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  About the SKIN - Sunlight and Sun Protection  
Basic Recommendations for Sun Protection

UVA rays can penetrate down into the connective tissue and are the primary cause of immunosuppression and chronic sun-induced damage like premature skin ageing. UVB rays can reach as far as the deepest cell layers of the epidermis and are the main cause of sunburn, DNA damage and skin cancer.

With the help of an advice table, it is easy to determine the suitable individual protection factor...
With this advice table, it is easy to determine the suitable individual sun protection factor you based on your skin's sensitivity to the sun (skin pigmentation) and the radiation intensity.


Correct Use of Sunscreens
  • At the beach you often see people putting on sunscreen after they arrive, but sun protection products need at least 30 minutes to develop their protective potential, as the chemical filters must first bond to the horny layer. The result for the user is a sunburn despite sunscreen application. It is especially important for people with skin types I - III to apply sunscreens at least 30 to 45 minutes before sun exposure.
  • Shadow as a sunblock? Assuming that shade or a beach umbrella guarantees complete protection from UV radiation can lead to a painful sunburn. The reason is that scattering of shorter wavelengths is very pronounced, giving the skin too high a dose of UV radiation even without being in direct sunlight. The "shadow rule” is very important to remember for UV protection of the skin: If your shadow is shorter than you are, then there is a danger of UV-induced skin damage.
  • Water - protection by cooling? The widely held belief that being under water protects you from UV radiation is a misconception: Even one meter below the water’s surface the intensity of UVB radiation is still almost 50%, which means a sunburn can occur even here. The cooling effect of water can also mask pain.
  • We supply Lip Balm with Sunscreen in India
Golden Sun Rules for Sensitive Sun Protection
  • Extensive sun exposure at peak hours between 11 a.m. and 3. p.m. and direct sun should be avoided.
  • Apply sun protection products generously before sun exposure and re-apply every two hours - especially after sweating, swimming and towelling.
  • Do not expose babies and small children under 3 years of age to direct sunlight.
  • Regard your phototype.
  • Overexposure to the sun is a serious health risk, especially for small children. Use high sun protection factors and cover-up with protective clothes, sun hat and sun glasses.
  • After peelings and laser treatments and in case of drug-induced photo-sensitisations, avoid sun and use very high sun protection factors (SPF 50+).
Solar Spectrum
Sunlight and sun protection Sunlight consists of a spectrum of various visible and invisible types of radiation with wavelengths ranging from 280 nm to 3000 nm. Radiation emitted by the sun is partly absorbed by the ozone layer.


Sunlight consists of a spectrum of several visible and invisible types of radiation with wavelengths ranging from 280 nm to 3000 nm. Radiation emitted by the sun is partly absorbed by the ozone layer, by clouds and by air pollutants.

The most important in terms of pathological damage to the skin are the invisible UVA and UVB rays, which stimulate the body's own photoprotective mechanisms in the different skin layers. According to leading photobiologists the shortwave UVC radiation, which has strong erythematogenic and carcinogenic effects on human skin, is completely absorbed in the stratosphere and atmosphere and never reaches the earth's surface.

Some types of radiation reach the earth directly and others indirectly after being scattered in the different layers of the earth's atmosphere. The amount of scattering depends on the wavelength: the shorter the wavelength, the greater the scattering. Only small doses of sunlight are needed to have positive effects on the human organism.

UV rays and their effect on the skin
  • With increasing wavelengths both the percentage of penetrating radiation and the depth of penetration increase. At 300 nm, which is in the UVB region, 10 percent of the radiation still reaches the basal cell layer of the skin. 
  • The highly erythematogenic UVB rays are the main cause of DNA damage and sunburn (erythema solare), the most common acute light-induced damage. They are additionally responsible for epidermal changes accompanying chronic, light-induced damage.
  • The skin-burdening UVB portion of sunlight is influenced by geographical factors such as latitude and altitude (alpine, coastal regions, etc.), as well as the time of day and level of air pollution. Thinning of the ozone layer in particular has led to a rise in UVB radiation.
  • UVB radiation acts as a local immunosuppressant by damaging the Langerhans cells, which are responsible for antigen presentation in the epidermis. Langerhans cells respond to UV radiation by leaving the epidermis. Immunological studies on persons after prolonged exposure to UVB radiation reveal an additional, systemic immunosuppression. It is assumed that keratinocytes in the epidermis release immunosuppressive factors to the immune system.
  • UVA rays penetrate as far as the connective tissue and cause changes in the dermis which can result in irreversible long turn damage, e.g. premature skin ageing (photoageing). In addition, they are primarily responsible for the formation of cell-damaging free radicals.
  • Distribution of Langerhans cells (dark-coloured).
Other dermatological impacts of UVA radiation :
Most important trigger of sun allergy - polymorphous light eruptions (PLE) PLE is the most common sun-induced skin disease. The formation of free radicals induced by UV radiation is considered a causative factor in this disease which occurs mostly in younger women.
  • Photoallergic and phototoxic skin reactions.
  • Photoallergic and phototoxic reactions can be triggered by chemical substances - including certain active ingredients in sunscreen and skincare products - under the influence of sunlight and/or by staying in the sun when taking certain medications.
Formation of free radicals (oxidants)
UV radiation, particularly UVA, triggers skin damage through the formation of free radicals. Free radicals are chemical compounds with a free electron that are highly reactive. Free radicals damage the cells of the epidermis and dermis. The cumulative action of these processes over years gradually leads to the signs of chronic light-induced damage. They are also considered triggers polymorphous light eruptions (PLE).

Skin's Intrinsic Photo protection

Its own protection mechanisms make the skin able to protect itself against the negative effects of UV radiation. These mechanisms include...

Sunlight has many positive effects on the body: It increases our vitality and well-being, promotes circulation and metabolic processes and activates vitamin D production. Just a small dose of sunlight is enough to achieve this "feeling of well-being". Through its own protective mechanisms the skin is able to protect itself from the negative effects of UV radiation. These mechanisms include :
  • Pigmentation
  • Thickening of the horny layer
  • DNA repair mechanisms
  • Formation of the body’s own UV filtering substances, such as urocanic acid
  • Activation of the body’s own antioxidants
It takes about 2 to 4 weeks at a low UV dosage level for the skin to produce the pigmentation and thickening of the horny layer necessary for its own photoprotection.

Protective mechanisms

Pigment formation (melanin synthesis)
Tanning results from the synthesis of melanin in pigment- forming cells (melanocytes) of the epidermis. Pigment formation is induced by UV radiation.

In the epidermis, melanin pigments form a natural protection from the sun by reducing the radiation energy through dispersion and absorption. Formation of new melanin is stimulated (indirect pigmentation).

Direct or immediate pigmentation is triggered mainly by UVA radiation : Weakly coloured melanin precursors are darkened by oxidation. However, this immediate tanning of the skin is transitory and offers only inadequate protection from the sun.


Melanosomes are transferred from the melanocytes to the keratinocytes via the pigment units (one melanocyte per 36 keratinocytes). The released melanin protects the DNA by surrounding the cell nuclei. The pigment subsequently migrates to the skin surface with the epidermal cells.

A feedback mechanism triggered by the increased activity of the enzyme tyrosinase needed for melanin formation possibly also slows cell renewal, causing a thickening in the horny layer of the skin.

Pigmentation types :

An individual's sensitivity to UV radiation and proneness to sunburn are determined by the thickness of the skin's horny layer and its pigment content. Europeans are classified into 4 different pigmentation types :


Stratum corneum thickening
Exposure to sunlight stimulates physiological photoprotection, leading not only to melanin formation but also a considerable thickening of the horny layer (hyperkeratosis). Together with melanin this thickening forms an effective shield against UV radiation.

DNA repair mechanisms
UVB irradiation can cause dose-dependent DNA damage to the epidermal cells. The skin has DNA repair mechanisms (excision repair and photoreactivation) that can somewhat reduce the amount of cell damage caused by the action of light.

In excision repair (dark repair), damaged DNA segments are recognised and removed by enzymes. The damaged DNA segments are replaced by intact segments produced by enzymatic synthesis.

In photoreactivation, damaged DNA segments are repaired by an energy-dependent enzyme in two steps. The enzyme obtains the energy required for this by absorbing UVA radiation in the region of 340 to 430 nm.

However, if the skin is exposed for too long and left in the sun unprotected, such as when on holiday, the skin's photoprotection is inadequate, and the DNA repair mechanisms will be overburdened. The cells either die from too much radiation damage or they mutate and pass on false genetic information. The result is chronic light-induced damage with solar elastosis, precancerous lesions and squamous cell carcinomas. Unlike acute light-induced damage (sunburn), these chronic manifestations of light-induced damage are irreversible.

Urocanic acid
Urocanic acid is formed from the amino acid histidine in the keratinocytes of the stratum corneum and found only in sweat. After exposure to UVB radiation the trans isomer of urocanic acid is converted to the higher energy cis isomer, thus protecting the skin by absorbing and dissipating the harmful radiation energy.

Radical scavengers (antioxidants)
The cells of the skin are equipped with enzymes (such as superoxide dismutase and peroxidases) for protection against the cell-damaging effects of free radicals. Among the most effective radical scavengers are tocopherol, ascorbic acid and ß-carotene, all of which are assimilated with food. Melanin formed by the melanocytes also acts as a radical scavenger.

3-dimensional Sun Protection
Physical sunscreens are inorganic substances that reflect or scatter UV radiation reaching their surface but do not allow it to penetrate the skin.

When exposed to the sun, suitable sunscreen products should be used to support the skin’s own protection mechanisms. Important ingredients of a sunscreen product are the filter substances that act as a shield between the sun and the skin.

A distinction is made between physical and chemical sunscreens.

Physical sunscreens are inorganic substances that reflect or scatter UV radiation reaching their surface but do not allow it to penetrate the skin. Normally they are mineral pigments such as titanium dioxide. An important development have been micronized pigments with a particle size between 10 and 50 nm. When used in a suitable base (cream, lotion), physical sunscreens are not a cosmetic problem.

Chemical sunscreens are organic aromatic compounds that can absorb UV radiation. A distinction is made between UVB, UVA and broadband filters depending on the wavelength range absorbed. The absorbed energy is released again as thermal radiation.

Photoprotection for Highly Exposed Areas
Because facial skin is permanently exposed to the sun and has a thin epidermis, it is at particular risk and unable to respond to the constant UV exposure with adequate thickening of the horny layer.

Photoprotection for sensitive facial skin
While biological ageing is genetically determined, premature ageing of the skin, particularly on the face and hands, can be attributed to exogenous stress. There is no doubt that UV radiation is one of the most important factors in premature ageing of the skin. The face is especially affected for the following reasons :

Due to permanent sun exposure the facial skin with its thin epidermis is at particular risk and unable to respond to the constant UV-burden with adequate thickening of the horny layer. In addition, the lips in particular cannot form pigmentation. The consequences of frequent exposure to the sun are wrinkling, premature UV-induced skin changes (premature ageing), and skin tumours.

Damage to the epidermis and connective tissue markedly reduces the stability and elasticity of the skin. The visible effects of damaged connective tissue are often described as "sagging". Damage to DNA of the epidermis can cause actinic keratosis, basal cell carcinomas and squamous cell carcinomas to develop. This is especially true for people who stay outdoors unprotected on a daily basis.

Results of a study have shown that daily application of a sunscreen over a 2-year period can significantly reduce damage to the dermal connective tissue (solar elastosis) and protect from actinic keratosis.

Photoprotection for scalp and hairy areas
The scalp has a thin epidermis, and when lelft uncovered is exposed to direct and therefore more intense UV radiation especially in areas where hair growth is reduced. Other hairy areas of the body, also those with sparse hair growth, should also be protected with appropriate clothing and special sunscreen preparations that are easy to apply.

Photoprotection for Allergy-Prone Skin
Recommended are sunscreen products containing no fragrance or emulsifiers such as products based on hydrodispersion gels with a high sun protection factor.

Sun Protection for Medical Conditions

UV radiation can provoke or aggravate a number of skin disorders including lupus erythematosus or herpes simplex and rosacea. UV radiation can provoke or aggravate a number of skin diseases. Skin diseases provoked or worsen by UV radiation.
  • Lupus erythematosus, an autoimmune disease accompanied by scaly rashes on both cheeks and the bridge of the nose, can be aggravated by UVB and/or UVA radiation. In such cases, sunscreen products with a high sun protection factor should be used for skin protection, especially on the face.
  • In the hereditary disease xeroderma pigmentosum, the DNA repair mechanism is defective. Any damage to the DNA caused by UVB can never be repaired. As a result, precancerous lesions develop on skin areas exposed to light even at a young age followed by skin carcinomas and melanomas. These patients should avoid UV radiation at all times and use sunblocks.
  • Herpes simplex recidivans is a recurring disease with itching, a feeling of tightness and clusters of crusted blisters frequently occurring on the face (lips, nose) that is sometimes painful, and accompanied by regional swelling of lymph glands. Since UV radiation can cause a further outbreak, a sunblock or a protective stick with a high sun protection factor should be used before exposure to the sun.
  • Rosacea is a disease occurring in people with a high sensitivity to external noxae that is manifested as reddening of the facial skin. The first stage of the illness is also known as couperose. Any triggering effect, and particularly UV radiation, must be avoided. To protect the skin from sunlight, sufferers should use a sunblock or daily sun protection product with a high protection factor, especially for the sensitive facial skin.
  • Albinism is a congenital absence of the pigment melanin affecting the whole body or parts of it. Melanocytes are present, but the enzyme responsible for melanin formation is dysfunctional. These patients should use sunscreens that have a high sun protection factor and are ultra waterproof. 
  • Patients with vitiligo display defined, depigmented skin areas occurring roughly symmetrically on both sides of the body. Skin areas protected from light such as the armpits and genital area can also be affected. No melanin formation can take place in these areas. Only horny layer thickening is possible. Because of the reduced capacity of the skin's own protective mechanisms, the affected areas need to be additionally protected with suitable sunscreen products with a high sun protection factor. UV radiation induces cell damage in different layers of the skin, especially in people with pigmentation disorders.
  •  Patients with a history of UV-induced skin tumours (basaliom, spinaliom, melanom) are at a high risk of developing further skin tumours and must be especially protected from all forms of UV radiation. Therefore medicinal sunscreen products with a high sun protection factor that should also replenish lipids are required.
Photoprotection after Therapy

After acne therapy, peels and anti-aging treatments as well as on scars and after laser treatments.

Following acne therapy, peels or treatments for premature ageing It has been observed in acne patients with photodamaged skin that application of tretinoin not only improves acne but also reduces the photodamage clinically and histologically. It could be shown that precancerous lesions were eliminated. The desired peeling effect makes the skin thinner and thus more photosensitive. Therefore, it must be protected from sunlight. All skincare products must offer ample moisturising factors.

Chronic photodamage is characterised by thin, dry, scaly, itchy skin with loose connective tissue, elastosis, actinic keratosis, wrinkles and age spots. Treatment of premature skin ageing with retinoic acid (tretinoin, vitamin A acid) has keratolytic, anticarcinogenic, and, when administered orally, antiseborrheic effects.

When on Medication

Many medicines can trigger photodynamic reactions, and these reactions can be phototoxic and/or photoallergic. Foremost among them are the antibiotics of the tetracycline group, followed by sulphonamides and certain substance groups found in antidiabetics, diuretics, neuroleptics, antidepressants and antirheumatics. Topically applied medications can also show such adverse effects. It is therefore necessary to include any medications when determining the medical history of any photodermatosis. Naturally, these patients must receive an appropriate medicinal sunscreen product with a high SPF selected according to the skin type.

For scars and after laser therapy
Rigorous sun protection with a high SPF is recommended in such instances, and a product with micropigments is especially indicated, since these sunscreens do not penetrate into the skin and will place no additional burden on the affected areas.