From the AAD: Skin Cancer Public Service Advertisements

The ADD has a campaign targeting teens to try to prevent them from using tanning beds. A Swedish study presents strong evidence that indoor tanning increases the risk of melanoma, especially when indoor tanning begins at an early age.

Fact Sheets

Indoor Tanning Fact Sheet 
Skin Cancer Fact Sheet (2006)
Melanoma Fact Sheet (2006)

Articles from The Journal of the American Academy of Dermatology

The indoor UV tanning industry: A review of skin cancer risk, claims, and regulation 
Do adolescent tanners exhibit dependency?
Sunlight, tanning booths and vitamin D

Articles from other scientific, peer-reviewed journals

Pediatrics

Use of sunscreen, sunburning rates, and tanning bed use among more than 10,000 US children and adolescents

Pamphlets

The Darker Side of Tanning
Ultraviolet Index 
Skin Cancer
Basal Cell Carcinoma
Squamous Cell Carcinoma
Melanoma

More information on skin cancer

SkinCancerNet

Acne & Bacteria

A bacteria, known as Propionibacterium acnes, is a normal inhabitant of the skin. It uses sebum as a nutrient for growth, therefore increases in follicles during puberty. People with acne have more Propionibacterium acnes in their follicles than people without acne. The presence of bacteria attracts white blood cells to the follicle. These white blood cells produce an enzyme that damages the wall of the follicle, allowing the contents of the follicle to enter the dermis. This process causes an inflammatory response seen as papules (red bumps), pustules, and nodules. The bacteria also cause the formation of free fatty acids, which are irritants, increasing the inflammatory process in the follicle.

Normal Follicles

Sebum produced by the sebaceous gland combines with cells being sloughed off within the hair follicle and "fills up" the hair follicle. When the follicle is "full", the sebum spreads over the skin surface giving the skin an oily appearance. When this process works correctly, the skin is moisturized and remains healthy.

Obstructed Follicles

Problems arise when the sebum is trapped in the hair follicle. For reasons that are still unclear, some hair follicles become obstructed. The sebum is produced but gets trapped on the way out, and the cells that are normally sloughed off become "sticky", plugging up the follicle. The process of obstructing follicles is called comedogenesis. It causes some follicles to form a type of acne called comedones, also known as blackheads and whiteheads.

Hormones

For most people with acne, it begins at puberty. This is when the body starts to produce hormones called androgens. Androgens cause the enlargement and overstimulation of the sebaceous glands in people with acne. Sensitivity to these androgens also cause acne to appear during the menstrual cycle and sometimes in pregnancy. The extra sebum (oil) that the sebaceous glands produce mixes with dead skin cells and bacteria on the skin's surface and this blocks pores. Inside the blocked pore, bacteria multiply and cause inflammation leading to the spots and pustules associated with acne.

There are more theories of aging than facts. Aging clearly occurs at different rates for different species, and even within a species, aging occurs at different rates among different individuals. The only reasonable conclusion is that aging must be genetically controlled, at least to some extent. Both within and between species, lifestyle and exposures may alter the aging process.

Most gerontologists view senescence as a collection of degenerative entropic processes related only by the fact that they occur over time. Some theories of aging address what controls these processes and why the controls exist as they do. Other theories of aging address the issues of whether senescence is more programmed than random entropy, thus offering some advantage for a species. For example, senescence may have evolved because without it, a species would accumulate ill-adapted older members. These members would compete with potentially better adapted younger members, slowing the rate at which adaptive mutations are introduced.

Loose cannon theory: This theory posits that an entropy-producing agent--free radicals or glucose--slowly disrupts cellular macromolecular constituents. Theoretically, free radicals, generated during oxidative phosphorylation, can variously modify macromolecules, primarily through oxidation. Considerable evidence suggests that oxidative damage increases with age. For example, in older organisms, specific amino acids in specific proteins tend to be oxidized residues, leading to decreases in the specific activity of these proteins. Additionally, specific oxidized derivatives of nucleotides from DNA increase in frequency. Experimentally induced simultaneous overexpression of superoxide dismutase and catalase (enzymes that attenuate free-radical damage) increases the life span of fruit flies by about 30%.

Glucose is thought to promote senescence mainly through nonenzymatic attachment to proteins and nucleic acids, through the same process that produces glycated hemoglobin. Glycated protein levels increase with age. Otherwise, there is little direct evidence that glycation has a major role in senescence. However, because dietary restriction increases maximum life span and also reduces blood glucose and the rate of glycation, interest in glycation's role in senescence continues.

Rate of living theory: This theory posits that smaller mammals tend to have high metabolic rates and thus tend to die at an earlier age than larger mammals. Thus, this theory is related to the idea that free radicals and other metabolic by-products play a role in senescence. However, studies of metabolic rates have shown wide variation in the correlation between size and longevity, undermining the credibility of this theory.

Weak link theory: This theory posits that a specific physiologic system--usually the neuroendocrine or immune system--is particularly vulnerable (presumably to entropic processes) during senescence. Failure of the weak system accelerates dysfunction of the whole organism. Failure of the neuroendocrine system would be expected to produce profound impairments in homeostatic systems, including loss of reproductive function and metabolic regulation, which occur with age. Failure of the immune system would be expected to produce an increased susceptibility to infection and a decreased ability to reject tumor cells. However, there is little evidence that failure of either system directly contributes to age-related diseases or to mortality (in contrast, for example, to the direct contribution of a compromised immune system to mortality in patients with AIDS). Furthermore, even if this theory explains some manifestations of aging in higher organisms, it does not explain aging in lower organisms, and little is known about the primary mechanism behind such weakness.

Error catastrophe theory: This theory posits that errors in DNA transcription or RNA translation eventually lead to genetic errors that promote senescence. Although data suggest that older organisms have altered proteins reflective of such genetic changes, this theory does little to explain most observed age-related changes.

Master clock theory: This theory is one of the oldest theories of aging and no longer has high credibility; it states that aging is under direct genetic control. Teleologically, it suggests that the rate of aging within each species has developed for the good of each species. Individual variation develops because of maladaption, exposure, and lifestyle. In the wild, such maladapted individuals tend to die out and the well-adapted ones persist, altering longevity in the best interest of the species.

Exactly what controls the rate of aging is unknown. It could be a gene that controls telomere shortening or some other process of cell division. Or it could be genetic control of another cellular process not involved in division, such as DNA repair, thus resulting in apoptosis.

Having built a community of plastic surgeons, dermatologists, and cosmetic physicians at Medical Spa MD, the need arose for a place for patients and those interested in knowing more about treatments, benefits, and complications to have a place to share information. Hence, Switch MD.

I started this website in June 2008 to provide the same type of straight shooting information for patients who want to know about how some treatments are better than others, you don't want multiple facelifts, and why your plastic surgeon, dermatologist or medical spa is telling you some things, but not others.

This website is for patients of cosmetic medicine who want to be smarter and know what's going on behind clinic counter. If you're looking for the same old BS that covers every magazine and web site you're in the wrong place. This is a no bullshit zone. Since this site takes both time and money to run I run some advertisements on it and am creating a directory of plastic surgeons, dermatologists and medical spas. I think it's a fair trade.