell membrane appears to enhance membrane activity, such as exchange of nutrients and wastes of the cellular environment. This also enhances cellular function and repair.

Methods and compositions of the present invention are particularly useful for treating damaged skin tissue, particularly various types of dermatitis, skin conditions such as rosacea, seborrhea, eczema, xerosis (dry skin), psoriasis, thermal and radiation burns, and other types of inflammation. Acetyl carnitine compositions of the invention are useful in treating both contact dermatitis and atopic dermatitis. Topical application of acetyl carnitine according to the invention can also be effective to prevent symptoms in aging persons for the inhibition of microscarring of the dermis and to promote collagen production. It is an advantage of the invention that that treatment or preventive measures employ, as an active ingredient, natural compounds. It is another advantage of the invention that topical application of acetyl carnitine with phosphatidylcholine and/or ascorbyl fatty acid esters provides a simple, non-invasive, nontoxic, over-the-counter topical method for treating all kinds of skin damage.

All references cited herein are hereby incorporated by reference, as are additional ingredients and methods set out in U.S. Pat. Nos. 4,775,530, 5,376,361, 5,409,693, 5,545,398, 5,574,063, 5,643,586, 5,709,868, 5,879,690, 5,965,618, and 5,968,618. Generally, these compositions contain other active ingredients summarized above that enhance the effect of active ingredients of the invention.

The above description is for the purpose of teaching the person of ordinary skill in the art how to practice the present invention, and it is not intended to detail all those obvious modifications and variations of it which will become apparent to the skilled worker upon reading the descrip In one embodiment, the composition contains fromtion. It is intended, however, that all such obvious modifications and variations be included within the scope of the invention in any sequence which is effective to meet the objectives there intended, unless the context specifically indicates the contrary.

Claims

1. A method for the treatment of skin damage comprising topically applying to the skin a composition containing an effective amount of acetyl carnitine and a second ingredient selected from the group consisting of phosphatidylcholine, fatty acid esters of ascorbic acid, and mixtures thereof.

2. A method according to claim 1 wherein the acetyl carnitine is L-acetyl carnitine.

3. A method according to claim 1 wherein the fatty acid ester of ascorbic acid is a saturated fatty acid ester selected from the group consisting of ascorbyl laurate, ascorbyl myristate, ascorbyl palmitate, ascorbyl stearate, ascorbyl behenate, and mixtures thereof.

4. A method according to claim 11 wherein the fatty acid ester of ascorbic acid is ascorbyl palmitate.

5. A method according to claim 3 wherein the composition contains from about 0.5% to about 7% by weight fatty acid esters of ascorbic acid.

6. A method according to claim 1 wherein the composition contains from about 0.025% to about 5% by weight acetyl carnitine.

7. A method according to claim 6 wherein the composition contains from about 0.5% to about 2% acetyl carnitine.

8. A method according to claim 1 wherein the composition contains an α-hydroxy acid adjunct ingredient selected from the group consisting of lactic acid, glycolic acid, and mixtures thereof.

9. A method according to claim 8 wherein the α-hydroxy acid is glycolic acid.

10. A method according to claim 1 wherein the composition consists essentially of acetyl carnitine in food grade lecithin.

11. A method according to claim 10 wherein the composition consists essentially of acetyl carnitine and ascorbyl palmitate in food grade lecithin.

14. A method according to claim 1 wherein the skin damage is selected from the group consisting of eczema, atopic dermatitis, contact dermatitis, seborrhea, xerosis, rosacea, thermal or radiation burns, psoriasis, and aging.

15. A method for the treatment of skin damage comprising topically applying to the skin areas subject to such damage a composition containing an effective amount of L- acetyl carnitine and an effective amount of ascorbyl palmitate in a carrier in amounts sufficient to deliver the acetyl carnitine active ingredient into skin cells.

16. A method according to claim 15 wherein the carrier comprises phosphatidylcholine.

17. A method according to claim 17 wherein the composition contains from about 0.025% to about 5% by weight acetyl carnitine and from about 0.5% to about 7% ascorbyl palmitate.

18. A method according to claim 15 wherein the skin damage is selected from the group consisting of eczema, atopic dermatitis, contact dermatitis, seborrhea, xerosis, rosacea, thermal or radiation burns, and psoriasis.

19. A method according to claim 15 wherein the skin damage is inflammation or aging.

20. A method for the treatment of skin damage comprising topically applying to the skin areas subject to such damage a composition containing from about 0.5% to about 2% by weight L-acetyl carnitine, from about 1 % to about 5% by weight ascorbyl palmitate, and food grade lecithin.