Stress related skin article from a radio show with a derm

[Guest guest]

I know this article is not directly about rosacea but

thought it may be of interest to those of us who

suffer from the dry skin as well as the acne...

Stress-Associated Skin Disorders

Broadcast Monday 28 May 2001

with Norman Swan

Summary:

Research from the U.S. found that stress can reduce

the skin permeability barrier and skin conditions can

become worse.

Transcript:

Norman Swan: Welcome to the program.

Today on The Health Report, Zen and the Art of Skin

Maintenance; some myths about bedwetting, some

surprises about what it can lead to; and a chance to

test your surgical skills.

Let’s start with the stuff that keeps our insides in.

There’s now objective evidence that stress can

directly affect your skin in a potentially harmful

way.

Results from the United States and both animals and

humans have shown that stress can reduce what’s called

the skin permeability barrier, our protection against

the outside world.

It confirms the impression of many people with skin

problems that at times of stress, their rashes become

worse.

Dr Elias is Professor of Dermatology at the

University of California, San Francisco.

Elias: Almost all the important diseases that we

see in dermatology such as eczema, atopic dermatitis,

and psoriasis, are associated with the permeability

barrier abnormality. The permeability barrier function

is so important for survival of ourselves as

terrestrial creatures that when there’s any

abnormality in the barrier, a whole host of signalling

molecules are released that are continually attempting

to bring about repair of the barrier. These signalling

molecules don’t just repair the barrier, but they also

initiate the inflammation in the deeper layers of the

skin. And this is consistent with everything that we

know about atopic dermatitis and psoriasis. In

addition are a host of other risk factors that

increase the tendency, or aggravate disease

expression, and one of these factors is psychological

stress.

Norman Swan: So tell me about the work that you did.

Elias: We started out with some simple studies

in mice, where we first took completely normal mice

and did three different things with them. The first

was simply to have different numbers of mice living

together in the same sized cages for varying periods

of time, up to ten mice from one to ten mice per page.

The second model was to simply take a mouse and

transfer him from the cage that he was used to into a

brand-new cage. So a ‘new cage environment’. And the

third model was a frustration model, where the mouse

was in a little hammock suspended so his feet could

not touch the ground but he could still have all the

water and food that he needed. In all three of those

models we discovered that what had previously been

completely normal skin barrier function became

abnormal, very quickly. And this abnormality was due

to an increase in the body’s production of adrenal

corticosteroids, glucocorticoids, which are part of

the stress response in humans, and we could block the

increase in steroids and prevent the deterioration in

barrier function by giving either tranquilisers, or by

giving inhibitors that would block the action of the

glucocorticoid’s receptor antagonist such as the drug

that’s well-known to even your general audience,

RU486, which is a glucocorticoid receptor antagonist.

Norman Swan: RU486 being mifepristone, the

controversial so-called abortion drug.

The key here is that they concluded that these

glucocorticoids, these cortisone-like hormones

produced by the adrenal gland just above the kidneys,

seemed to be harmful to the skin.

Elias then went on to study stress and skin

permeability in a group of medical students, before,

during and after their final exams. He compared their

skin responses to objective measures of how much

stress they were under.

Elias: In all the students they had relatively

low scores after the vacations, much higher scores on

both scales during exam periods and the students who

had the highest stress levels had the greatest

deterioration in permeability barrier function.

Norman Swan: Could you relate that to the abnormal

cortisone production from the adrenal gland?

Elias: For logistical reasons we couldn’t assess

that aspect but other workers elsewhere in the world

and the United States have shown that different types

of psychological stress, for example in high divers

and parachutists and people like that, they generate

much higher levels of glucocorticoids when they’re

under that type of stress.

Norman Swan: Was the relationship strong enough that

you would say it was cause and effect, that the stress

was causing the change in the skin function?

Elias: The stress based on the studies in the

animals, is definitely directly causing the

deterioration barrier function. Now the significance

here is again, that that would simply amplify the

tendency for people who already have either a marginal

barrier or a tendency for diseases like eczema and

psoriasis It’s a trigger factor.

Norman Swan: And just explain the change in the

barrier itself.

Elias: The barrier I’m talking about here is

called the permeability barrier. This is what keeps

the water inside your body, and prevents you from

desiccating, in this terrestrial environment, and

that’s the function that’s most critical, the most

critical barrier function of the skin, and that’s the

one that drives everything else underneath and

therefore impacts on everything else underneath.

Norman Swan: So when you add stress, what happens

exactly to that barrier, is your ability to hold in

water reduced and therefore the skin dries out, which

in fact is what happens in eczema and psoriasis?

Elias: Patients with eczema and psoriasis have

an abnormal barrier to begin with. In the case of

eczema, even the uninvolved skin has an abnormal

barrier, so they’re always right at a trigger point.

So now you add psychological stress, which causes a

further compromise in the barrier. You get a further

increase in the signalling molecules, which are always

attempting to repair the barrier, but they can’t ever

repair the barrier.

Norman Swan: And the side effect is inflammation?

Elias: The side effect is inflammation and

recruitment of these specific inflammatory and immune

cells that are characteristic of the disease.

Norman Swan: And what about skin moisture, has it got

anything to do with that at all?

Elias: It really doesn’t. Moisturisation is

really more of a cosmetic issue. It is a little bit

important; moisturisation in the stratum corneum does

act as a biosensor and it does indeed sense changes in

external moisture independent of the barrier, and that

does regulate functions underneath, but not as

profoundly as these changes in stress that impact on

the barrier.

Norman Swan: If you’re implying here that one of the

causes of this, that the mechanism is increased

stress, affects your adrenal glands, the stress

hormones, there, increased cortisone-like hormones and

that changes the barrier, it makes you worry just

about the only drug that dermatologists have got to

treat skin disease, which is steroids, which is in

fact the very same analogues, if you like, of these

hormones you’re using to treat; are you saying that

we’re using the wrong drugs to treat these skin

diseases?

Elias: Well I think the problem is that these

drugs are seductive, because they are so effective at

reducing inflammation, and we all use them; I use them

in my practice extensively. But we must not rely on

them entirely because the skin becomes dependent on

them, they have side effects in the skin, and they

become less effective over time and you tend to get

rebound flares of these diseases.

Norman Swan: But if one of the primary problems is

skin permeability, and these endogenous, inbuilt, if

you like, cortisone hormones are bad for skin

permeability, does that not mean the drugs are bad for

skin permeability and therefore you’re not really

helping the condition in the long run?

Elias: It’s a trade-off. If you’re getting more

effect on inflammation when things are very

inflammatory, then it’s beneficial. But as your skin

inflammation declines, then you begin to see more and

more of the potential negative effects of steroids.

Norman Swan: What about interventions, like is RU486 a

potential treatment, turning it into a cream, is that

a potential treatment for these skin diseases, or is

stress reduction?

Elias: Stress reduction makes a lot of sense,

and in the case of skin diseases there’s even one

study by the Zen physician, Kabat-Zinn, who’s

published a lot of books on Zen approaches as

adjunctive therapy where he’s taken patients with

psoriasis and divided them into two randomised groups

and given them the same therapy. And one half of the

patients were given in addition to that, some

intensive meditation sessions, and they cleared much

faster with standard therapy than did the patients who

were treated with the standard therapy alone.

Norman Swan: What about RU486?

Elias: I don’t know of any experience with this

agent used topically in humans, or even in animals for

that matter, and the idea that it could be useful as

topical agent hasn’t even been considered yet.

Norman Swan: Elias is Professor of Dermatology

at the University of California, San Francisco.

Reference:

Garg A. et al. Archives of Dermatology 2001;137:53-59

Guests:

Dr. Elias

Professor of Dermatology,

University of California, San Francisco

Veterans Affairs Medical Center,

4150 Clement St.,

San Francisco CA 94121

U.S.A.

email: eliaspm@...

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