Monday, February 27, 2012

New path discovered by which vitamin D reduces inflammation

Scientists have identified a new path by which vitamin D reduces inflammation.

According to a group led by Elena Goleva at National Jewish Health Center in Denver, vitamin D binds to a receptor in monocytes, a type of white blood cell. The receptor then binds to DNA in the cells and directs the cells to make more of an enzyme that shuts down inflammatory signaling.

The researchers found that vitamin D at or above a concentration of 30 nanograms per milliliter was enough to do the job. 30 ng/ml is a widely accepted lower limit for vitamin D in blood serum. (I recently had my own vitamin D level assayed and found it was 32 ng/ml.)

The research was published in the Journal of Immunology. [paper] [media summary] The authors say that vitamin D not only is important in maintaining calcium levels and bone health, but also plays an important role in the immune response.

That’s what I’ve found in my reading, although there’s also a lot of people on the internet who would like you to believe that taking vitamin D supplements—sometimes to an extreme degree—is a good idea for your health and in particular for relieving eczema. I remain wary. If vitamin D is so important then you need to maintain a proper level, not overdose yourself.  All drugs are toxic when ingested beyond ranges established to be safe in clinical trials.

What I like about this paper is that the authors have gone out of their way to conduct their experiments in an environment that is similar to the human body, as far as concentrations of various substances go (including vitamin D). They also used monocytes taken from human donors instead of cells from some purified, genetically altered strain, as is so often the case with cell biologists dabbling in medical applications. So their results mean something to you and me.

One question that I do have is whether the same kind of inflammation studied here—caused by LPS, a bacterial molecule that triggers an anti-infection response—is at work in chronic eczema. Is there one major inflammatory response, or are there several?

Thursday, February 23, 2012

Habit reversal works for scalp itching

Training myself in habit-reversal, to replace compulsive scratching with more socially acceptable behavior, has not been easy.

It's hard because you have to be on all the time. You have to intercept those impulses to scratch before the action happens. Of course the goal is to make the behavior automatic, so you don't have to consciously think about it, but you do at the start.

And I fail all the time. I'll just discover my hand doing something it's not supposed to, and I'll have to yank it away. Fortunately the inventors of habit-reversal acknowledge that you'll fail. You just have to try your best.

I haven't quantified the results yet but I do see one significant improvement. I've been able to stop scratching my scalp, especially on the days that I wash my hair with shampoo (tar shampoo, naturally). Just a few weeks ago, my scalp was covered with dry skin and little scabs that I was picking at. It's annoying to feel itchy all the time, and everyone knows how embarrassing dandruff is.

But, in this completely unscientific experiment lacking any sort of control, I observe that I am hardly scratching my head at all any more. To some extent, I have broken the itch-scratch cycle for this specific behavior. And that's great.

However, elsewhere on my body, particularly the backs of my knees, I've got red and inflamed skin from scratching that I haven't brought under control. It's like a different type of itch, although there's certainly a psychological contribution.

My ability to implement habit-reversal is strongest in the morning. Later in the day--especially after I get back from work and the circus of getting the kids through bathtime and into bed begins--the stress mounts and I find myself scratching various places vigorously. (Not the scalp though.) I'd guess that's because whatever part of my brain I need to control scratching is busy thinking about how to keep the kids disciplined instead. Or it could just be that the urge to scratch gets brought on by stress, and there's little more stressful than fighting with your two- and five-year olds to brush their damn teeth and get into the tub and stop trying to drown your sister and stop whining and crying about how she's got your rubber dolphin, etc.

I need some stress-reduction technique--something more powerful than the beer I open after the kids are in bed.

Wednesday, February 15, 2012

Staph aureus throws a party in untreated eczema patches

We are not alone. Wherever we go, we carry our personal microbiological party along with us--in our gut, in our intestine, and naturally on our skin. We're crawling, even the healthiest of us, with ten bacteria, viruses, protozoa, etc. for every cell in our body.

New research has revealed an interesting difference between the skin microbiomes of patients who do and don't use pharmaceuticals to control their eczema. A recent study in the journal Genome Research finds that Staphylococcus aureus has pooped the party--it dominates the population of bacteria in untreated skin. On the skin of patients who use steroids, calcineurin inhibitors such as Protopic, or antibiotics, S. aureus shares its living quarters much more equitably with its bacterial cousins.

The authors of the paper, led by Heidi Kong and Julia Segre at NIH, used a technique called "16S ribosomal RNA bacterial gene sequencing" to catalog the bacterial population in two body locations at which eczema commonly occurs--the insides of the elbows and the backs of the knees--in 12 kids with eczema and 11 healthy controls.

(They used this type of sequencing because the method usually used to assay bacteria, which is to swab and try to grow a culture, may favor the growth of certain species over others. 16S sequencing provides a snapshot of all bacteria species present at any one time.)

S. aureus dominates flareup regions in patients who don't treat eczema. (Fig 3A.  from Kong et al.)
In the controls and the eczema patients before flareups, the bacterial populations were quite similar, with the eczema patients hosting populations in which S. aureus owned twice as much market share as it did in the controls.But during flares, the main finding was that in the patients who didn't treat their eczema (to be specific: they hadn't taken an oral antibiotic for the previous 4 weeks, or applied a topical treatment in the previous week), 90% of the bacterial population was Staphylococcus, compared to 20% for the patients who had treated their skin.

The scientists observed other shifts in the bacterial population on untreated skin, too. Several other species increased their relative numbers--especially Staphylococcus epidermidis, often thought to be a "commensal"--which I take to mean relatively harmless--species on healthy skin. It appears that S. aureus and S.epidermidis have some kind of symbiotic relationship--the two are helping each other out, or one is parasitic on the other in some way.

Very interesting research, although there's not much for an eczema patient to take away. Naively, one might think that this shows it is better to treat one's eczema than not. But there was nothing about the eczema in untreated skin being worse; the number of patients in the study is small; and there's a lot of variation (of course) among the data for the patients who treated their skin. What did they treat it with? We don't know. Could it be that applying a steroid helps keep down the S. aureus population? That would be weird indeed, because S. aureus folliculitis is a known side effect of strong steroid use. I'll go out on a limb and say that antibiotics are probably better than steroids for keeping S. aureus down in the short term.

One small frustrating point is that the 16S sequencing technique doesn't seem to provide absolute numbers. I'll exaggerate to make the point: Maybe there are 100 bacteria total in your elbow to start, 20 of which are S. aureus, and during a flare there are now 100,000 bacteria, but 90,000 of them are S. aureus. Or maybe there are 90 billion S. aureus out of 100 billion during a flare. This paper doesn't give you any idea of the scale.

Friday, February 10, 2012

Eczema occurrence increases from north to south in Australia. Is sunshine responsible?

An Australian/British study connecting eczema and exposure to sunshine (in press) in the Journal of Allergy and Clinical Immunology has been getting a lot of media attention of late. [media summary] [paywall link to paper, which I mysteriously got for free a few days ago]

The media coverage has been misleading, at least in the titles. Makes it sound like you should send your kids out in the sun. "Playing in the sun ‘reduces risk of eczema and food allergies in children.'" "Sunlight may help ward off allergies." Irresponsible, really, when Australia faces an epidemic of melanoma caused by exposure to UV through the ozone hole.

That doesn't mean the results aren't interesting. The authors of the paper analyzed data from a national database, for two cohorts of 3312 and 4331 children (aged 4-5 and 8-9) so the number of subjects isn't a concern. They stratified the kids by geographical location from north to south and found that the incidence of eczema and allergy to peanut and egg increased from north to south. (Asthma showed no correlation.)

Strangely, the authors don't quantify how much sunlight children might be exposed to in these regions, even in crude average numbers. You'd think that if they are going to make the claim, as they do, that their numbers provide support for the hypothesis that kids are developing eczema and allergies because they aren't getting enough sunlight--or to go further and say that the lack of sunlight is reducing vitamin D levels in these kids and THIS is what is causing the eczema and allergies--that they might make some effort to refer to how much sun kids are exposed to. But no.

This leaves me wondering what other factors might account for the incidence of eczema and allergies increasing as you go southward through Australia. Also, I wonder whether it might be true that sunlight helps keep eczema down (I have no personal experience with this) by some other mechanism than vitamin D production. Perhaps exposure to long-wavelength--safer--UV radiation affects skin cells in some beneficial way that I'm not aware of.

I had my own vitamin D level measured last week. According to Kaiser Permanente, the normal range for 25-hydroxy vitamin D in the blood is 25-79 ng/ml. My level is 32 ng/ml. Relatively low, but in the normal range. So it's unlikely that for me personally a lack of vitamin D is what's causing my eczema.

Once I'm done with my habit-reversal trial, it might be worth taking some supplemental vitamin D to see whether it has any effect.

Tuesday, February 7, 2012

First day of the habit-reversal regimen

This is the first day of the self-training phase of my habit-reversal project.

It's gone pretty well so far, probably helps that I'm not having a flare-up or a stressful day.

Yesterday by 7 pm I'd logged 503 separate scratching events, by making marks on business cards--a convenient, inconspicuous data storage medium. Roughly half of the events occurred before lunch and half afterward. As I mentioned yesterday, a surprising number of the events involved nervous touching of the face, to quell tiny itches or crawling-ant-like sensations.

Making marks on business cards is a tedious way to enter data. (Really, you need a clicker or some kind of smartphone app.) I lost interest in doing it toward the end of the day and probably under-reported my scratching. And then, at 7 pm, bedtime for the kids started and I gave up entirely. But the point is that I expect habit-reversal to have a significant effect, and after two weeks I'll repeat the measurement--I hope to see the scratching drop down to less than 100, possibly 50, events.

Today I've had some luck intercepting scratch attempts before my nails hit skin. I've been clenching my fist on whatever side is affected. If I feel a more intense itch, I've been pressing a nail hard into the itchy spot, which does seem to reduce the itch, sometimes to the point where I forget about it.

One problem is that many of the itches originate on my face, and poking your fingernail into your skin leaves a dent and sometimes a blanched spot. I am not sure this is more socially acceptable than scratching. But, so I understand, habit reversal breaks the itch-scratch cycle, and eventually I'll feel fewer itchy sensations on my face.

Often after I wash my hair, my scalp is particularly dry and I tend to pick at it. Then I get scabs or dandruff. Eww! This behavior is largely nervous and compulsive and I hope to eliminate it by habit reversal.

Monday, February 6, 2012

Habit reversal: The hyperactive monkey records scratching events

Today, as the first part of an effort to reduce the frequency of obsessive scratching that contributes to my problems with eczema, I counted the number of times that I scratched throughout the day--every motion, whether a light skin brush or a deep nail dig, that I made to relieve an itch or satisfy a nervous compulsion.

My method was hardly high-tech. I made marks on the back of a business card. (Possibly the most practical use I have made of one.) In fact I made so many marks by noontime (254) that I ran out of space and had to start a second one.
A highly scientific data collection method.
These are separate events. Wow, I knew I had an issue with this but I wasn't aware I scratched so often. And that's the point of this stage of the habit-reversal process: to become aware of the scratching, so you can make a conscious effort to recognize the motion and stop it.

Usually, from what I gather, patients use some sort of clicking device instead of making marks. I bet that you could go further and use a smart device that records the time of each scratch. That way you could see when intense bouts of scratching occur through the day, and link them to triggers, and perhaps deal with issues psychologically.

Also best would be an initial step to record scratching events that the patient is not aware are being recorded. All day today I have gone through this thought process:
  1. unconscious urge to scratch
  2. motion to scratch
  3. realization that I'm doing it
  4. stop! Don't do it!
  5. no! It's OK to do it and record it!
  6. scratch. oh yeah.
  7. repeat
Even marking the stuff down is weird. You can see that instead of making marks in some places I have written down numbers. I did this when I couldn't use a pen and had to keep track in my head--like when I was changing the kids' diapers, or riding the subway, or talking to someone in the office.

I'm glad that I only have to do this once at the start and once later on. It's really interfering with getting work done.

Several things are interesting. For example, the number of times I sneakily merge a scratch with a motion that would otherwise seem natural, such as smoothing my hair (or what's left of it). Also, the vast majority of scratch entries so far correspond to nervous touching of my face and head.

What an interesting process. Even better if the psychological training works and I can stop looking like a hyperactive monkey.

Thursday, February 2, 2012

A wider perspective on habit reversal to reduce eczema scratching

I've done as much armchair research as PubMed will allow, and I've found that the psychological technique called "habit reversal" seems to be a valuable component of total therapy for eczema—but it's not covered much in the scientific literature, and in my personal experience, it’s almost completely ignored by the medical system.

Why? There’s little profit in it, sure, but it’s also unsexy—it requires patients to commit to a training regimen and then not deviate from proper practice, and it requires repeated input from nursing staff and a medium-term follow-up. It’s low-budget, time-consuming, and probably effective. But only when combined with traditional therapy such as topical steroids.

Habit reversal is a technique to reduce obsessive, compulsive scratching not generated by intense itch. The patient, instead of scratching, clenches his/her fist, and/or applies strategic pain to the itchy area by poking it with a fingernail.

I searched on PubMed and read the papers I could access on the topic. Here are the two that were most informative, besides the ones by Noren and colleagues that I wrote about previously:

Habit reversal training for the itch-scratch cycle associated with pruritic skin conditions (2007) An instruction manual for nursing staff. The authors are from Australia. They recommend four training sessions spaced a week apart, with a follow-up session one or two months later.

The effects of psychological intervention on atopic dermatitis. A systematic review and meta-analysis (2007)  The authors, from the UK and Japan, consider eight journal articles studying psychological treatment for eczema. Their conclusion: “Taken together, the most effective psychological intervention for AD would seem to be a combination of stress-managing psychotherapy, relaxation techniques and habit reversal behavioral therapy.”

Interesting. Habit reversal is not the only game in town when it comes to psychology. Someone even tried aromatherapy, but it didn't pan out.

It’s time for me to give habit reversal a shot. I’m going to train myself starting next Monday. In the initial phase, “registration,” you record how many times a day you scratch. The point is to make the patient conscious of scratching action that was previously unconscious. I’ll be making little marks with a pencil on the back of a business card. When I’m done for the day, I’ll post a photo of the card.