Dermatologists, Sun Bathing and Eczema

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Dermatologists can be accused of having contradictory attitudes towards sun exposure. On the one hand, to prevent skin cancer we routinely advise against sun bathing, but on the other, we often treat common skin disorders like eczema (“atopic dermatitis“) or psoriasis with ultraviolet (UV) light.  Now there is even reason to think that too little exposure to sunlight may be why allergic diseases, like atopic dermatitis, have become so much more common in recent years.  What is going on with sunlight and the skin?

Unquestionably, sunburns damage the skin and promote the development of skin cancer.  There is no known “safe” amount of sun exposure that does not produce the biochemical changes in skin which are linked to cancer.  For this reason, dermatologists do not consider suntans to be healthy for the skin, either.  Suntans, like freckles, are properly considered an injury response of the skin to excessive sun exposures. Hence, our general recommendation is to: cover up, use sunscreens on sun exposed areas and get your necessary vitamin D through diet and dietary supplements.

Yet, ultraviolet light therapy is a time honored and effective treatment for inflammatory skin conditions, like atopic dermatitis and psoriasis. Typically these treatments which use the sunburning, UV-B, portion of the sun spectrum are given in the physician’s office, to prevent over-dosage.  The desired exposures are ‘sub-erythemogenic’, meaning they are below those that will produce skin redness or sunburn. [Read more…]

What Is The Skin Barrier, And Why Does It Matter?

The skin barrier is like a brick wall. The cells or "bricks" are surrounded by fat (lipids) or "mortar"
The skin barrier is like a brick wall. The cells or “bricks” are surrounded by fat (lipids) or “mortar”. Credit: Mary L. Williams

Why Have A Skin Barrier?

Our skin barrier is what stands between us and the outside world. But the skin barrier is more than a mere fence or line drawn in the sand to separate “inside” from “outside”, or “here” from “over there”. Our skin barrier protects from many different types of threats to our well-being. We probably think of these primarily as perils coming from the outside, such as bacteria or other microbes. Or toxic chemicals. Or sunburn. Or mechanical injury.

While our skin barrier does work to protect against such external assaults, its most  important task by far  is to protect us from a terrible threat coming from the inside.  This hazard of all hazards, peril beyond measure, is the escape of our precious body water.

Let us go back many eons in time and imagine that first fish as it attempted to venture out onto land. Bear in mind that most creatures and most cells are about 80% water. How could our fish retain its body water, as it left its wet surroundings to live on dry land? How could it keep the water in its cells from evaporating away into the dessicating air? This new world was a hostile one that threatened to turn our fish explorer from a plum into a prune? This newcomer to land needed some type of ‘permeability barrier’; it needed some form of waterproofing. Biologists call the outer protective covering of plants and animals, their ‘integument’; we call ours ‘skin’.  In every species, whether plant or animal, the most critical function of the integument (including our skin) is to protect against loss of body water.  Our skin barrier’s number one task is to hold our body water inside.  [Read more…]

Do pores on the skin need to breathe?

pores on the skin shown in drawing of skin|Credit: Jessica Kraft

Drawing showing pores on the skin where hairs and ducts of sweat glands come to the surface.
Credit: Jessica Kraft


Pores on the skin represent openings of hair follicles and sweat ducts.  These pores do not ‘breathe’ in the usual sense – our lungs take care of that need.  Yet, it can help to keep your pores open.  Sweat gland openings can become obstructed – for example, by wearing skin tight clothing when we exercise.  This can result in an itchy heat rash, or miliaria,  Hence, it is advisable to avoid overdressing when it is hot, and to remove sweaty clothing and shower as soon as possible after exercising.  The widespread plugging of sweat (or ‘eccrine’) glands can result in heat intolerance – with the risk of heat stroke.  Individuals who have one of the skin disorders called ichthyosis,  where the outermost layer of skin, the stratum corneum, is too thick over most or all of their body, often experience overheating because their sweat ducts are obstructed by scales.

Similarly, when the pores of sebaceous glands on the face, chest and back become plugged with sebum and keratinous debri, we develop blackheads.  These are often an early sign of acne and an indication that it’s time for a visit to our dermatologist.  While blackheads are not caused by too infrequent face washing, they can be produced by some of the products we put on our skin, such as oily cosmetics.  Look for the label “non-comedogenic” on cosmetic products, which will indicate a safer product to use.  And avoid oily scalp pomades.pores

Highlights from the 2013 IID. Part 7: Is Acne a Disorder of the Skin Barrier?

It has been known for decades that the formation of keratinous plugs in the outlet of the sebaceous follicles is the first step in the process of acne vulgaris.  These ‘comedones’, (called ‘open comedones’ (blackheads) if the opening of the pore is wide and the plug is visible; and ‘closed comedones’ (whiteheads) if it is tiny and the plug buried under the surface), precede the development of inflammatory lesions (what we call pimples). It has also been known for a long time that individuals who develop more than their fair share of acne have oily skin.  Or, more precisely, they tend to have high rates of sebum production.

Downing and colleagues linked these two observations together and proposed that comedones are the result of essential fatty acid deficiency in the follicular orifice.  Deficiency of the essential fatty acid, linoleic acid, produces a dermatitis characterized by scaling, redness or erythema, and a defective permeability barrier.  This is because linoleic acid is a critical constituent of some of the ceramides that are required  for the skin barrier. Sebum is rich in other fatty acids, but it lacks linoleic acid. Therefore, the epidermal cells lining the follicle, which are continually bathed in this deficient lipid mixture, could develop a form of localized essential fatty acid deficiency. The more sebum being produced, the greater this dilutional effect. Little has been done to test the Downing hypothesis since it was first espoused twenty five years ago.  A first step in that direction would be to determine whether or not there is a barrier defect in the follicular epithelium.

In the studies reported here, we examined the barrier integrity of different regions of the hair follicle in biopsies of non-inflamed, open comedones, using a water-soluble tracer that can be seen with an electron microscope. While normal follicles show an intact barrier from the skin surface all the way down to the opening of the sebaceous gland, follicle walls surrounding open comedones leaked abundant tracer.

Bottom Line: These studies indicate that an barrier defect in the hair follicle wall is present in the earliest lesions of acne.  It raises the possibility that treatments aimed at restoration of the barrier in early acne lesions might prevent the later development of inflammatory acne.

Highlights of the IID. Part 5: The microbiome of normal skin and atopic dermatitis

The gut and its bacterial flora – its ‘microbiome’ – is receiving a lot of attention from scientists and their findings are being closely followed by the lay press.  The skin’s microbiome, too, has become a hot topic among dermatologic researchers, as evidenced by the number of papers and reports dealing with the subject at the 2013 International Investigative Dermatology meeting in Edinburgh.  Of these reports, several dealt with the microbiome in atopic dermatitis (or eczema).  This is of particular importance to clinical dermatology because infections with Staph. aureus is a common trigger of disease flares among atopics. [Read more…]

Highlights of the IID 2013. Part 2: Promising New Drug for Atopic Dermatitis

An important feature of the inflammation in atopic dermatitis (and in the other ‘atopic’ disorders, such as asthma) is the overproduction of ‘bad’ cytokines, such as interleukin 4 (IL-4), by a subgroup of Th2-type lymphocytes. After secretion from Th2 cells, IL-4 percolates up into the epidermis where it decreases the production of both lipids and proteins that are critical for normal barrier function (see our recent series of articles on atopic dermatitis for more information on the link between the barrier and Th2 cytokines).

One would anticipate, therefore, that if one could block the actions of IL-4, the dermatitis might improve. This is just what Lisa Beck’s group at the University of Rochester reported at the recent IID meeting in Edinburgh. [Read more…]