<![CDATA[Transformation Beauty Studio Cosmetic Tattoo & Skin Care SPA - Stuart, FL - Beauty Blog +]]>Fri, 27 Mar 2020 16:22:57 -0400Weebly<![CDATA[Is your natural beauty hidden behind a mask of dark, irregular patches]]>Fri, 24 Mar 2017 21:12:24 GMThttp://transformationbeautystudio.com/beauty-blog/is-your-natural-beauty-hidden-behind-a-mask-of-dark-irregular-patchesPicture
Is your natural beauty hidden behind a mask of dark, irregular patches on the upper cheek, the nose, lips, upperlip, and/or your forehead? Would you prefer lighter/brighter skin?
And if you think you´re silently suffering alone, think again. An estimated six million women throughout the U.S. are currently affected by this distressing cosmetic concern.
Melasma is a tan or dark facial skin discoloration or hyperpigmentation. Although it can affect anyone, melasma is particularly common in women, especially pregnant women and those who are taking oral contraceptives or hormone replacement therapy (HRT) medications. However, this condition develops spontaneously in some women who are neither pregnant, taking oral contraceptives, nor HRT medications. It is also prevalent in men and women of Native American descent (on the forearms) and in men and women of German/Russian Jewish descent (on the face).
The cheeks, the upper lip, the chin, and the forehead are the most common locations, but it can occasionally occur in other sun-exposed locations. Chloasma is a synonymous term sometimes used to describe the occurrence of melasma during pregnancy (also known as the mask of pregnancy). Chloasma is derived from the Greek word chloazein, meaning “to be green.” Melas, also Greek, means “black.”
Race: Persons of any race can be affected. However, it is much more common in constitutionally darker skin types than in lighter skin types, and it may be more common in light brown skin types, especially Hispanics and Asians, from areas of the world with intense sun exposure. 
Sex: Melasma is much more common in women than in men. Women are affected in 90% of cases. When men are affected, the clinical and histologic picture is identical. 
 Age: Melasma is rare before puberty and most commonly occurs in women during their reproductive years. 
The color of human skin is differentiated by the nature and quantity of the natural pigment, melanin present in the epidermal layers of the skin.
Cutaneous pigmentation is the outcome of two events: the synthesis of melanin by melanocytes (MC) and the donation of melanin in melanosomes (organelles within the cells) to surrounding keratinocyte cells. The rate of melanin synthesis is determined by intracellular enzymes, the best characterized of which are tyrosinase, and the two tyrosinase-related proteins (TRP)-1 and TRP-2 or DOPAchrome tautomerase (DT). 
The formation of melanin from amino acid tyrosine involves several biogenetic steps mediated initially by the enzyme tyrosinase. Tyrosine is first oxidized by tyrosinase to dihydroxyphenylalanine (I-dopa), then to dopaquinone. Dopaquinone is then converted into eumelanin (black, white, and Asian skin types; skin color is dependent on the quantity of eumelanin in skin), or phaeomelanin (red-haired skin types). This conversion proceeds through the intermediate formation of leucodopachrome and dopachrome (eumelanin), or cysteinyldopa (phaeomelanin).
Causes of Melasma
Melasma is thought to be the result of stimulation of melanocytes or pigment-producing cells by the female sex hormones estrogen and progesterone to produce more melanin pigments when the skin is exposed to sun. Women with a light brown skin type who are living in regions with intense sun exposure are particularly susceptible to developing this condition.
A direct relationship with female hormonal activity appears to cause melanocytes or the pigment-producing cells to produce and deposit excess pigments, because it occurs with pregnancy and with the use of oral contraceptive pills. Other factors implicated in melasma are photosensitizing medications, mild ovarian or thyroid dysfunction, and certain cosmetics. 
Genetic predisposition is also a major factor in determining whether someone will develop melasma. It is much more common in women than in men. Persons with light brown skin types from regions of the world with intense sun exposure are much more prone to the development of melasma. More than 30% of patients have a family history of melasma. Identical twins have been reported to develop melasma, while other siblings under similar conditions did not. 
Another major factor is exposure to sunlight. Ultraviolet radiation can cause peroxidation of lipids in cellular membranes, leading to generation of free radicals, which could stimulate melanocytes to produce excess melanin. Sunscreens that primarily block UV-B radiation (290-320 nm) are unsatisfactory because longer wavelengths (UV-A and visible radiation, 320-700 nm) also stimulate melanocytes to produce melanin. 
Hormonal influences play a role in some individuals. The mask of pregnancy is well known to obstetric patients. The exact mechanism by which pregnancy affects melasma is unknown. Estrogen, progesterone, and melanocyte-stimulating hormone (MSH) levels are normally increased during the third trimester of pregnancy. However, nulliparous patients with melasma have no increased levels of estrogen or MSH. In addition, the occurrence of melasma with estrogen- and progesterone-containing oral contraceptive pills and diethylstilbestrol treatment for prostate cancer has been reported. The observation that postmenopausal woman who are given progesterone develop melasma, while those who are given only estrogen do not, implicates progesterone as playing a critical role in the development of melasma. 
The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone replacement therapy.
The incidence of melasma also increases in people with thyroid disease. It is thought that the overproduction of melanocyte-stimulating hormone (MSH) brought on by stress can cause outbreaks of this condition. Other rare causes of melasma include allergic reaction to medications and cosmetics. 
One study found a 4-fold increase in thyroid disease in patients with melasma when compared with matched controls. A case report of 2 women who developed melasma after sudden and profound emotional stress implicated the release of MSH by the hypothalamus as a cause. Exactly which hormones and what mechanisms are involved in the development of melasma are yet to be determined. Genetic and hormonal influences in combination with ultraviolet radiation are the 2 most important causes of melasma, yet phototoxic and photoallergic medications and certain cosmetics have been reported to cause melasma in rare instances.
The most important factor in the development of melasma is exposure to sunlight. Without the strict avoidance of sunlight, potentially successful treatments for melasma are doomed to fail. 
Hyperpigmentation is an area of the skin where there is an overabundance of melanin relative to the surrounding cutaneous tissue. This can be the result of either an abnormally high concentration of melanocytes producing the melanin, or hyperactive melanocytes. Melanin is increased in the epidermis, in the dermis, or (most commonly) in both locations. Epidermal melanin is found in keratinocytes in the basal and suprabasal area. In most cases, the number of melanocytes is not increased, yet the melanocytes that are present are larger, more dendritic, and more active. Dermal melanin is found in the superficial and mid dermis within macrophages, which often congregate around small, dilated vessels. Inflammation is sparse or absent.
Excess melanin can be visually localized to the epidermis or the dermis by use of a Wood lamp (wavelength, 340-400 nm). 
Reduction of Hyperpigmentation 
Melasma can be difficult to treat. The pigment of melasma develops gradually, and resolution is also gradual. Resistant cases or recurrences occur often and are certain if strict avoidance of sunlight is not rigidly heeded. All wavelengths of sunlight, including the visible spectrum, are capable of inducing melasma. 
The cosmetic treatment of skin to produce a visible even-tone has been practiced since ancient times. The use of plant-derived extracts and salves to whiten or brighten dark colored skin has been very popular among Asian, African, and South American cultures. The even toning of age-related dark spots, skin pigmentation, freckles, and other skin pigmentation disorders with skin lightening products is gaining popularity among people of light-colored skin as well.
To date, the best-known active substance for de-pigmentation is hydroquinone, a bleaching agent which has the status of a FDA approved OTC drug active ingredient for skin whitening compositions. Kojic acid and arbutin, which are chemically related to hydroquinone, are also commonly used. If applied over long periods of time, hydroquinone can have serious side effects, which has led to its being permitted only in limited concentrations in some countries, and to its being completely forbidden for applications in cosmetic products in other countries (The chemical is under new scrutinity in the US and may soon be forbidden by the FDA). 
Furthermore, hydroquinone leads to permanent de-pigmentation, and thus to increased photosensitivity of the skin when exposed to UV light. Better-tolerated skin lightening substances currently being used are of natural origin, e.g., arbutin (from the leaves of the common bearberry, Uva ursi), liquorice extract (from liquorice root), ascorbic acid (vitamin C from citrus fruits) and their derivatives, as well as kojic acid (from carbohydrate solutions under the effect of certain bacteria). These substances, which are highly soluble in water, act on the tyrosinase as competitive inhibitors; however, they are unstable in some formulations, and have the disadvantage that only very small quantities penetrate the deeper skin layers and reach the melanocytes in the basal membrane. A further disadvantage of these substances is their low level of efficacy, which necessitates their being used in high concentrations. Compared to the quantity of hydroquinone used, 17 times as much ascorbic acid and over 100 times as much arbutin is required to achieve a similar effect.
Topical applications of ascorbic acid and its esters are also claimed to have skin-lightening property. Several botanical-based ingredients with claims such as "helps reduce the appearance of minor skin discoloration", "helps brighten skin and even-out skin tone", "helps reduce the appearance of dark spots, age-related spots, and freckles", and modifications of the above claims are made. 
Basically, the most effective strategy is to reduce the tyrosinase, for then you reduce the melanin. 
The most effective way to reduce the visible signs of hyperpigmentation, is to down-regulate melanin production. This is effective because areas where more melanin is being produced will show higher levels of efficacy and respond with a greater reduction in melanin. 

Treatment of Melasma
The dark spots usually go away by themselves - however, this process can take a very long time. It is not unusual to have the condition persist for months or years after giving birth or stopping taking birth control pill. Lotions with high SPF (sun protection factor) of 15 or greater should be worn if you have melasma, because sunlight and ultraviolet lights stimulate the production of melanin as a result of body's own protective response to such external stimuli. 
Treatment to lighten the dark spots include:
·  Cosmetic cover-ups to hide and reduce the appearance of spots. 
·  Non-prescription tyronsinase inhibitors ( vitamin C, Kojic Acid, and other ingredients available in High strength) applied to clean skin twice a day. Ideal for use under makeup
·  Chemical Peeling done by a professional and not at a deeper level and enzyme peels
 Treatments to hasten the fading of the discolored patches include:

Topical depigmenting agents, such as the ingredients listed above works by decreasing the production and increasing the breakdown of melanosomes (melanin pigment granules) in the skin's pigment cells (melanocytes). 

2.  Tretinoin or retinols, that increases skin cell (keratinocyte) proliferation and/or turnover. This treatment cannot be used during pregnancy. 

3.  Azelaic acid (20%), thought to decrease the activity of melanocytes. 

4.  Facial peel with alpha hydroxyacids or chemical peels with glycolic acid, Azelaic, Lactic, Mandelic.

Quick fixes with destructive modalities (eg, cryotherapy, medium-depth chemical peels, lasers) yield unpredictable results and are associated with a number of potential adverse effects, including epidermal necrosis, post inflammatory hyperpigmentation, and hypertrophic scars. The precise manner in which these modalities can be used has not been fully delineated. However, in some experienced hands, they have been anecdotally reported to be safe, effective, and produce results much quicker than topical medications. More careful study is needed before they can be recommended as a standard treatment. 
In all of these treatments the effects are gradual and a strict avoidance of sunlight is required. The use of broad-spectrum sunscreens with physical blockers, such as titanium dioxide and zinc dioxide is preferred over that with only chemical blockers. This is because UV-A, UV-B and visible lights are all capable of stimulating pigment production.
·  The mainstay of treatment remains topical depigmenting agents. Hydroquinone (HQ) is most commonly used. It is a hydroxyphenolic chemical that inhibits tyrosinase, leading to the decreased production of melanin. Additionally, cytotoxic metabolites may cause interference with melanocyte function and viability. HQ can be applied in cream form or as an alcohol-based solution. Concentrations vary from a 2% concentration available in the United States without a prescription to a standard 4% concentration and even higher when compounded. Efficacy is directly linked to concentration, but the incidence of adverse effects also increases with concentration. All concentrations can lead to skin irritation, phototoxic reactions with secondary postinflammatory hyperpigmentation, and irreversible exogenous ochronosis (reported even with long-term use of 2% HQ). Special care must be taken not to prescribe the monobenzyl ether of HQ (Benoquin), which causes an irreversible localized and generalized vitiligolike leukoderma. 
·  The use of tretinoin (trans-retinoic-acid) can be effective as monotherapy. However, the response to treatment is less than with HQ and can be slow, with improvement taking 6 months or longer. As such, combinations of tretinoin with HQ, with or without a topical corticosteroid, have been promoted. The retinoid is believed to work by increasing keratinocyte turnover and thus limiting the transfer of melanosomes to keratinocytes. The major adverse effect is skin irritation, especially when the more effective, higher concentrations are used. Temporary photosensitivity and paradoxical hyperpigmentation can also occur. 
·  Azelaic acid, available as a 20% cream-based formulation, appears to be as effective as 4% HQ and superior to 2% HQ in the treatment of melasma. The mechanism of action is not fully understood. DNA synthesis is reduced, and mitochondrial cellular energy products are inhibited in melanocytes. Unlike HQ, azelaic acid seems to target only hyperactive melanocytes and thus will not lighten skin with normally functioning melanocytes. The primary adverse effect is skin irritation. No phototoxic or photoallergic reactions have been reported. 
·  Other depigmenting agents that have been studied in the treatment of melasma are 4-N-butylresorcinol, phenolic-thioether, 4-isopropylcatechol, kojic acid, and ascorbic acid.
Regardless of the treatments used, all will fail if sunlight is not strictly avoided. Prudent measures to avoid sun exposure include hats and other forms of shade combined with the application of a broad-spectrum sunscreen at least daily. Sunscreens containing physical blockers, such as titanium dioxide and zinc oxide, are preferred over chemical blockers because of their broader protection. UV-B, UV-A, and visible light are all capable of stimulating melanogenesis. In addition, clients should be forewarned that resolution is gradual and may take many months.
Mild Exfoliation Combined With Accelerated Skin Renewal & Melanin Inhition 
In an attempt to hasten resolution, many practitioners attempt mild exfoliation with superficial chemical peels. The rational is that if melanogenesis is inhibited with bleaching agents and keratinocyte turnover is increased as a reaction to mild exfoliation, the time to resolution can be reduced. A number of studies have shown that treating melasma with superficial chemical peels and a bleaching agent is safe and effective. 
Skin pigmentation and tanning are related to the amount and distribution of melanin in epidermal melanosomes. The epidermis cell population includes keratinocytes and the melanocytes that supply the keratinocytes with melanosomes, i.e., melanin containing pigment granules, via dendritic processes. Melanin is a dark pigment that is produced by the oxidation of tyrosine to dopa and dopaquinone by the enzyme tyrosinase, to produce compounds that polymerize to form melanin. 
Get Rid Of Melasma, Hyperpigmentation, Sun & Age Spots While Revitalizing and Protecting the Skin From The Effects of Free Radicals
A deeply moisturizing natural skin care cream that replenishes the lipid barrier of the skin and triggers the repair of cells damaged by UV radiation and Free Radicals. Also gets rid of melasma, hyperpigmentation, brown, sun and age spots and all types of skin blemishes. The novel ingredients with an added natural substance that reduces melanin biosynthesis and a biomimetic peptide that inhibits the accumulation of melanin pigments. 
**portions reprinted from bioskin.

<![CDATA[Hyperpigmentation and Skin of Color]]>Thu, 23 Mar 2017 15:55:41 GMThttp://transformationbeautystudio.com/beauty-blog/hyperpigmentation-and-skin-of-colorHyperpigmentation and Skin of Color
By: Jennifer Linder, MD
Posted: August 23, 2010, from the September 2010 issue of Skin Inc. Magazine.

Much of the world’s population is considered Fitzpatrick type IV–VI. (See Fitzpatrick Scale.) By 2050, according to the U.S. Census Bureau in 2000, 50% of Americans will be of darker-skinned racial backgrounds. One of the most common skin conditions in higher Fitzpatrick clients is hyperpigmentation. Although many of the popular treatments performed on a regular basis on Caucasians may be well-tolerated by clients with darker skin, special considerations need to be taken to ensure positive treatment outcomes for such clients. A deeper understanding of the causes of hyperpigmentation, and of the myriad of ingredients available for its treatment, will help spa professionals develop highly effective therapies for all of their clients, regardless of ethnicity.
Beyond black and white
Within any ethnic background, a variety of Fitzpatrick skin types can be identified. Darker skin can commonly be seen in Hispanics, Latinos, Africans, African-Americans, Caribbeans, Native Americans, Pacific Islanders, East Indians, Pakistanis, Eskimos, Koreans, Chinese, Vietnamese, Filipinos, Japanese, Thai, Cambodians, Malaysians, Indonesians and Aleuts, according to dermatologist Pearl Grimes, MD.1 With this broad global representation in mind, spa professionals should expect to see an increase in clients of one or mixed racial backgrounds with darker skin.
The most apparent difference in the skin of those from different ethnicities is, of course, the color, although there are also differences in skin thickness, vascularity, and predispositions to certain skin conditions and diseases. Hyperpigmentation can occur due to UV exposure, cutaneous trauma or hormonal fluctuations. Studies by dermatologist Susan Taylor in 2005 demonstrate that up to 86% of women of Latino, Asian and African descent are concerned about skin discolorations.2
Melanogenesis and skin color
Melanin is the complex molecule that is responsible for the pigment in the body; specifically eyes, hair and skin. Melanin works to protect by reducing the penetration of UV rays into the skin and, even more importantly, into the nuclei of cells where DNA resides. Those with both dark and light skin have the same number of melanocytes—the cells responsible for melanogenesis or melanin production—although their level of responsiveness differs. Clients whose genetic heredity is that of global regions with extreme UV exposure have melanocytes that will, out of protective necessity, instigate the process of melanin deposition much more quickly than someone with lighter skin. Some clients with mixed genetic heritage may have lighter skin, but still have a greater predisposition for hyperpigmentation than a typical Fitzpatrick skin type I or II.
As a result of inflammation or hormonal fluctuations, the following process is stimulated.
Melanocyte stimulating hormone (MSH) is triggered and released. Within the melanocyte, a chain of events is activated that begins with the enzyme tyrosinase being released from the rough endoplasmic reticulum (RER) and acting on the amino acid tyrosine to convert it to L-DOPA.
Then, tyrosinase binds with copper and acts on L-DOPA, converting it into melanosomes. These melanosomes are packets of pigment that can either be eumelanin (brown/black pigment) or pheomelanin (orange/red pigment). Dark skin tends to have more eumelanin. This more vigorous type of melanin contributes to the increased occurrence of hyperpigmentation in darker skin.
Those with fairer skin, and especially red hair, will predominantly have pheomelanin. The final color of a person’s skin will be slightly different based on the ratio of eumelanin to pheomelanin, as well as the quantity of sustained UV exposure to which their skin is subjected.
The melanosomes produced are then transported along the dendrites, or arms, of the melanocyte and transferred into the keratinocyte. They then congregate in an umbrellalike pattern over the nucleus to protect the DNA within the cell, resulting in visible hyperpigmentation. Protease-activated receptor-2 (PAR-2) is the receptor located in the keratinocytes that regulates whether or not the melanosomes that arrive at the keratinocyte are phagocytized—consumed or taken in. The keratinocytes in skin of color contain more of these PAR-2 receptors, increasing the amount of phagocytized melanosomes by keratinocytes.
Additionally, PAR-2 receptors are increased in number by UV exposure, which may explain the predisposition of darker skin to be more responsive to melanogenesis. All types of hyperpigmentation can affect any person, regardless of race, although this PAR-2 expression and upregulation makes it more prevalent in clients with darker skin.
Gentle treatment optionsMany of the ingredients that are used to treat hyperpigmentation can be topically irritating. Therapeutic ingredients must be selected with care when treating clients with darker skin to avoid causing undue irritation that will worsen the condition rather than improve it.
To avoid stimulating pigment deposition, it is wise to use lower percentages of ingredients in blends to prevent melanogenesis, rather than one ingredient at a high percentage that could potentially be surface-stimulating. Hydroquinone is very effective at the low over-the-counter (OTC) percentage of 2%, especially when used in concert with other effective ingredients, such as lactic, kojic, ascorbic and azelaic acids, just to name a few. Care must be taken when using hydroquinone at 4% or higher on darker skin, as these are more irritating and can trigger post-inflammatory hyperpigmentation. 
One of the most important steps in any daily care regimen or professional treatment is that of sun protection. A broad-spectrum moisturizer with an SPF of 30 or greater should be applied to all exposed areas every day and after any professional treatment. Although darker skin has more natural protection against UV exposure, this critical step cannot be omitted. With an understanding of the more reactive state of the melanocytes in clients with darker skin, along with blends of gentle, beneficial melanogenesis-inhibiting ingredients, great success can be achieved in treating Fitzpatrick type IV–VI clients.
REFERENCES1.      PE Grimes, Aesthetics and Cosmetic Surgery for Darker Skin Types, Lippincott Williams & Wilkins, Philadelphia, 2008 (pp 15–26)
2.      3. S Badreshia-Bansal and ZD Draelos, Insight into Skin Lightening Cosmeceuticals for Women of Color, J of Drugs in Dermatology 6 1 32–39 (2007) ​]]>