Skin microneedling with Dermapen

Skin microneedling with Platelet Rich Plasma

Skin microneedling is also known as Percutaneous Collagen Induction (PCI) or Collagen Induction Therapy (CIT). Microneedling is the term used when the needle length used for PCI is less than 1mm. Medical skin needling is the term used when the needle length used for PCI is greater than 1mm. Home skin microneedling kits have needle lengths of 0.5mm or less.

Skin microneedling is used for the treatment of scarring, stretch marks and to improve skin texture.

Besides skin microneedling, there are many other procedures that can be used to improve skin texture, stretch marks and scarring.

 

Treatments for skin texture, stretch marks and scarring
Chemical peels
Mechanical dermabrasion
Intense pulsed light therapy
Non-fraxionated, ablative CO2 and ER:YAG lasers
Fraxionated, ablative CO2 and Erbium:YAG lasers
Fraxionated, non-ablative, Erbium-glass (Fraxel) lasers
Medical microneedling without platelet rich plasma (PRP)
Medical microneedling with platelet rich plasma (PRP)


The non-fraxionated, ablative CO2 and ER:YAG lasers, deeper chemical peels and deeper dermabrasion will destroy the epidermis completely in the process of trying to improve skin texture and scarring. Optimally you want to only improve the skin anatomy, not damage certain parts and improve other parts. Perhaps unsurprisingly, the procedures that destroys the epidermis completely, can cause a persistent lightening (hypopigmenation) or darkening (hyperpigmentation) of the skin. Also, the epidermis can become thinner (atrophic) as a result. Scarring, including hypertrophic scarring, has been reported, especially on areas with thinner skin, like the neck.

I have therefore eliminated procedures that destroys the epidermis completely from the above list. Superficial chemical peels and superficial dermabrasion does not destroy the epidermis completely, which makes it safer compared to deeper chemical peels and deeper dermabrasion , but is also much less effective and are therefore also left out of the list. The following treatment options remain.

 

Safer, but still effective treatments for skin texture, stretch marks and scarring
Intense pulsed light therapy
Fraxionated, ablative CO2 and Erbium:YAG lasers
Fraxionated, non-ablative, Erbium-glass (Fraxel) lasers
Medical microneedling without platelet rich plasma (PRP)
Medical microneedling with platelet rich plasma (PRP)


Intense pulsed light is a fantastic treatment for pigmentation and blood vessels, but skin microneedling, for example, has at least a 2 times greater stimulating effect on collagen production.[Kim et al. Greater Collagen Deposition with the Microneedle Therapy System Than with Intense Pulsed Light. Dermatol Surg 2011;37:336–341]. 

 

Medical microneedling combined with Platelet Rich Plasma, the so-called Vampire Facial or Vampire Peel, has a 10-30% greater collagen stimulating effect than without Platelet Rich Plasma.

 

Dropping Intense Pulsed Light and Medical microneedling without PRP leaves us with the following options:

 

Treatments of choice for skin texture, stretch marks and scarring
Fraxionated, ablative CO2 and Erbium:YAG lasers
Fraxionated, non-ablative, Erbium-glass (Fraxel) lasers
Medical microneedling with platelet rich plasma (PRP)


When if comes to the safety of these treatments fraxionated CO2, Erbium:YAG, Fraxel and skin microneedling devices all injure the skin in a controlled, pixellated way, by puncturing tiny holes through the epidermis into the dermis. Only a small percentage of the total surface area of the epidermis is affected. Lasers punctures the skin with columns of light that heats water in the epidermis and dermis. Skin microneedling punctures the skin mechanically with tiny needles. The lasers involve heat, whereas needling does not. The greater the heat, the higher the risk of a thermal injury that can lead to pigment abnormalities and scarring. The advantage here goes to medical microneedling.

The lasers involve heat, whereas microneedling does not. The greater the heat, the higher the risk of a thermal injury that can lead to pigment abnormalities and scarring.

Considering the efficacy of the above three treatment option, the depth of penetration into the dermis for the various devices are as follows:

DeviceDepth of penetration
Fraxel laser0,3mm - 1,4 mm deep (avg 0,679 mm, median 0,580 mm)
Fraxionated Er:YAG laser0,3 mm - 1,162 mm (avg 0,825 mm, median 0,525 mm)
Fraxionated CO2 laser0,3 - 2,52 mm deep (avg 0,895 mm, median 0,600 mm)
Needling devices0,2 mm - 3 mm


Please see:

Sherling et al. Consensus Recommendations on the Use of an Erbium-Doped 1,550-nm Fractionated Laser and Its Applications in Dermatologic Laser Surgery. Dermatol Surg 2010;36:461–469
Kabir et al. Histological Validity and Clinical Evidence for Use of Fractional Lasers for Acne Scars. Cutan Aesthet Surg 2012 Apr-Jun; 5(2): 75-90.

Medical skin microneedling devices can therefore penetrate deeper, but it is unclear how much the depth of penetration actually matters for the improvement of scarring and the induction of new collagen formation. 

To date (March 2014), there are no definitive double blind studies comparing the beneficial effect of different lasers to microneedling on different types of scarring and skin texture. To get an idea of relative efficacy we therefore have to look at papers reporting on the effect of an individual treatment on scarring and skin texture and then try to compare these papers as best we can.

A recent review article in the British Journal of Dermatology [Ong MWS, Bashir SJ. Fractional laser resurfacing for acne scars: a review. British Journal of Dermatology 2012;166:1160–1169] looked at 428 papers on the treatment of acne scarring with non-ablative (Fraxel) and ablative (CO2 and ER:YAG) lasers. They summarize their results as follows:

“Patients who opt for fractional laser resurfacing with a nonablative FP laser (Fraxel) will experience: erythema for between 1 and 3 days which should resolve within 1 week; less likelihood of developing PIH, and if it does occur, it should resolve within 1 week; scar improvement of 26–50%; and a relatively comfortable procedure”.

There are no papers involving large numbers of patient on the treatment of acne scarring with skin microneedling. Looking at the individual published papers [Leheta T et al. Percutaneous Collagen Induction Versus Full-Concentration Trichloroacetic Acid in the Treatment of Atrophic Acne Scars. Dermatol Surg 2011;37:207–216] on the treatment of acne scarring with skin microneedling, improvement for rolling scars is in the range of 30-80%.

It is therefore not possible to draw a definitive conclusion from the lasers studies vs the microneedling studies. It seems safe to say that both fractionated lasers and microneedling works very well for acne scars, but the fractionated lasers might be slightly better for box car type scars and skin microneedling might be slightly better for rolling acne scars. There is in my estimation no clearly demonstrated advantage for either the fractionated lasers or skin microneedling in the treatment of acne scarring and by extension skin texture. Furthermore, additional treatments will result in further improvement with both fractionated lasers and skin needling. This raises the possibility that with enough treatments both the lasers and microneedling will eventually reach the same level of improvement, even if there is a difference in efficacy with individual treatments.

 

Cost for a full face treatment for scarring or skin texture improvement 
Medical skin needling without platelet rich plasma (PRP)R1900
Medical skin needling with platelet rich plasma (PRP)R2600
Fraxionated Erbium-glass (Fraxel) lasersR7500
Fraxionated CO2 and Erbium:YAG lasers R15000


Medical skin microneedling requires topical anesthetic ointment for pain relief during the procedure. Fraxionated Erbium-glass (Fraxel) laser requires topical anesthetic ointment with or without oral analgesics and sedatives. There are multiple pain relief options for fraxionated CO2 and Erbium:YAG lasers. Option 1 is topical anesthetic ointment, plus oral analgesics, plus oral sedatives, plus multiple local anesthetic injections; options 2 is conscious sedation and option 3 is general anesthetic.

Until the definitive comparative studies are done I think similar efficacy, decreased cost, increased safety and less downtime makes medical microneedling with Platelet Rich Plasma the treatment of choice for scarring, stretch marks and to improve skin texture.

 

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Adult Acne

Adult acne first develops in the twenties or later. The strict definition of Adult Acne is Acne that first develops after 25, but definitions vary slightly.

Adult acne is common. In America 50% of adult women has Acne in their twenties, 35% in their thirties, 26% in their forties and 15% in their fifties.

Teenage and adult acne is due to excessive sebum production from oil (sebum) glands. The increased sebum production leads to changes in the mouth of the hair follicle, the infundibulum, which enlarges and becomes plugged with open comedones (black heads) and closed comedones (white heads). A bacterium that normally occurs on the skin, Propionibacterium Acnes, proliferates in the excess sebum, which leads to inflammation, pimples and worse blackheads and whiteheads via biofilm formation.

Adult Acne is common around the jaw line area and is mostly inflammatory (pimply), whereas teenage acne occurs more in the T-panel and is often a mix of inflammatory lesions (pimples) and comedones (blackheads and whiteheads).

In the teenage years increased sebum production is due to the natural surge in hormones that occurs at puberty. This clearly cannot be the cause of Adult Acne.

The causes of Adult Acne include unnaturally increased testosterone levels from a variety of sources, a genetically increased sensitivity to testosterone, increased insulin-like growth factor 1 (IGF-1) that mimics the effect of testosterone, oral medication, cosmetics, smoking and possibly raised insulin levels.

Causes of unnaturally increased testosterone levels:

  • Polycystic ovarian disease
  • Overproduction of testosterone from a tumor of the ovaries or testis
  • Overproduction of testosterone from adrenal gland hyperplasia or an adrenal gland tumor
  • Overproduction of testosterone in the skin, due to stress induced increased release of Corticotrophin Releasing Hormone (CRH) from the brain
  • a Relative excess of testosterone versus estrogen around the middle of the menstrual cycle
  • a Relative excess of testosterone versus estrogen around the menopause

Causes of increased Insulin-like growth factor (IGF-1):

Oral medications that can cause Adult Acne:

  • Oral Contraceptive pills (OCP’s) that contain 1st generation progestins, like norgesterol
  • OCP’s that contain 2nd generation progestins, like norethindrone, ethynodiol diacetate, and levonorgestrel
  • OCP’s that contain third generation progestins, like norgestimate or desogestrel
  • Vitamins B2,B6,B12 and D2
  • SSRI’s, like Prozac
  • Lithium
  • The Tuberculosis drugs, Isoniazid and Ethionamide
  • The epilepsy drugs, Phenytoin and Phenobarbital
  • Glucocorticosteroids, like Prednisone
  • Anabolic steroids
  • Corticosteroid creams and ointments
  • Iodides and Bromides. Iodides are found in cold and asthma preparations, kelp and vitamin & mineral supplements. Bromides are found in sedatives, analgesics and cold remedies

Other causes of Adult Acne;

  • Cosmetics, especially occlusive petroleum bases moisturizers
  • Smoking
  • Increased insulin levels (hyperinsulinemia) can stimulate sebum production.

Often, what appears to be Adult Acne, is in fact another condition mimicking acne. These Acne mimics include:

The diagnosis of Adult Acne requires a detailed history and careful examination. In addition to Adult Acne an irregular or absent menstrual cycle, excess hair on the face and body (hirsutism), loss of hair from the scalp (androgenetic alopecia), oily facial skin (seborrhea), a milky discharge from the breasts (galactorrhea), enlargement of the clitoris (cliteromegaly), a coarser voice and infertility are all signs of raised testosterone levels.

If the diagnosis is Adult Acne the next step is to identify and treat any underlying cause. If there is an identifiable cause for the Adult Acne, eliminating it will most likely clear the Acne.

Laboratory blood tests for FSH & LH (brain/pituitary gland origin), DHEA-S (adrenal gland origin) , Free Testosterone & Total Testosterone (ovarian origin), Prolactin (brain/pituitary gland origin), SHBG (liver origin), delta-4-androstenedione (adrenal gland origin), 17-hydroxyprogesterone (adrenal gland origin) and insulin might be requested. In women blood tests must be done within a few days of menstruation, when hormonal levels are naturally at their lowest, to avoid confusing results and women should also not be on the oral contraceptive pill. Abnormal hormone values might require closer examination of the ovaries, adrenal glands or pituitary gland.

Oral medication, vitamin supplements and cosmetics might be stopped or changed. Adult acne patients need to stop smoking. A low glycemic index (low carbohydrate/high fat – LCHF) diet to lower IGF-1 release and insulin levels might be required. Lower stress levels, to reduce Corticotrophin Releasing Hormone (CRH) levels, could be helpful.

Some patients will have no identifiable cause for their Adult Acne. Also, patients that have eliminated possible causes of Adult Acne, might still get Adult Acne. These patients will require general anti-Acne therapies, as used for Acne in puberty.

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Acne in pregnancy

Acne in pregnancy is not uncommon. The course and severity of Acne in pregnancy is unpredictable. Pregnancy can lead to an improvement or worsening of Acne. It is possible to get Acne and pimples for the first time when pregnant. The treatment of Acne in pregnancy is complicated by the fact that only certain medications and procedures can be used safely.

The Food and Drugs Administration (FDA) have graded medications into 5 categories of safety:

Category A: Adequate and well-controlled studies have failed to demonstrate a risk to the foetus in the first trimester of pregnancy, and there is no evidence of risk in later trimesters.

Category B: Animal reproduction studies have failed to demonstrate a risk to the foetus and there are no adequate and well-controlled studies in pregnant women.

Category C: Animal reproduction studies have shown an adverse effect on the foetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

Category D: There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

Category X: studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits.

Only medication from category A, category B and occasionally category C can be used in pregnancy. Personally, I’ll only consider medications from category A or category B. At present (March 2014), there are no medications in category A for the treatment of Acne in pregnancy. That leaves us with the following category B medications.

Topical anti-Acne products (creams and lotions) that can be used in pregnancy:

  • Clindamycin phosphate (e.g. Dalacin T™)
  • Erythromycin (e.g. Ilotycin T.S.™)
  • Azeleic Acid (e.g. Skinoren™)
  • Benzoyl peroxide gel and wash (e.g. Benzac AC 5™) – Category C, not an option for me.
  • Topical glycolic acid and salicylic acid – Not categorised by the FDA, so also not an option for me.
  • Topical retinoid agents – Category C, so not an option for me.

First line oral anti-Acne medications that can be used in pregnancy:

  • Amoxicillin 250mg-500mg 2 x per day
  • Cephalosporins i.e., Cephalexin 500mg PO BD

Second line oral anti-Acne medications that can be used in pregnancy:

  • Azithromycin 500mg on Monday, Wednesday and Friday
  • Erythromycin stearate (not Erythromycin estolate or Erythromycin ethylsuccinate) 250mg-500mg 2-4 x per day

Third line oral anti-Acne medications that can be used in pregnancy:

  • Clindamycin 75mg-150mg 2 x per dag

Anti-acne procedures that can be used in pregnancy:

  • Red light therapy
  • Intense Pulsed light therapy
  • Skin needling
  • Pulsed-dye laser therapy
  • Photodynamic therapy with Aminolevulinic acid (ALA) as light sensitiser has been described in the literature, but ALA is FDA category C and therefore not something I would use.
  • Narrowband (311nm) UVB light therapy has also been described in the literature, but this is also not a treatment option for me, because prolonged UVB exposure leads to depressed Folic Acid levels.

For very mild cases of Acne in pregnancy I generally start with Clindamycin phosphate with or without Azeleic Acid combined with a sebum reducing face wash.

More severe cases might require the addition of an oral antibiotic, like Amoxicillin or Cephalexin. If the patient is allergic to one of these antibiotics, or the Acne is non-responsive to the antibiotics, Azithromycin or Erythromycin stearate is the next choice of oral antibiotic.

Clindamycin can be used in the unlikely scenario where none of the previous antibiotics can be used.

The only safe Erythromycin in pregnancy is Erythromycin stearate. Erythromycin estolate causes reversible liver toxicity in 10% of patients. Erythromycin ethylsuccinate can cause fetal heart defects when used in the first trimester. To avoid accidental dispensing mistakes, it is perhaps best rather to avoid all Erythromycins in the first trimester.

My approach for the most severe cases of Acne in pregnancy is the combination of a topical product plus an oral antibiotic plus skin needling. Skin needling has the added advantage of improving skin texture and acne scarring.

The treatment of Acne in pregnancy is challenge. There is no medication that is 100% safe. Even if a medication has shown no negative effects on a fetus, the mother can still have a reaction to a medication, which in turn might affect the pregnancy.

Acne in pregnancy can be treated successfully, but the pros and cons of the different treatment options needs to be weighed up carefully.

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Skin tags

Skin tags are small 2-6mm wide, 10-20mm high, flesh coloured, benign growths of the skin that can develop on the neck, underarms, around the eyes and the inner upper legs. Skin tags are not dangerous and has no real medical importance.

They can be unsightly and bothersome in the neck area and irritating in the underarm and groin area. When skin tags are damaged from shaving, rubbing or some other mechanical irritation, they can become red and painful, or even bleed. If the blood supply to the skin tag is damaged they can turn alarmingly black, but will eventually fall off.

Anyone can develop skin tags, but weight gain, a genetic tendency, Syndrome X, pregnancy and diabetes are predisposing factors. The medical name for skin tags are fibroepithelial polyps or Acrochordons. They are also known as “vleismoesies” and “muistepels” in Afrikaans. “Vleismoesie” translates roughly to “meaty mole” and “muistepel” translates roughly to “mouse nipple”.

Dermatosis Papulosis Nigra is a similar growth to skin tags, but they are darkly pigmented and occur on the face of people with dark skin.

Skin tags are easily removed with shave excision, nipping them off with a special pair of curved scissors, freezing them with liquid nitrogen, or with light cautery. Flat skin tags can be removed with light liquid nitrogen therapy or preferably light cautery, which is more accurate. The elevated ones are removed with curved scissors, shave excision or light cryotherapy, depending on the size of the skin tag.

Liquid nitrogen does not require any local anaesthetic, but the surgical options and cautery most often do. To minimize discomfort a patient can have a numbing ointment applied for two hours, before the procedure. The bigger skin tags can then be further numbed with a local anaesthetic injection.

These procedures can result in scarring or excessive pigmentation if not done with the correct intensity. I will therefore, in some patients, initially remove only one or two skin tags to first test a patients healing response. If the patient is happy with the result, we can then remove the remaining skin tags.

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Sensitive skin

Sensitive skin is not an uncommon problem. It is almost always a problem of facial skin, but can occur anywhere or everywhere on the body. The most common complaint is that facial products start to burn, tingle or sting when applied. The product often needs to be washed off quickly to relieve the sensation.

Sensitive skin is a symptom. It is not a specific disease, like asthma. Therefore, the question to ask when you have sensitive skin is: “What is the underlying condition that is causing the sensitive skin?”

From a purely anatomical or physiological perspective any condition that can disturb the epidermis, which is the top layer of the skin, can lead to a sensitive skin. Nerve fibres terminate in the epidermis, so any condition that disturbs the area around a nerve fibre can result in that nerve fibre becoming too easily stimulated. This over sensitivity of nerve fibres is experienced by the patient as sensitive skin.

The two most common causes of a sensitive skin are Atopic Dermatitis and Irritant Dermatitis.

Atopic Dermatitis is a genetic condition that results in many different signs and symptoms, but a tendency to dryness is perhaps the most common symptom. Dryness leads to an abnormal epidermis, disturbs the environment of the epidermal nerve endings and opens the door for sensitive skin to develop. Because dryness is the primary problem, the cornerstone of the treatment of Atopic Dermatitis is moisturisers and the avoidance of products that can dry the skin even more, like regular soaps and cleansers. Over time, this will improve the epidermis, normalize the area around the nerve fibre and result in less sensitivity. In many patients Atopic Dermatitis only manifests later in life.

Irritant dermatitis is caused by exposure to irritants. These irritants are most often soaps, cleansers, toners and other cosmetic preparations. Very often these products are advertised as mild, natural and non-irritant. The cornerstone of the treatment if Irritant Dermatitis is to avoid the irritant. With complete avoidance of the irritant and other supplementary measures, the skin sensitivity will gradually subside over a period of weeks to months.

Irritant dermatitis can often be superimposed on Atopic dermatitis. The patient with Atopic dermatitis already has an abnormal epidermis and is therefore already much more sensitive to the potential irritant effects of soaps and other cosmetic products. Patients often find it difficult to believe that their facial products or facial cosmetic routine can play a role in their sensitive skin. “Doctor, but I have used those products for years”, is a common explanation for why the facial products cannot possibly play a role. But, it can.

There are two possible explanations why an existing product can suddenly start stinging. Either the person himself/herself has changed or the product ingredients or way of use have changed.

Here are some examples of the “person has changed” scenario:

  • Perhaps an oral medication was started that makes the skin drier. Statins, used to treat elevated cholesterol levels, often leads to dry skin and then increased skin sensitivity.
  • Perhaps the work or home environment changed. Air conditioners can sometimes tip the scale towards dryness.
  • Perhaps a Contact dermatitis has developed. Contact dermatitis is a type of skin allergy that can be investigated by doing an allergy tests, called patch tests.
  • Stress has been showed to influence the epidermis in dramatic ways.
  • The thyroid gland might have become under active, leading to a disturbed epidermis and increased skin sensitivity.
  • The normal ageing process and sun damage leads to increased skin dryness that can then lead to sensitive skin.
  • After the menopause the skin becomes significantly drier and prone to sensitivity

To figure out what exactly tipped the scale towards a sensitive skin and to treat sensitive skin will often require the help of a dermatologist.

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Melasma Treatment Steps

Melasma is a disorder of facial pigmentation. Melasma treatment is a multistep process. The number of steps required differ for patients, but all patients start with step 1 and then progress from there.

Step 1 – Things you can do before seeing a dermatologist

  • If possible, stop the oral contraceptive pill, or switch to an intrauterine device, like the Mirena
  • Apply sunblock at least twice a day, if not wearing make-up. If you do use make-up apply a good sunblock before applying the make-up
  • Use an over the counter depigmenting agent at night

Step 2 – If the above is not effective after 8 weeks, make an appointment to see the dermatologist

  • For milder cases of Melasma the dermatologist might prescribe Azeleic Acid cream or a retinoid cream
  • For more severe cases of Melasma the dermatologist might prescribe a Hydroquinone containing cream at night

Step 3 – If the above is not effective after 8 weeks, the following treatments will be considered

  • Tranexamic acid tablets has recently been investigated in the treatment of Melasma and works well in some patients
  • Topical Tranexamic acid needling or Tranexamic acid intradermal injections
  • Pulsed light treatments
  • Fraxel laser

Once the Melasma is brought under control, the treatment falls back to controlling it, which involves Step 1 above. The treatment of Melasma therefore never actually stops, but is an ongoing process.

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Sunscreen and SPF

SPF is an abbreviation for sun protection factor. It is a slight misnomer, because SPF only indicates a sunscreens ability to block ultraviolet B light. It says nothing about the other type of ultraviolet light that the sun emits, ultraviolet A light. Make sure that your sunblock blocks UVA light as well. If it does not say so on the tube, then rather assume it does not block UVA.

Sunscreen and SPF
The tube should state the SPF value and that it blocks UVA

There is some confusion around what the SPF value indicates and how often you should apply sunscreen. As mentioned, the SPF value indicates a sunscreens ability to block ultraviolet B light.

If it normally takes Y minutes before you sunburn, by using a sunblock cream it would take Y minutes multiplied by the SPF value, before you will sunburn. If you get a sunburn after 10 minutes without a sunscreen, by using a SPF 15, you will get a sunburn after 150 minutes. If you get a sunburn after 8 minutes without a sunscreen, by using a SPF 30, you will get a sunburn after 240 minutes.

Irrespective of the above formula, you should always reapply sunblock cream after 2 hours or so, because sweating and rubbing will removed the sunscreen from your skin. This is why sunscreens with a very high SPF value are overkill. A sunscreen only has to protect you from ultraviolet light for 2 hours or so, before you should anyway reapply the sunscreen.

If you normally get a sunburn after 10 minutes without a sunscreen, then with a SPF 15 sunscreen, you will get a sunburn after 150 minutes, which is 30 minutes longer than needed, because after 2 hours you should anyway reapply the sunscreen.

For most people a SPF 30 sunblock cream that also block UVA light is more than enough. Use it and reapply the sunscreen every 2 hours. Reapply the sunblock directly after swimming as well. Wear a hat, ultraviolet blocking sunglasses and protective clothing. Also, try to avoid sun exposure around midday.

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Sun damage

Sun damage is a result of DNA damage to skin cells. DNA, the brain of the cell, absorbs Ultraviolet B light and this damages the genetic code. Damaged genes are incapable of maintaining normal cell function. The visible result is sun damage.

The four categories of sun damage are colour change, texture change, loss of tightness and skin cancer.

Sun damage on chest
Sun damage on chest

Colour changes are either red, brown or white.

Brown blotches are caused by an irregular increase in a pigment called Melanin. Melanin is normally spread evenly through the epidermis. DNA damage to melanocytes, the cells that produce melanin, causes irregular production of the melanin pigment.

A decrease in melanin production leads to lighter or even white spots. An increase in melanin production results in brown, dark brown or even black spots.

Red blotches are a result of more prominent blood vessels. Blood vessels can increase in number and in size due to sun damage. An increase in the number of blood vessels is a result of inflammation. When you get a sun burn and the skin goes red and sore, it is due to inflammation. Inflammation is the bodies attempt to heal itself and in the process new blood vessels form by a process called neovascularisation.

Damage to the connective tissue, collagen fibres, elastic fibres and fibroblasts around blood vessels weakens the support structure of blood vessels and causes blood vessel to dilate and increase in size.

The second category of sun damage, a rougher skin texture, is the result of sun damage to the connective tissue in the dermis, sun induced enlargement in oil glands, enlargement of pores and dehydration of the skin.

Loss of tightness of the skin is also due to ultraviolet light (especially ultraviolet A) damage to elastic and collagen fibres and DNA damage to fibroblast cells that make collagen and elastic fibres. Eventually this leads to skin sagging.

The fourth category of sun damage is skin cancer. Sun induced skin cancer is a result of progressive and cumulative damage to the DNA of the epidermal cells. There are two main cell types in the epidermis. Damage to the DNA of melanocytes, the pigment forming cells, leads to Melanoma. Melanoma is a highly aggressive form of cancer, with a tendency to spread (metastasize) throughout the body early.

Damage to the DNA of keratinocytes, the cells that make up the bulk of the epidermis, causes the most common skin cancer in humans, Solar Keratosis. Eventually more aggressive skin cancers like Squamous cell carcinoma and Basal cell carcinoma develops.

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