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Saturday, January 29, 2022

Sunburn

From Wikipedia, the free encyclopedia

Sunburn
Sunburn Treatment Practices.jpg
A sunburned neck
SpecialtyDermatology
ComplicationsSkin cancer
Risk factorsWorking outdoors, skin unprotected by clothes or sunscreen, skin type, age
PreventionUse of sunscreen, sun protective clothing

Sunburn is a form of radiation burn that affects living tissue, such as skin, that results from an overexposure to ultraviolet (UV) radiation, usually from the Sun. Common symptoms in humans and other animals include: red or reddish skin that is hot to the touch or painful, general fatigue, and mild dizziness. Other symptoms include blistering, peeling skin, swelling, itching, and nausea. Excessive UV radiation is the leading cause of (primarily) non-malignant skin tumors, and in extreme cases can be life-threatening. Sunburn is an inflammatory response in the tissue triggered by direct DNA damage by UV radiation. When the cells' DNA is overly damaged by UV radiation, type I cell-death is triggered and the tissue is replaced.

Sun protective measures including sunscreen and sun protective clothing are widely accepted to prevent sunburn and some types of skin cancer. Special populations, including children, are especially susceptible to sunburn and protective measures should be used to prevent damage.

Signs and symptoms

Blisters from sunburn

Typically, there is initial redness, followed by varying degrees of pain, proportional in severity to both the duration and intensity of exposure.

Other symptoms can include blistering, swelling (edema), itching (pruritus), peeling skin, rash, nausea, fever, chills, and fainting (syncope). Also, a small amount of heat is given off from the burn, caused by the concentration of blood in the healing process, giving a warm feeling to the affected area. Sunburns may be classified as superficial, or partial thickness burns. Blistering is a sign of second degree sunburn.

Variations

Minor sunburns typically cause nothing more than slight redness and tenderness to the affected areas. In more serious cases, blistering can occur. Extreme sunburns can be painful to the point of debilitation and may require hospital care.

Duration

Sunburn can occur in less than 15 minutes, and in seconds when exposed to non-shielded welding arcs or other sources of intense ultraviolet light. Nevertheless, the inflicted harm is often not immediately obvious.

After the exposure, skin may turn red in as little as 30 minutes but most often takes 2 to 6 hours. Pain is usually strongest 6 to 48 hours after exposure. The burn continues to develop for 1 to 3 days, occasionally followed by peeling skin in 3 to 8 days. Some peeling and itching may continue for several weeks.

Skin cancer

Ultraviolet radiation causes sunburns and increases the risk of three types of skin cancer: melanoma, basal-cell carcinoma and squamous-cell carcinoma. Of greatest concern is that the melanoma risk increases in a dose-dependent manner with the number of a person's lifetime cumulative episodes of sunburn. It has been estimated that over 1/3 of melanomas in the United States and Australia could be prevented with regular sunscreen use.

Causes

The cause of sunburn is the direct damage that a UVB photon can induce in DNA (left). One of the possible reactions from the excited state is the formation of a thymine-thymine cyclobutane dimer (right).

Sunburn is caused by UV radiation from the sun, but "sunburn" may result from artificial sources, such as tanning lamps, welding arcs, or ultraviolet germicidal irradiation. It is a reaction of the body to direct DNA damage from UVB light. This damage is mainly the formation of a thymine dimer. The damage is recognized by the body, which then triggers several defense mechanisms, including DNA repair to revert the damage, apoptosis and peeling to remove irreparably damaged skin cells, and increased melanin production to prevent future damage.

Melanin readily absorbs UV wavelength light, acting as a photoprotectant. By preventing UV photons from disrupting chemical bonds, melanin inhibits both the direct alteration of DNA and the generation of free radicals, thus indirect DNA damage. However, human melanocytes contain over 2,000 genomic sites that are highly sensitive to UV, and such sites can be up to 170-fold more sensitive to UV induction of cyclobutane pyrimidine dimers than the average site These sensitive sites often occur at biologically significant locations near genes.

Sunburn causes an inflammation process, including production of prostanoids and bradykinin. These chemical compounds increase sensitivity to heat by reducing the threshold of heat receptor (TRPV1) activation from 109 °F (43 °C) to 85 °F (29 °C). The pain may be caused by overproduction of a protein called CXCL5, which activates nerve fibres.

Skin type determines the ease of sunburn. In general, people with lighter skin tone and limited capacity to develop a tan after UV radiation exposure have a greater risk of sunburn. The Fitzpatrick's Skin phototypes classification describes the normal variations of skin responses to UV radiation. Persons with type I skin have the greatest capacity to sunburn and type VI have the least capacity to burn. However, all skin types can develop sunburn.

Fitzpatrick's skin phototypes:

  • Type 0: Albino
  • Type I: Pale white skin, burns easily, does not tan
  • Type II: White skin, burns easily, tans with difficulty
  • Type III: White skin, may burn but tans easily
  • Type IV: Light brown/olive skin, hardly burns, tans easily
  • Type V: Brown skin, usually does not burn, tans easily
  • Type VI: Black skin, very unlikely to burn, becomes darker with UV radiation exposure

Age also affects how skin reacts to sun. Children younger than six and adults older than sixty are more sensitive to sunlight.

There are certain genetic conditions, for example xeroderma pigmentosum, that increase a person's susceptibility to sunburn and subsequent skin cancers. These conditions involve defects in DNA repair mechanisms which in turn decreases the ability to repair DNA that has been damaged by UV radiation.

Medications

The risk of a sunburn can be increased by pharmaceutical products that sensitize users to UV radiation. Certain antibiotics, oral contraceptives, antidepressants, acne medications, and tranquillizers have this effect.

UV intensity

The UV Index indicates the risk of getting a sunburn at a given time and location. Contributing factors include:

  1. The time of day. In most locations, the sun's rays are strongest between approximately 10am and 4pm daylight saving time.
  2. Cloud cover. UV is partially blocked by clouds; but even on an overcast day, a significant percentage of the sun's damaging UV radiation can pass through clouds.
  3. Proximity to reflective surfaces, such as water, sand, concrete, snow, and ice. All of these reflect the sun's rays and can cause sunburns.
  4. The season of the year. The position of the sun in late spring and early summer can cause a more-severe sunburn.
  5. Altitude. At a higher altitude it is easier to become burnt, because there is less of the earth's atmosphere to block the sunlight. UV exposure increases about 4% for every 1000 ft (305 m) gain in elevation.
  6. Proximity to the equator (latitude). Between the polar and tropical regions, the closer to the equator, the more direct sunlight passes through the atmosphere over the course of a year. For example, the southern United States gets fifty percent more sunlight than the northern United States.
Erythemal dose rate at three Northern latitudes. (Divide by 25 to obtain the UV Index.) Source: NOAA.

Because of variations in the intensity of UV radiation passing through the atmosphere, the risk of sunburn increases with proximity to the tropic latitudes, located between 23.5° north and south latitude. All else being equal (e.g., cloud cover, ozone layer, terrain, etc.), over the course of a full year, each location within the tropic or polar regions receives approximately the same amount of UV radiation. In the temperate zones between 23.5° and 66.5°, UV radiation varies substantially by latitude and season. The higher the latitude, the lower the intensity of the UV rays. Intensity in the northern hemisphere is greatest during the months of May, June and July — and in the southern hemisphere, November, December and January. On a minute-by-minute basis, the amount of UV radiation is dependent on the angle of the sun. This is easily determined by the height ratio of any object to the size of its shadow (if the height is measured vertical to the earth's gravitational field, the projected shadow is ideally measured on a flat, level surface; furthermore, for objects wider than skulls or poles, the height and length are best measured relative to the same occluding edge). The greatest risk is at solar noon, when shadows are at their minimum and the sun's radiation passes most directly through the atmosphere. Regardless of one's latitude (assuming no other variables), equal shadow lengths mean equal amounts of UV radiation.

The skin and eyes are most sensitive to damage by UV at 265–275 nm wavelength, which is in the lower UVC band that is almost never encountered except from artificial sources like welding arcs. Most sunburn is caused by longer wavelengths, simply because those are more prevalent in sunlight at ground level.

Ozone depletion

In recent decades, the incidence and severity of sunburn have increased worldwide, partly because of chemical damage to the atmosphere's ozone layer. Between the 1970s and the 2000s, average stratospheric ozone decreased by approximately 4%, contributing an approximate 4% increase to the average UV intensity at the earth's surface. Ozone depletion and the seasonal "ozone hole" have led to much larger changes in some locations, especially in the southern hemisphere.

Tanning

Suntans, which naturally develop in some individuals as a protective mechanism against the sun, are viewed by most in the Western world as desirable. This has led to an overall increase in exposure to UV radiation from both the natural sun and tanning lamps. Suntans can provide a modest sun protection factor (SPF) of 3, meaning that tanned skin would tolerate up to three times the UV exposure as pale skin.

Sunburns associated with indoor tanning can be severe.

The World Health Organization, American Academy of Dermatology, and the Skin Cancer Foundation recommend avoiding artificial UV sources such as tanning beds, and do not recommend suntans as a form of sun protection.

Diagnosis

Skin showing sunburn below the shorts line

Differential diagnosis

The differential diagnosis of sunburn includes other skin pathology induced by UV radiation including photoallergic reactions, phototoxic reactions to topical or systemic medications, and other dermatologic disorders that are aggravated by exposure to sunlight. Considerations for diagnosis include duration and intensity of UV exposure, use of topical or systemic medications, history of dermatologic disease, and nutritional status.

  • Phototoxic reactions: Non-immunological response to sunlight interacting with certain drugs and chemicals in the skin which resembles an exaggerated sunburn. Common drugs that may cause a phototoxic reaction include amiodarone, dacarbazine, fluoroquinolones, 5-fluorouracil, furosemide, nalidixic acid, phenothiazines, psoralens, retinoids, sulfonamides, sulfonylureas, tetracyclines, thiazides, and vinblastine.
  • Photoallergic reactions: Uncommon immunological response to sunlight interacting with certain drugs and chemicals in the skin. When in excited state by UVR, these drugs and chemicals form free radicals that react to form functional antigens and induce a Type IV hypersensitivity reaction. These drugs include 6-methylcoumarin, aminobenzoic acid and esters, chlorpromazine, promethazine, diclofenac, sulfonamides, and sulfonylureas. Unlike phototoxic reactions which resemble exaggerated sunburns, photoallergic reactions can cause intense itching and can lead to thickening of the skin.
  • Phytophotodermatitis: UV radiation induces inflammation of the skin after contact with certain plants (including limes, celery, and meadow grass). Causes pain, redness, and blistering of the skin in the distribution of plant exposure.
  • Polymorphic light eruption: Recurrent abnormal reaction to UVR. It can present in various ways including pink-to-red bumps, blisters, plaques and urticaria.
  • Solar urticaria: UVR-induced wheals that occurs within minutes of exposure and fades within hours.
  • Other skin diseases exacerbated by sunlight: Several dermatologic conditions can increase in severity with exposure to UVR. These include systemic lupus erythematosus (SLE), dermatomyositis, acne, atopic dermatitis, and rosacea.

Additionally, since sunburn is a type of radiation burn, it can initially hide a severe exposure to radioactivity resulting in acute radiation syndrome or other radiation-induced illnesses, especially if the exposure occurred under sunny conditions. For instance, the difference between the erythema caused by sunburn and other radiation burns is not immediately obvious. Symptoms common to heat illness and the prodromic stage of acute radiation syndrome like nausea, vomiting, fever, weakness/fatigue, dizziness or seizure can add to further diagnostic confusion.

Prevention

Sunburn effect (as measured by the UV Index) is the product of the sunlight spectrum at the earth's surface (radiation intensity) and the erythemal action spectrum (skin sensitivity). Long-wavelength UV is more prevalent, but each milliwatt at 295 nm produces almost 100 times more sunburn than at 315 nm.
 
Skin peeling on the arm as a result of sunburn – the destruction of lower layers of the epidermis causes rapid loss of the top layers
 
Tanning of the forearm (visible darkening of the skin) after extended sun exposure

The most effective way to prevent sunburn is to reduce the amount of UV radiation reaching the skin. The World Health Organization, American Academy of Dermatology, and Skin Cancer Foundation recommend the following measures to prevent excessive UV exposure and skin cancer:

  • Limiting sun exposure between the hours of 10am and 4pm, when UV rays are the strongest
  • Seeking shade when UV rays are most intense
  • Wearing sun-protective clothing including a wide brim hat, sunglasses, and tightly-woven, loose-fitting clothing
  • Using sunscreen
  • Avoiding tanning beds and artificial UV exposure

UV intensity

The strength of sunlight is published in many locations as a UV Index. Sunlight is generally strongest when the sun is close to the highest point in the sky. Due to time zones and daylight saving time, this is not necessarily at 12 noon, but often one to two hours later. Seeking shade including using umbrellas and canopies can reduce the amount of UV exposure, but does not block all UV rays. The WHO recommends following the shadow rule: "Watch your shadow – Short shadow, seek shade!"

Sunscreen

Commercial preparations are available that block UV light, known as sunscreens or sunblocks. They have a sun protection factor (SPF) rating, based on the sunblock's ability to suppress sunburn: The higher the SPF rating, the lower the amount of direct DNA damage. The stated protection factors are correct only if 2 mg of sunscreen is applied per square cm of exposed skin. This translates into about 28 mL (1 oz) to cover the whole body of an adult male, which is much more than many people use in practice. Sunscreens function as chemicals such as oxybenzone and dioxybenzone that absorb UV radiation (chemical sunscreens) or opaque materials such as zinc oxide or titanium oxide to physically block UV radiation (physical sunscreens). Chemical and mineral sunscreens vary in the wavelengths of UV radiation blocked. Broad-spectrum sunscreens contain filters that protect against UVA radiation as well as UVB. Although UVA radiation does not primarily cause sunburn, it does contribute to skin aging and an increased risk of skin cancer.

Sunscreen is effective and thus recommended for preventing melanoma and squamous cell carcinoma. There is little evidence that it is effective in preventing basal cell carcinoma. Typical use of sunscreen does not usually result in vitamin D deficiency, but extensive usage may.

Recommendations

Research has shown that the best sunscreen protection is achieved by application 15 to 30 minutes before exposure, followed by one reapplication 15 to 30 minutes after exposure begins. Further reapplication is necessary only after activities such as swimming, sweating, and rubbing. This varies based on the indications and protection shown on the label — from as little as 80 minutes in water to a few hours, depending on the product selected. The American Academy of Dermatology recommends the following criteria in selecting a sunscreen:

  • Broad spectrum: protects against both UVA and UVB rays
  • SPF 30 or higher
  • Water resistant: sunscreens are classified as water resistant based on time, either 40 minutes, 80 minutes, or not water resistant

Eyes

The eyes are also sensitive to sun exposure at about the same UV wavelengths as skin; snow blindness is essentially sunburn of the cornea. Wrap-around sunglasses or the use by spectacle-wearers of glasses that block UV light reduce the harmful radiation. UV light has been implicated in the development of age-related macular degeneration, pterygium and cataract. Concentrated clusters of melanin, commonly known as freckles, are often found within the iris.

The tender skin of the eyelids can also become sunburned, and can be especially irritating.

Lips

The lips can become chapped (cheilitis) by sun exposure. Sunscreen on the lips does not have a pleasant taste and might be removed by saliva. Some lip balms (ChapSticks) have SPF ratings and contain sunscreens.

Feet

The skin of the feet is often tender and protected, so sudden prolonged exposure to UV radiation can be particularly painful and damaging to the top of the foot. Protective measures include sunscreen, socks, and swimwear or swimgear that covers the foot.

Diet

Dietary factors influence susceptibility to sunburn, recovery from sunburn, and risk of secondary complications from sunburn. Several dietary antioxidants, including essential vitamins, have been shown to have some effectiveness for protecting against sunburn and skin damage associated with ultraviolet radiation, in both human and animal studies. Supplementation with Vitamin C and Vitamin E was shown in one study to reduce the amount of sunburn after a controlled amount of UV exposure. A review of scientific literature through 2007 found that beta carotene (Vitamin A) supplementation had a protective effect against sunburn, but that the effects were only evident in the long-term, with studies of supplementation for periods less than 10 weeks in duration failing to show any effects. There is also evidence that common foods may have some protective ability against sunburn if taken for a period before the exposure.

Protecting children

Babies and children are particularly susceptible to UV damage which increases their risk of both melanoma and non-melanoma skin cancers later in life. Children should not sunburn at any age and protective measures can ensure their future risk of skin cancer is reduced.

  • Infants 0–6 months: Children under 6mo generally have skin too sensitive for sunscreen and protective measures should focus on avoiding excessive UV exposure by using window mesh covers, wide brim hats, loose clothing that covers skin, and reducing UV exposure between the hours of 10am and 4pm.
  • Infants 6–12 months: Sunscreen can safely be used on infants this age. It is recommended to apply a broad-spectrum, water-resistant SPF 30+ sunscreen to exposed areas as well as avoid excessive UV exposure by using wide-brim hats and protective clothing.
  • Toddlers and Preschool-aged children: Apply a broad-spectrum, water-resistant SPF 30+ sunscreen to exposed areas, use wide-brim hats and sunglasses, avoid peak UV intensity hours of 10am-4pm and seek shade. Sun protective clothing with a SPF rating can also provide additional protection.

Artificial UV exposure

The WHO recommends that artificial UV exposure including tanning beds should be avoided as no safe dose has been established. When one is exposed to any artificial source of occupational UV, special protective clothing (for example, welding helmets/shields) should be worn. Such sources can produce UVC, an extremely carcinogenic wavelength of UV which ordinarily is not present in normal sunlight, having been filtered out by the atmosphere.

Treatment

The primary measure of treatment is avoiding further exposure to the sun. The best treatment for most sunburns is time; most sunburns heal completely within a few weeks.

The American Academy of Dermatology recommends the following for the treatment of sunburn:

Non-steroidal anti-inflammatory drugs (NSAIDs; such as ibuprofen or naproxen), and aspirin may decrease redness and pain. Local anesthetics such as benzocaine, however, are contraindicated. Schwellnus et al. state that topical steroids (such as hydrocortisone cream) do not help with sunburns, although the American Academy of Dermatology says they can be used on especially sore areas. While lidocaine cream (a local anesthetic) is often used as a sunburn treatment, there is little evidence for the effectiveness of such use.

A home treatment that may help the discomfort is using cool and wet cloths on the sunburned areas. Applying soothing lotions that contain aloe vera to the sunburn areas was supported by multiple studies, though others have found aloe vera to have no effect. Note that aloe vera has no ability to protect people from new or further sunburn. Another home treatment is using a moisturizer that contains soy.

A sunburn draws fluid to the skin’s surface and away from the rest of the body. Drinking extra water is recommended to help prevent dehydration.

Sun tanning

From Wikipedia, the free encyclopedia

A visible tan line on a woman whose skin has been darkened by ultraviolet exposure, except where covered

Sun tanning or simply tanning is the process whereby skin color is darkened or tanned. It is most often a result of exposure to ultraviolet (UV) radiation from sunlight or from artificial sources, such as a tanning lamp found in indoor tanning beds. People who deliberately tan their skin by exposure to the sun engage in a passive recreational activity of sun bathing. Some people use chemical products which can produce a tanning effect without exposure to ultraviolet radiation, known as sunless tanning.

Impact on skin health

Moderate exposure to direct sunlight contributes to the production of melanin and vitamin D by the body, but excessive exposure to ultraviolet rays has negative health effects, including sunburn and increased risk of skin cancer, as well as depressed immune system function and accelerated aging of the skin. Some people tan or sunburn more easily than others. This may be the result of different skin types and natural skin color, and these may be a result of genetics.

The term "tanning" has a cultural origin, arising from the color tan. Its origin lies in the Western culture of Europe when it became fashionable for young women to seek a less pale complexion (see Cultural history below).

Tanning process

A sun tanned arm showing browner skin where it has been exposed

Melanin is a natural pigment produced by cells called melanocytes in a process called melanogenesis. Melanocytes produce two types of melanin: pheomelanin (red) and eumelanin (very dark brown). Melanin protects the body by absorbing ultraviolet radiation. Excessive UV radiation causes sunburn along with other direct and indirect DNA damage to the skin, and the body naturally combats and seeks to repair the damage and protect the skin by creating and releasing further melanin into the skin's cells. With the production of the melanin, the skin color darkens. The tanning process can be triggered by natural sunlight or by artificial UV radiation, which can be delivered in frequencies of UVA, UVB, or a combination of both. The intensity is commonly measured by the UV Index.

Cross-sectional view showing skin tone becoming darker due to the production of more melanin to overcome DNA damage caused by UV radiation

There are two different mechanisms involved in the production of a tan by UV exposure: Firstly, UVA radiation creates oxidative stress, which in turn oxidizes existing melanin and leads to rapid darkening of the melanin. UVA may also cause melanin to be redistributed (released from melanocytes where it is already stored), but its total quantity is unchanged. Skin darkening from UVA exposure does not lead to significantly increased production of melanin or protection against sunburn.

In the second process, triggered primarily by UVB, there is an increase in production of melanin (melanogenesis), which is the body's reaction to direct DNA photodamage (formation of pyrimidine dimers) from UV radiation. Melanogenesis leads to delayed tanning, and typically becomes visible two or three days after exposure. The tan that is created by increased melanogenesis typically lasts for a few weeks or months, much longer than the tan that is caused by oxidation of existing melanin, and is also actually protective against UV skin damage and sunburn, rather than simply cosmetic. Typically, it can provide a modest Sun Protection Factor (SPF) of 3, meaning that tanned skin would tolerate up to 3 times the UV exposure as pale skin. However, in order to cause true melanogenesis-tanning by means of UV exposure, some direct DNA photodamage must first be produced, and this requires UVB exposure (as present in natural sunlight, or sunlamps that produce UVB).

The ultraviolet frequencies responsible for tanning are often divided into the UVA and UVB ranges.

UVA

Ultraviolet A (UVA) radiation is in the wavelength range 320 to 400 nm. It is present more uniformly throughout the day, and throughout the year, than UVB. Most UVA is not blocked by the atmosphere's ozone layer. UVA causes the release of existing melanin from the melanocytes to combine with oxygen (oxidize) to create the actual tan color in the skin.

UVA is blocked less than UVB by many sunscreens, but is blocked to some degree by clothing. UVA is known both to cause DNA damage and to be carcinogenic. However, it operates not by inducing direct DNA damage, but by producing reactive oxygen species which damage DNA indirectly. UVA (see above) induces a cosmetic tan but little extra melanin protection against sun damage, sun burn, or cancer.

UVB

Ultraviolet B (UVB) radiation is in the wavelength range 280 to 320 nm. Much of this band is blocked by the Earth's ozone layer, but some penetrates. UVB:

  • triggers the formation of CPD-DNA damage (direct DNA damage), which in turn induces an increased melanin production.
  • is more likely to cause a sunburn than UVA as a result of overexposure. The mechanism for sunburn and increased melanogenesis is identical. Both are caused by the direct DNA damage (formation of CPDs).
  • produces Vitamin D in human skin.
  • is reduced by virtually all sunscreens in accordance with their SPF.
  • is thought, but not proven, to cause the formation of moles and some types of skin cancer.
  • causes skin aging (but at a slower rate than UVA).
  • stimulates the production of new melanin, which leads to an increase in the dark-colored pigment within a few days.

Tanning behavior of different skin colors

A person's natural skin color affects their reaction to exposure to the sun. An individual's natural skin color can vary from a dark brown to a nearly colorless pigmentation, which may appear white. In 1975, Harvard dermatologist Thomas B. Fitzpatrick devised the Fitzpatrick scale which described the common tanning behavior of various skin types, as follows:

Type Also called Sunburning Tanning behavior von Luschan scale
I Very light or pale Often Occasionally 1–5
II Light or light-skinned Usually Sometimes 6–10
III Light intermediate Rarely Usually 11–15
IV Dark intermediate Rarely Often 16–21
V Dark or "brown" type No Sometimes darkens 22–28
VI Very dark or "black" type No Naturally black-brown skin 29–36

Health aspects

Sunburn peeling
 
Disappearing sun tan, revealing the individual's naturally light-colored skin.

The most common risk of exposure to ultraviolet radiation is sunburn, the speed and severity of which vary among individuals. This can be alleviated at least to some extent by the prior application of a suitable-strength sunscreen, which will also hinder the tanning process due to the blocking of UV light.

Overexposure to ultraviolet radiation is known to cause skin cancer, make skin age and wrinkle faster, mutate DNA, and impair the immune system. Frequent tanning bed use triples the risk of developing melanoma, the deadliest form of skin cancer, according to a 2010 study. The study suggests that the melanoma risk is linked more closely to total exposure than it is to the age at which an individual first uses a tanning bed. The International Agency for Research on Cancer places the use of tanning beds in the highest cancer risk category, describing them as carcinogenic to humans even if used as recommended.

Several organizations, such as the World Health Organization (WHO), the American Cancer Society and the US Surgeon General have issued guidelines warning about sun tanning and UV radiation exposure, either from the sun or from indoor tanning.

Production of vitamin D is essential for human health. Moderate exposure (avoiding sunburn) to UV radiation provides benefits such as increased vitamin D, as well as other possible benefits that are still being studied.

Several tanning activators have used different forms of psoralen, which are known to be photocarcinogenic. Health authorities have banned psoralen since July 1996.

Cultural history

La promenade (1875) by Claude Monet. At that time in the West, the upper social class used parasols, long sleeves and hats to avoid sunlight's tanning effects.

Tanning has gone in and out of fashion. In the United States and Western Europe before the 1920s, tanned skin was associated with the lower classes, because they worked outdoors and were exposed to the sunlight. Women went to great lengths to preserve pale skin, as a sign of their "refinement".

Women's outdoor clothing styles were tailored to protect against sunlight exposure, with full-length sleeves, and sunbonnets and other large hats, headscarves, and parasols shielding the head. Lead- and arsenic-based cosmetics were used to artificially whiten the skin. The preference for fair skin continued until the end of the Victorian era.

By the early 20th century, the therapeutic benefits of sunlight began to be recognized. In 1903, Niels Finsen was awarded the Nobel Prize in Medicine for his “Finsen Light Therapy”. The therapy was a cure for diseases such as lupus vulgaris and rickets. Vitamin D deficiency was found to be a cause of rickets, and exposure to sunlight would allow vitamin D to be produced in a person. Therefore, sunlight exposure was a remedy to curing several diseases, especially rickets. In 1910 a scientific expedition went to the island of Tenerife to test the wider health benefits of "heliotherapy", and by 1913 "sunbathing" was referred to as a desirable activity for the leisured class.

Shortly thereafter, in the 1920s, fashion-designer Coco Chanel accidentally got sunburnt while visiting the French Riviera. When she arrived home, she arrived with a sun tan and her fans apparently liked the look and started to adopt darker skin tones themselves. Tanned skin became a trend partly because of Coco’s status and the longing for her lifestyle by other members of society. In addition, Parisians fell in love with Josephine Baker, a "caramel-skinned" singer in Paris, and idolized her dark skin. These two women were leading figures of the transformation that tanned skin underwent, in which it became perceived as fashionable, healthy, and luxurious. Jean Patou capitalized on the new tanning fad, launching the first sun tan oil "Huile de Chaldee" in 1927.

Just before the 1930s, sunlight therapy became a popularly subscribed cure for almost every ailment from simple fatigue to tuberculosis. In the 1940s, advertisements started appearing in women's magazines which encouraged sunbathing. At the same time, swimsuits' skin coverage began decreasing, with the bikini radically changing swimsuit style after it made its appearance in 1946. In the 1950s, many people used baby oil as a method to increase tanning. The first self-tanner came about in the same decade and was known as "Man-Tan", although it often led to undesirable orange skin. Coppertone, in 1953, marketed its sunscreen with a drawing of a little blond girl and her cocker spaniel tugging on her bathing suit bottom, revealing her bare bottom and tan line; this advertisement was modified around the turn of the 21st century and now shows a little girl wearing a one-piece bathing suit or shorts. In the latter part of the 1950s, silver metallic reflectors were common to enhance one’s tan.

In many European countries women may sunbathe without covering their breasts.

In 1962, sunscreen commenced to be SPF rated, although SPF labeling in the US was not standardized by the FDA until 1978. In 1971, Mattel introduced Malibu Barbie, which had tanned skin, sunglasses, and her very own bottle of sun tanning lotion. In 1978, both sunscreen with an SPF 15 rating as well as tanning beds first appeared. In 2007, there were an estimated 50,000 outlets for indoor tanning; it was a five-billion-dollar industry in the United States, and had spawned an auxiliary industry for indoor tanning lotions including bronzers, intensifiers, and accelerators. Since then, the indoor tanning industry has become more constrained by health regulations. In China, darker skin is still considered by many to be the mark of the lower classes. As recently as 2012, in some parts of China, ski masks were becoming popular items to wear at the beach in order to protect the wearer's face from the effects of sunlight.

A 1969 innovation is tan-through swimwear, which uses fabric perforated with thousands of micro holes that are nearly invisible to the naked eye, but which transmit enough sunlight to approach an all-over tan, especially if the fabric is stretched taut. Tan-through swimwear typically allows more than one-third of UV rays to pass through (equivalent to SPF 3 or less), and an application of sunscreen even to the covered area is recommended.

Sunless tanning

A tanning bed emits UV radiation.
 

To avoid exposure to UVB and UVA rays, or in seasons without strong sunshine, some people take alternative steps to appear with darkened skin. They may use sunless tanning (also known as self-tanners); stainers which are based on dihydroxyacetone (DHA); or cosmetics such as bronzers.

Many sunless tanning products are available in the form of darkening creams, gels, lotions, and sprays that are self-applied on the skin. There is also a professional spray-on tanning option or “tanning booth” that is offered by spas, salons, and tanning businesses. Spray tanning does not involve a color being sprayed on the body, instead it uses a colorless chemical which reacts with proteins in the top layer of the skin, resulting in a brown color.

Light therapy

From Wikipedia, the free encyclopedia

Light therapy
Light Therapy for SAD.jpg
Example of light therapy for winter depression
ICD-10-PCS6A6, GZJ
ICD-999.83, 99.88
MeSHD010789

Light therapy—or phototherapy, classically referred to as heliotherapy—is a method recognized by scientific medicine for the treatment of various diseases. It includes exposure to outdoor daylight or specific indoor artificial light sources.

The care guideline for unipolar depression recommends light therapy especially for depression that follows a seasonal pattern (seasonal affective disorder). There is tentative evidence to support its use to treat depressive disorders that are not seasonally dependent. As a treatment for disorders of the skin, the second kind of light therapy, called ultraviolet light therapy, is meant to treat neurodermatitis, psoriasis, acne vulgaris, eczema and neonatal jaundice.

Medical uses

A newborn infant in neonatal care placed under blue light (420–470 nm) phototherapy lamp without clothes or just wearing a diaper to treat newborn jaundice (hyperbilirubinemia).

Skin conditions

High-intensity blue light (425 nm) used for the attempted treatment of acne.

Light therapy treatments for the skin usually involve exposure to ultraviolet light. The exposures can be to a small area of the skin or over the whole body surface, as in a tanning bed. The most common treatment is with narrowband UVB, which has a wavelength of approximately 311–313 nanometers. Exposure to photons (light) at these specific wavelengths enables the body to produce vitamin D. Full body phototherapy can be delivered at a doctor's office or at home using a large high-power UVB booth. Tanning beds, however, generate mostly UVA light, and only 4% to 10% of tanning bed light is in the UVB spectrum.

Atopic dermatitis

Light therapy is considered one of the best monotherapy treatments for atopic dermatitis (AD) when applied to patients who have not responded to traditional topical treatments. The therapy offers a wide range of options: UVA1 for acute AD, NB-UVB for chronic AD, and balneophototherapy have proven their efficacy. Patients tolerate the therapy safely but, as in any therapy, there are potential adverse effects and care must be taken in its application, particularly to children.

Psoriasis

For psoriasis, UVB phototherapy has been shown to be effective. A feature of psoriasis is localized inflammation mediated by the immune system. Ultraviolet radiation is known to suppress the immune system and reduce inflammatory responses. Light therapy for skin conditions like psoriasis usually use 313 nanometer UVB though it may use UVA (315–400 nm wavelength) or a broader spectrum UVB (280–315 nm wavelength). UVA combined with psoralen, a drug taken orally, is known as PUVA treatment. In UVB phototherapy the exposure time is very short, seconds to minutes depending on intensity of lamps and the person's skin pigment and sensitivity.

Vitiligo

About 1% of the human population suffers from vitiligo which causes painless distinct light-colored patches of the skin on the face, hands, and legs. Phototherapy is an effective treatment because it forces skin cells to manufacture melanin to protect the body from UV damage. Prescribed treatment is generally 3 times a week in a clinic or daily at home. About 1 month usually results in re-pigmentation in the face and neck, and 2–4 months in the hands and legs. Narrowband UVB is more suitable to the face and neck and PUVA is more effective at the hands and legs.

Acne vulgaris

As of 2012 evidence for light therapy and lasers in the treatment of acne vulgaris was not sufficient to recommend them. There is moderate evidence for the efficacy of blue and blue-red light therapies in treating mild acne, but most studies are of low quality. While light therapy appears to provide short-term benefit, there is a lack of long-term outcome data or data in those with severe acne.

Cancer

According to the American Cancer Society, there is some evidence that ultraviolet light therapy may be effective in helping treat certain kinds of skin cancer, and ultraviolet blood irradiation therapy is established for this application. However, alternative uses of light for cancer treatment – light box therapy and colored light therapy – are not supported by evidence. Photodynamic therapy (often with red light) is used to treat certain superficial non-melanoma skin cancers.

Other skin conditions

Some types of phototherapy may be effective in the treatment of polymorphous light eruption, cutaneous T-cell lymphoma and lichen planus. Narrowband UVB between 311–313 nanometers is the most common treatment.

Wound healing

Low level laser therapy has been studied as a potential treatment for chronic wounds, and higher-power lasers have sometimes been successfully used to close acute wounds as an alternative to stitching. However, as of 2012 and due to inconsistent results and the low quality of extant research, reviews in the scientific literature have not supported its widespread application.

Retinal conditions

There is preliminary evidence that light therapy is an effective treatment for diabetic retinopathy and diabetic macular oedema.

Mood and sleep related

Seasonal affective disorder

The effectiveness of light therapy for treating seasonal affective disorder (SAD) may be linked to the fact that light therapy makes up for lost sunlight exposure and resets the body's internal clock. Studies show that light therapy helps reduce the debilitating and depressive behaviors of SAD, such as excessive sleepiness and fatigue, with results lasting for at least 1 month. Light therapy is preferred over antidepressants in the treatment of SAD because it is a relatively safe and easy therapy. Two methods of light therapy, bright light and dawn simulation, have similar success rates in the treatment of SAD.

It is possible that response to light therapy for SAD could be season dependent. Morning therapy has provided the best results because light in the early morning aids in regulating the circadian rhythm. People affected by SAD have low levels of energy and have difficulty concentrating. They usually have a change in appetite and experience trouble sleeping.

A 2007 systematic review by the Swedish agency SBU found insufficient evidence that light therapy was able to alleviate symptoms of depression or seasonal affective disorder. The report recommended that: "Approximately 100 participants are required to establish whether the therapy is moderately more effective than placebo". Although treatment in light therapy rooms was well established in Sweden, no satisfactory, controlled studies had been published on the subject. This led to the closure of a number of clinics offering light therapy in Sweden.

A Cochrane review conducted in 2019 states the evidence that light therapy's effectiveness as a treatment for the prevention of seasonal affective disorder is limited, although the risk of adverse effects are minimal. Therefore, the decision to use light therapy should be based on a person's preference of treatment.

Non-seasonal depression

Light therapy has also been suggested in the treatment of non-seasonal depression and other psychiatric mood disturbances, including major depressive disorder, bipolar disorder and postpartum depression. A meta-analysis by the Cochrane Collaboration concluded that "for patients suffering from non-seasonal depression, light therapy offers modest though promising antidepressive efficacy." A 2008 systematic review concluded that "overall, bright light therapy is an excellent candidate for inclusion into the therapeutic inventory available for the treatment of nonseasonal depression today, as adjuvant therapy to antidepressant medication, or eventually as stand-alone treatment for specific subgroups of depressed patients." A 2015 review found that supporting evidence for light therapy was limited due to serious methodological flaws.

A 2016 meta-analysis showed that bright light therapy appeared to be efficacious, particularly when administered for 2–5 weeks' duration and as monotherapy.

Chronic circadian rhythm sleep disorders (CRSD)

In the management of circadian rhythm disorders such as delayed sleep phase disorder (DSPD), the timing of light exposure is critical. Light exposure administered to the eyes before or after the nadir of the core body temperature rhythm can affect the phase response curve. Use upon awakening may also be effective for non-24-hour sleep–wake disorder. Some users have reported success with lights that turn on shortly before awakening (dawn simulation). Evening use is recommended for people with advanced sleep phase disorder. Some, but not all, totally blind people whose retinae are intact, may benefit from light therapy.

Circadian rhythm sleep disorders and jet lag

Situational CRSD

Light therapy has been tested for individuals with shift work sleep disorder and for jet lag.

Sleep disorder in Parkinson's disease

Light therapy has been trialed in treating sleep disorders experienced by patients with Parkinson's disease.

Sleep disorder in Alzheimer's disease

Studies have shown that daytime and evening light therapy for nursing home patients with Alzheimer’s disease, who often struggle with agitation and fragmented wake/rest cycles effectively led to more consolidated sleep and an increase in circadian rhythm stability.

Neonatal jaundice (Postnatal Jaundice)

A newborn infant undergoing white-light phototherapy to treat neonatal jaundice.

Light therapy is used to treat cases of neonatal jaundice. Bilirubin, a yellow pigment normally formed in the liver during the breakdown of old red blood cells, cannot always be effectively cleared by a neonate’s liver causing neonatal jaundice. Accumulation of excess bilirubin can cause central nervous system damage, and so this buildup of bilirubin must be treated. Phototherapy uses the energy from light to isomerize the bilirubin and consequently transform it into compounds that the newborn can excrete via urine and stools. Bilirubin is most successful absorbing light in the blue region of the visible light spectrum, which falls between 460-490 nm. Therefore light therapy technologies that utilize these blue wavelengths are the most successful at isomerizing bilirubin.

Techniques

Photodynamic therapy

Photodynamic therapy is a form of phototherapy using nontoxic light-sensitive compounds that are exposed selectively to light, whereupon they become toxic to targeted malignant and other diseased cells.

One of the treatments is using blue light with aminolevulinic acid for the treatment of actinic keratosis. This is not a U.S. FDA-approved treatment for acne vulgaris.

Light boxes

Light intensity of a light therapy lamp in a room. Daylight only penetrates into the room filtered and restricted from the window curtain and protruding roof. In modern society people often spend too little time outdoors, where the light is significantly brighter than in closed rooms.
 

The production of the hormone melatonin, a sleep regulator, is inhibited by light and permitted by darkness as registered by photosensitive ganglion cells in the retina. To some degree, the reverse is true for serotonin, which has been linked to mood disorders. Hence, for the purpose of manipulating melatonin levels or timing, light boxes providing very specific types of artificial illumination to the retina of the eye are effective.

Light therapy uses either a light box which emits up to 10,000 lux of light at a specified distance, much brighter than a customary lamp, or a lower intensity of specific wavelengths of light from the blue (460 nm) to the green (525 nm) areas of the visible spectrum. A 1995 study showed that green light therapy at doses of 350 lux produces melatonin suppression and phase shifts equivalent to 10,000 lux white light therapy, but another study published in May 2010 suggests that the blue light often used for SAD treatment should perhaps be replaced by green or white illumination, because of a possible involvement of the cones in melatonin suppression.

Risks and complications

Ultraviolet

Ultraviolet light causes progressive damage to human skin and erythema even from small doses. This is mediated by genetic damage, collagen damage, as well as destruction of vitamin A and vitamin C in the skin and free radical generation. Ultraviolet light is also known to be a factor in formation of cataracts. Ultraviolet radiation exposure is strongly linked to incidence of skin cancer.

Visible light

Optical radiation of any kind with enough intensity can cause damage to the eyes and skin including photoconjunctivitis and photokeratitis. Researchers have questioned whether limiting blue light exposure could reduce the risk of age-related macular degeneration. According to the American Academy of Ophthalmology, there is no scientific evidence showing that exposure to blue light emitting devices result in eye damage. According to Harriet Hall, blue light exposure is reported to suppress the production of melatonin, which affects our body's circadian rhythm and can decrease sleep quality. It is reported that bright light therapy may activate the production of reproductive hormones, such as testosterone, luteinizing hormone, follicle-stimulating hormone, and estradiol.

Modern phototherapy lamps used in the treatment of seasonal affective disorder and sleep disorders either filter out or do not emit ultraviolet light and are considered safe and effective for the intended purpose, as long as photosensitizing drugs are not being taken at the same time and in the absence of any existing eye conditions. Light therapy is a mood altering treatment, and just as with drug treatments, there is a possibility of triggering a manic state from a depressive state, causing anxiety and other side effects. While these side effects are usually controllable, it is recommended that patients undertake light therapy under the supervision of an experienced clinician, rather than attempting to self-medicate.

Contraindications to light therapy for seasonal affective disorder include conditions that might render the eyes more vulnerable to phototoxicity, tendency toward mania, photosensitive skin conditions, or use of a photosensitizing herb (such as St. John's wort) or medication. Patients with porphyria should avoid most forms of light therapy. Patients on certain drugs such as methotrexate or chloroquine should use caution with light therapy as there is a chance that these drugs could cause porphyria.

Side effects of light therapy for sleep phase disorders include jumpiness or jitteriness, headache, eye irritation and nausea. Some non-depressive physical complaints, such as poor vision and skin rash or irritation, may improve with light therapy.

History

Child patients with external forms of tuberculosis, especially of the bones and joints, laying on beds on a terrace outside Treloar Hospital in Alton, Hampshire, England, in sunlight as part of their light therapy, ca. first half of the 20th century

Many ancient cultures practiced various forms of heliotherapy, including people of Ancient Greece, Ancient Egypt, and Ancient Rome. The Inca, Assyrian and early German settlers also worshipped the sun as a health bringing deity. Indian medical literature dating to 1500 BCE describes a treatment combining herbs with natural sunlight to treat non-pigmented skin areas. Buddhist literature from about 200 CE and 10th-century Chinese documents make similar references.

The Faroese physician Niels Finsen is believed to be the father of modern phototherapy. He developed the first artificial light source for this purpose. Finsen used short wavelength light to treat lupus vulgaris, a skin infection caused by Mycobacterium tuberculosis. He thought that the beneficial effect was due to ultraviolet light killing the bacteria, but recent studies showed that his lens and filter system did not allow such short wavelengths to pass through, leading instead to the conclusion that light of approximately 400 nanometers generated reactive oxygen that would kill the bacteria. Finsen also used red light to treat smallpox lesions. He received the Nobel Prize in Physiology or Medicine in 1903. Scientific evidence for some of his treatments is lacking, and later eradication of smallpox and development of antibiotics for tuberculosis rendered light therapy obsolete for these diseases.

From the late nineteenth century until the early 1930s, light therapy was considered an effective and mainstream medical therapy in the UK for conditions such as varicose ulcer, 'sickly children' and a wide range of other conditions. Controlled trials by the medical scientist Dora Colebrook, supported by the Medical Research Council, indicated that light therapy was not effective for such a wide range of conditions.

Seasonal affective disorder

From Wikipedia, the free encyclopedia

Seasonal affective disorder
Other namesSeasonal mood disorder, depressive disorder with seasonal pattern, winter depression, winter blues, summer depression, seasonal depression
Light Therapy for SAD.jpg
Bright light therapy is a common treatment for seasonal affective disorder and for circadian rhythm sleep disorders.
SpecialtyPsychiatry

Seasonal affective disorder (SAD) is a mood disorder subset in which people who have normal mental health throughout most of the year exhibit depressive symptoms at the same time each year, most commonly in winter. Common symptoms include sleeping too much, having little to no energy, and overeating. The condition in the summer can include heightened anxiety.

In the Diagnostic and Statistical Manual of Mental Disorders DSM-IV and DSM-5, its status was changed. It is no longer classified as a unique mood disorder but is now a specifier, called "with seasonal pattern", for recurrent major depressive disorder that occurs at a specific time of the year and fully remits otherwise. Although experts were initially skeptical, this condition is now recognized as a common disorder. However, the validity of SAD has been questioned by a 2016 analysis by the Center for Disease Control, in which no links were detected between depression and seasonality or sunlight exposure.

Video explanation

In the United States, the percentage of the population affected by SAD ranges from 1.4% of the population in Florida, to 9.9% in Alaska. SAD was formally described and named in 1984 by Norman E. Rosenthal and colleagues at the National Institute of Mental Health.

History

SAD was first systematically reported and named in the early 1980s by Norman E. Rosenthal, M.D., and his associates at the National Institute of Mental Health (NIMH). Rosenthal was initially motivated by his desire to discover the cause of his own experience of depression during the dark days of the northern US winter, called polar night. He theorized that the reduction in available natural light during winter was the cause. Rosenthal and his colleagues then documented the phenomenon of SAD in a placebo-controlled study utilizing light therapy. A paper based on this research was published in 1984. Although Rosenthal's ideas were initially greeted with skepticism, SAD has become well recognized, and his 1993 book, Winter Blues has become the standard introduction to the subject.

Research on SAD in the United States began in 1979 when Herb Kern, a research engineer, had also noticed that he felt depressed during the winter months. Kern suspected that scarcer light in winter was the cause and discussed the idea with scientists at the NIMH who were working on bodily rhythms. They were intrigued, and responded by devising a lightbox to treat Kern’s depression. Kern felt much better within a few days of treatments, as did other patients treated in the same way.

Signs and symptoms

SAD is a type of major depressive disorder, and sufferers may exhibit any of the associated symptoms, such as feelings of hopelessness and worthlessness, thoughts of suicide, loss of interest in activities, withdrawal from social interaction, sleep and appetite problems, difficulty with concentrating and making decisions, decreased libido, a lack of energy, or agitation. Symptoms of winter SAD often include falling asleep earlier or in less than 5 minutes in the evening, oversleeping or difficulty waking up in the morning, nausea, and a tendency to overeat, often with a craving for carbohydrates, which leads to weight gain. SAD is typically associated with winter depression, but springtime lethargy or other seasonal mood patterns are not uncommon. Although each individual case is different, in contrast to winter SAD, people who experience spring and summer depression may be more likely to show symptoms such as insomnia, decreased appetite and weight loss, and agitation or anxiety.

Bipolar disorder

With seasonal pattern is a specifier for bipolar and related disorders, including bipolar I disorder and bipolar II disorder. Most people with SAD experience major depressive disorder, but as many as 20% may have a bipolar disorder. It is important to discriminate between diagnoses because there are important treatment differences. In these cases, people who have the With seasonal pattern specifier may experience a depressive episode either due to major depressive disorder or as part of bipolar disorder during the winter and remit in the summer. Around 25% of patients with bipolar disorder may present with a depressive seasonal pattern, which is associated with bipolar II disorder, rapid cycling, eating disorders, and more depressive episodes. Differences in biological sex display distinct clinical characteristics associated to seasonal pattern: males present with more Bipolar II disorder and a higher number of depressive episodes, and females with rapid cycling and eating disorders.

Cause

In many species, activity is diminished during the winter months in response to the reduction in available food, the reduction of sunlight (especially for diurnal animals) and the difficulties of surviving in cold weather. Hibernation is an extreme example, but even species that do not hibernate often exhibit changes in behavior during the winter. The preponderance of women with SAD suggests that the response may also somehow regulate reproduction.

Various proximate causes have been proposed. One possibility is that SAD is related to a lack of serotonin, and serotonin polymorphisms could play a role in SAD, although this has been disputed. Mice incapable of turning serotonin into N-acetylserotonin (by serotonin N-acetyltransferase) appear to express "depression-like" behavior, and antidepressants such as fluoxetine increase the amount of the enzyme serotonin N-acetyltransferase, resulting in an antidepressant-like effect. Another theory is that the cause may be related to melatonin which is produced in dim light and darkness by the pineal gland, since there are direct connections, via the retinohypothalamic tract and the suprachiasmatic nucleus, between the retina and the pineal gland. Melatonin secretion is controlled by the endogenous circadian clock, but can also be suppressed by bright light.

One study looked at whether some people could be predisposed to SAD based on personality traits. Correlations between certain personality traits, higher levels of neuroticism, agreeableness, openness, and an avoidance-oriented coping style, appeared to be common in those with SAD.

Pathophysiology

Seasonal mood variations are believed to be related to light. An argument for this view is the effectiveness of bright-light therapy. SAD is measurably present at latitudes in the Arctic region, such as northern Finland (64°00′N), where the rate of SAD is 9.5%. Cloud cover may contribute to the negative effects of SAD. There is evidence that many patients with SAD have a delay in their circadian rhythm, and that bright light treatment corrects these delays which may be responsible for the improvement in patients.

The symptoms of it mimic those of dysthymia or even major depressive disorder. There is also potential risk of suicide in some patients experiencing SAD. One study reports 6–35% of sufferers required hospitalization during one period of illness. At times, patients may not feel depressed, but rather lack energy to perform everyday activities.

Subsyndromal Seasonal Affective Disorder is a milder form of SAD experienced by an estimated 14.3% (vs. 6.1% SAD) of the U.S. population. The blue feeling experienced by both SAD and SSAD sufferers can usually be dampened or extinguished by exercise and increased outdoor activity, particularly on sunny days, resulting in increased solar exposure. Connections between human mood, as well as energy levels, and the seasons are well documented, even in healthy individuals.

Diagnosis

According to the American Psychiatric Association DSM-IV criteria, Seasonal Affective Disorder is not regarded as a separate disorder. It is called a "course specifier" and may be applied as an added description to the pattern of major depressive episodes in patients with major depressive disorder or patients with bipolar disorder.

The "Seasonal Pattern Specifier" must meet four criteria: depressive episodes at a particular time of the year; remissions or mania/hypomania at a characteristic time of year; these patterns must have lasted two years with no nonseasonal major depressive episodes during that same period; and these seasonal depressive episodes outnumber other depressive episodes throughout the patient's lifetime. The Mayo Clinic describes three types of SAD, each with its own set of symptoms.

Management

Treatments for classic (winter-based) seasonal affective disorder include light therapy, medication, ionized-air administration, cognitive-behavioral therapy and carefully timed supplementation of the hormone melatonin.

Light therapy

Photoperiod-related alterations of the duration of melatonin secretion may affect the seasonal mood cycles of SAD. This suggests that light therapy may be an effective treatment for SAD. Light therapy uses a lightbox which emits far more lumens than a customary incandescent lamp. Bright white "full spectrum" light at 10,000 lux, blue light at a wavelength of 480 nm at 2,500 lux or green (actually cyan or blue-green) light at a wavelength of 500 nm at 350 lux are used, with the first-mentioned historically preferred.

Bright light therapy is effective with the patient sitting a prescribed distance, commonly 30–60 cm, in front of the box with her/his eyes open but not staring at the light source for 30–60 minutes. A study published in May 2010 suggests that the blue light often used for SAD treatment should perhaps be replaced by green or white illumination. Discovering the best schedule is essential. One study has shown that up to 69% of patients find lightbox treatment inconvenient and as many as 19% stop use because of this.

Dawn simulation has also proven to be effective; in some studies, there is an 83% better response when compared to other bright light therapy. When compared in a study to negative air ionization, bright light was shown to be 57% effective vs. dawn simulation 50%. Patients using light therapy can experience improvement during the first week, but increased results are evident when continued throughout several weeks. Certain symptoms like hypersomnia, early insomnia, social withdrawal, and anxiety resolve more rapidly with light therapy than with cognitive behavioral therapy. Most studies have found it effective without use year round but rather as a seasonal treatment lasting for several weeks until frequent light exposure is naturally obtained.

Light therapy can also consist of exposure to sunlight, either by spending more time outside or using a computer-controlled heliostat to reflect sunlight into the windows of a home or office. Although light therapy is the leading treatment for seasonal affective disorder, prolonged direct sunlight or artificial lights that don't block the ultraviolet range should be avoided due to the threat of skin cancer.

The evidence base for light therapy as a preventive treatment for seasonal affective disorder is limited. The decision to use light therapy to treat people with a history of winter depression before depressive symptoms begin should be based on a persons preference of treatment.

Medication

SSRI (selective serotonin reuptake inhibitor) antidepressants have proven effective in treating SAD. Effective antidepressants are fluoxetine, sertraline, or paroxetine. Both fluoxetine and light therapy are 67% effective in treating SAD according to direct head-to-head trials conducted during the 2006 Can-SAD study. Subjects using the light therapy protocol showed earlier clinical improvement, generally within one week of beginning the clinical treatment. Bupropion extended-release has been shown to prevent SAD for one in four people, but has not been compared directly to other preventive options in trials. In a 2021 updated Cochrane review of second-generation antidepressant medications for the treatment of SAD a definitive conclusion could not be drawn due to lack of evidence and the need for larger randomized controlled trials.

Modafinil may be an effective and well-tolerated treatment in patients with seasonal affective disorder/winter depression.

Another explanation is that vitamin D levels are too low when people do not get enough Ultraviolet-B on their skin. An alternative to using bright lights is to take vitamin D supplements. However, studies did not show a link between vitamin D levels and depressive symptoms in elderly Chinese nor among elderly British women given only 800IU when 6,000IU is needed. 5-HTP (an amino acid that helps to produce serotonin and is often used to help those with depression) has also been suggested as a supplement that may help treat the symptoms of SAD, by lifting mood and regulating sleep schedule for sufferers. However, those who take antidepressants are not advised to take 5-HTP, as antidepressant medications may combine with the supplement to create dangerously high levels of serotonin – potentially resulting in 'serotonin syndrome'.

Other treatments

Depending upon the patient, one treatment (e.g., lightbox) may be used in conjunction with another (e.g., medication).

Negative air ionization, which involves releasing charged particles into the sleep environment, has been found effective with a 47.9% improvement if the negative ions are in sufficient density (quantity).

Physical exercise has shown to be an effective form of depression therapy, particularly when in addition to another form of treatment for SAD. One particular study noted marked effectiveness for treatment of depressive symptoms when combining regular exercise with bright light therapy. Patients exposed to exercise which had been added to their treatments in 20 minutes intervals on the aerobic bike during the day along with the same amount of time underneath the UV light were seen to make quick recovery.

Of all the psychological therapies aimed at the prevention of SAD, cognitive-behaviour therapy, typically involving thought records, activity schedules and a positive data log, has been the subject of the most empirical work, however, evidence for CBT or any of the psychological therapies aimed at preventing SAD remains inconclusive.

Epidemiology

Nordic countries

Winter depression is a common slump in the mood of some inhabitants of most of the Nordic countries. Iceland, however, seems to be an exception. A study of more than 2000 people there found the prevalence of seasonal affective disorder and seasonal changes in anxiety and depression to be unexpectedly low in both sexes. The study's authors suggested that propensity for SAD may differ due to some genetic factor within the Icelandic population. A study of Canadians of wholly Icelandic descent also showed low levels of SAD. It has more recently been suggested that this may be attributed to the large amount of fish traditionally eaten by Icelandic people, in 2007 about 90 kilograms per person per year as opposed to about 24 kg in the US and Canada, rather than to genetic predisposition; a similar anomaly is noted in Japan, where annual fish consumption in recent years averages about 60 kg per capita. Fish are high in vitamin D. Fish also contain docosahexaenoic acid (DHA), which help with a variety of neurological dysfunctions.

Other countries

In the United States, a diagnosis of seasonal affective disorder was first proposed by Norman E. Rosenthal, M.D. in 1984. Rosenthal wondered why he became sluggish during the winter after moving from sunny South Africa to (cloudy in winter) New York. He started experimenting increasing exposure to artificial light, and found this made a difference. In Alaska it has been established that there is a SAD rate of 8.9%, and an even greater rate of 24.9% for subsyndromal SAD.

Around 20% of Irish people are affected by SAD, according to a survey conducted in 2007. The survey also shows women are more likely to be affected by SAD than men. An estimated 3% of the population in the Netherlands suffer from winter SAD.

Lie point symmetry

From Wikipedia, the free encyclopedia https://en.wikipedia.org/wiki/Lie_point_symmetry     ...