Eczema Free Forever™ Eczema Free Forever™

Immunity persists for at least 3 years after receipt of new shingles vaccine

Immune responses to the latest shingles vaccine (Shingrix) last for at least three years following vaccination. The robust immune responses develop and persist in all age groups, according to a recent study in The Journal of Infectious Diseases.
Dermatology Times – Dermatology

40-60 years old not even walking for 10 minutes once a month

According to a report by Public Health England (PHE), middle aged men and woman are not getting enough exercise. In fact a staggering 41% are not even managing a 10 minute brisk walk once a month!

Dr Jenny Harries, Deputy Medical Director at PHE said: “I know first hand that juggling priorities of everyday life often means exercise takes a back seat.But walking to the shops instead of driving, or going for a brisk 10-minute walk on your lunch break each day, can add many healthy years to your life.”

In fact those in middle age can effect a 15% reduction in the risk of early death from at least one brisk 10 min walk per day.

The Government recommend people undertake at least 150 minutes of activity each week.

PHE also hopes by getting this age group active it will have a knock-on effect among those who have children.

PHE are recommending a free app called Active 10. In addition, there are a number of other apps that will track activity – it’s about finding the one that works best for you and one you will use.

Tell us your experience – were you inactive and turned things around? Would love to hear your story and what now works for you.

talkhealth Blog

4 Years TSW

Hi everyone, I feel I owe you a post and an explanation as to my whereabouts!

Can I just start with saying thank you so, so much to anyone who has asked after me, anyone who has taken the time to email me, comment or message me on other social media. I am so grateful for you all <3 For those who have gotten in touch with me who wanted answers I’m so sorry I’ve been unable to supply them. Life at the moment is pretty hectic.

I’ve been wanting to post for a long time but never quite knew what I was going to say. My 4 years TSW anniversary was May 22nd, I was looking to post then but just didn’t have the time or the will. It was only really this morning when I woke up a lot earlier than anticipated that I happened to look at a message on Facebook and discovered a whole section of unfiltered messages that contained an overwhelming amount of unread messages, dating all the way back to 2012! I am so annoyed that I’ve only now just been alerted to them and I can only but apologise for not getting back to you. I will say as well though that I don’t add people I don’t know to my personal Facebook account – if you want to talk to me I’d prefer it you emailed me. Alternatively I guess I could make a Facebook group…

So anyway. How am I? How is my skin?

I’m doing really good at the moment. I’ve landed a full time job in the city, which means hourly commuting each way. I’m in the process of buying a house, and have been since November so you can only dare to imagine the stress that I’ve been under! That is actually another reason I didn’t want to post yet – I was hoping I could update from the new house but hey ho – life just doesn’t always follow a plan.

At current my skin is pretty good. Dry, but good. I’m still taking Ciclosporin for now but I hope I can come off eventually or even start on Dupilumab, we will see. It hasn’t been plain sailing though, when I first started at my new job I had a horrible flare which was really quite embarrassing after being good for a few months and having to meet new people. It keeps coming and going but it’s bearable and I also put it down to the stress that comes with the house buying! Not only has my skin been bad but I’ve also been experiencing other unexplained health issues as well which we’re currently trying to figure out. Stress is a funny old thing.

Another thing I wanted to mention is heat – it’s really hot in the UK at the moment and I’m OK. I can deal with it now. I no longer come out in a full body heat urticaria rash, I’m starting to feel more confident that that is a thing of the past and was fully related to topical steroids, but until I flare again I’m not going to say that for definite.

There are moments that have me stopping and thinking, things now that I’ve been taking for granted, that I couldn’t even dream to do when I was in the deep grasps of TSW and it’s just astounding to see how far I’ve come. I have a full time commuters job, I can tolerate heat, my skin no longer comes off in gigantic flakes that compare to sunburn peel, I don’t have to vacuum my bed, I can take a 5-10 minute shower and be ready within an hour. I can stay at other people’s houses without thinking of myself as a hindrance or worrying that my skin or routines will be an issue. I’m no longer housebound. Touch wood I’ve not had a skin infection or a herpeticum outbreak, in fact I can’t even remember when I last had one!

The only things that are still problematic for me is the aforementioned dry skin but even then it’s not really that much of an issue – it’d just be nice to have suppler skin but dry skin has always be an issue of mine since day one. I’m also not yet confident I could live with a cat but I think that could be due to lack of exposure, I only spend time with cats once every couple of months so it will be hard to build up a tolerance, but gone are the days of full body rashes and acute asthma attacks when I so much as dare to look in the direction of one. I also still suffer from dermatillomania but I feel now that my skin has cleared up there’s not as many imperfections for me to pick at, but of course the tweezers still come everywhere with me! I also don’t wear make up but I’m cool with it… that’s the other thing, when going through such a traumatic illness you just start accepting your appearance for what it is. In my early 20s before the onslaught of TSW madness I used to wear make up every single day and when I became so ill it was a travesty, but over time you just accept that it’s your face. It’ll do.

And now onto the eagerly awaited awkward photos (that’s the other thing, it’s been so long since I’ve taken photos of myself I just can’t haha!):

I decided to take photos in a changing room because the lighting is always different.
Ignore the scab on my chin… it was a spot but dermatillomania and that…

I woke up like dis

Awkward flabby tummy pic

So as you can see, dry but currently rash free!

Hope everyone is well and I promise not to leave it so long next time.

Also I was emailed about this giveaway to share with you all which we can use to celebrate my 4 years of being steroid free!; Win some Dermasheets for your bed worth $ 270!

Good luck!

I Have Eczema

Why there will be no cure for eczema for at least 25 years

In a previous post, I made the Eeyore-like prediction that we are unlikely to see a cure for eczema during my lifetime, which means the next 40 years.

Upon reflection, I have become more optimistic: now I only think we might have 25 years to wait.

Several factors combine to make this so: our incomplete understanding of eczema; the ratchet-like course of the disease; its allergic component; and the expense and inertia of drug development.

As currently understood, eczema is initially a defective skin barrier that lets in allergens. In the first few years of life, children develop antibodies that protect them from disease over their lifetime. The defective barrier overstimulates this part of the immune system, and children build the capacity for allergic reactions to common things in the environment that most people don’t react to—pollen and foods for example.

The allergies get locked in. What may originally have been a leaky skin barrier now gets connected to allergies and inflammation.

In recent years scientists have discovered a number of genetic defects in various components of the skin barrier—the super-protein filaggrin, in particular. I can understand that the average patient must have the impression that with this genetic data is coming in, all that scientists have to do is develop targeted drugs to solve the defects. Or gene therapy to replace the bad genes. Surely these are on the horizon?

Here’s why they aren’t. Let’s start with gene therapy. Only one gene therapeutic has been approved anywhere in the world. The European Commission gave permission for Glybera to be used to treat a rare metabolic disease. Gene therapy is most famous in the US for the 1999 death of a teenager who signed up for a risky clinical trial. It is unlikely that over the next few decades we’ll see gene therapies emerge for anything but rare, fatal, incurable diseases. Eczema doesn’t qualify—and even if you could fix the skin barrier by gene therapy, you’d have to act within the first few months of life. What parent would let doctors give their newborn a potentially lethal treatment based only on the likelihood that the kid might grow up to have eczema?

Another possibility is RNA interference, a technique that blocks the conversion of genetic information into protein. RNAi was discovered sometime in the past two decades and recently the FDA approved the very first RNAi therapeutic, for a rare metabolic disease. To treat eczema, RNAi might be used to cut down on the amount of inflammatory molecules produced in the body or in the skin. A number of academic laboratories–I am aware of a couple in Japan–are looking at RNAi for eczema. However, there are no therapies anywhere near a clinical trial, and new “drugs” in this field would face even steeper regulatory hurdles than conventional drugs. Conversely, the reason to get excited about RNAi is that in theory it could allow us to choose which inflammatory molecules to turn off (rather than shutting down most of the immune system, as steroids do).

Now, let’s consider traditional drug discovery. Research does show that filaggrin defects are found in up to 50% of patients with severe eczema. (Naturally, there are apparently unaffected people who have filaggrin defects, as well as eczema patients who do not.)

So you’re going to develop some drug to target filaggrin? Irwin McLean, the filaggrin expert, says that targeting filaggrin could have a big payoff. But he admits that little is known about how the filaggrin gene is turned on or off. Eventually we will know, and perhaps that knowledge will suggest what drug might work.

The question is how a drug might fix or compensate for the defect. [See the comments for a couple possibilities.] And if we eventually find a drug that can correct for a single or double filaggrin mutation, there is still the question of how much benefit that will provide if a patient has already developed allergies.

Drugs are just not custom-designed—that is currently a pipe dream. Drug discovery is time-consuming and costly. It takes $ 1 billion and 15 years of trials to get a drug approved by the FDA. Scientists start with the protein of interest. Then they screen gigantic libraries of drugs to see if any of them affect the protein in useful ways. They tweak those initial “lead” compounds to make them better.

Then they file an application for a new drug. Then they proceed to animal trials: mice, rats, dogs, pigs, chimps. Then human trials—phase 1, 2, 3, 4. At any stage, and if you’re lucky it’s the early going, it can become apparent that your drug is ineffective or toxic.

And here’s another factor: many proteins are just not “druggable” for various reasons. Because of the shape of the molecule or the way it interacts with something else, tiny drug molecules can’t get to the active site; or they get in but can’t get out. Etc.

It is extremely difficult to develop new drugs.

Also, in the past few years the pharmaceutical industry has been in a slow-motion crash. Big companies are laying off scientists because a lot of the original big moneymaking drugs are coming off-patent and not generating enough income for R&D anymore.

Add to this the fact that there’s hardly anything in the pipeline for atopic dermatitis. I know Anacor has two candidates in Phase II trials—new topical anti-inflammatories. Great,  but hardly revolutionary. Regeneron has something interesting going: dupilumab, a monoclonal anti-IL4 antibody. It’s in Phase I.

Venture capital won’t even invest in startup companies unless their technology has passed Phase II.

You can understand my pessimism.

Next: why I might be wrong
End Eczema

Three years in: what has the $42M Atopic Dermatitis Research Network produced?

In July it will be three years since the NIH awarded National Jewish Health in Denver, CO $ 31 million to create and administer the Atopic Dermatitis Research Network, a consortium of five academic sites across the US. A contractor, Rho Federal Systems of Chapel Hill, NC, won an $ 11 million contract to operate a center to coordinate statistics and clinical trials for the project.

That makes $ 42 million—spread over five years—which puts the project on the large end of NIH funding for individual biomedical efforts. The typical NIH research grant ranges from $ 100 thousand to $ 2 million, and anything bigger is fodder for university news releases. Which raises the question: what have US taxpayers gotten in return?

I ask this as a patient who is grateful that these scientists are working to understand a disease that affects me, my family, and millions in the US and worldwide.

The answer is not obvious, since the publications page on the ADRN website hasn’t been updated since July 2011.

According to the website:

The Atopic Dermatitis Research Network (ADRN) is a consortium of academic medical centers that will conduct clinical research studies in an attempt to learn more about skin infections associated with atopic dermatitis (AD). The studies will focus on antibiotic-resistant Staphylococcus aureus infections and widespread viral infections of the skin, both of which are more prevalent among AD patients. The ADRN will build on the work of the Atopic Dermatitis and Vaccinia Network (ADVN) which conducted clinical studies focused on making smallpox vaccinations safer for people with AD. 

This research will lead to a greater understanding of the immune system in AD patients and may lead to novel therapeutic strategies to manage or prevent infectious complications associated with this disease. 

The ADRN will conduct a number of clinical studies over the next five years and will be enrolling large numbers of people with AD.

A search on clinicaltrials.gov returns two entries for the ADRN: one (open) to create a database of patients for the study of genetic markers connected to susceptibility to infections, and one (completed) to look into how AD patients respond to a new flu vaccine.

The ADRN’s NIH contract number is HHSN272201000020C. A search in the NIH’s PubMed database returns 12 papers that acknowledge funding by that contract number. Three of those are review papers (which did not involve new research).

So that makes  two clinical trials and nine research papers, three years into a five-year $ 42 million project.

Should US taxpayers expect more; be satisfied; or be impressed?

The answer is probably that we will have to wait to find out.

In each year, a typical top university research lab operates on about $ 2-3M a year and publishes somewhere around ten papers. That’s roughly $ 200k a paper.

Three of the five years in the ADRN contract are up; three-fifths of $ 42M is around $ 24M. We might therefore naively estimate that we should have seen upwards of 100 papers produced so far.

Most likely the reasons there are only 12 at the moment are that you don’t start publishing papers right at the outset of a project. The research must be done first and then written up; and the process of getting accepted to a journal takes months. And the ADRN appears largely to rely on clinical trials–which take time to set up.

So why do we only see two trials listed on clinicaltrials.gov?

I’ve never had anything to do with a clinical trial, but when I was a researcher, I conducted animal experiments, and there were formidable administrative hurdles to get over before I could start work. I imagine that trials with human subjects are heavily regulated by the government, and for good reason. So the apparently small output of the ADRN to date is, I’m guessing, because it takes a long time to plan trials, get approval, and conduct them, before you can begin analyzing data and reporting it.

    Still, let’s keep in mind that the ADRN is an extension of the ADVN. It’s not like the ADRN began from scratch—the scientists had the momentum of existing expertise and administration and research aims.

    Looking at the titles of the published papers, I can’t immediately judge which are the most important. So I emailed Donald Leung, the principal investigator for the ADRN (he’s a professor and head of the Division of Pediatric Allergy and Immunology at National Jewish Health), and asked him whether he could summarize the consortium’s findings so far and highlight key points. I hope to hear back from him soon and perhaps to interview him on the phone.

    I’d like to know what ADRN scientists have found that surprises them. What have they learned that is truly new?

    And what is going to be truly useful to patients in the end? Publishing papers should not be the be-all and end-all of scientific research. What about patents? I’d like to know whether anyone in the ADRN has thought about controlling intellectual property and commercialization. While it’s true that clinical studies may highlight the ideal dosing amount or schedule for existing therapies, and this does not involve creating a new commercial enterprise, most medical technology must pass through the marketplace before it can benefit the consumer/patient.

    Someone has to do the dirty work of developing scientific discovery into therapy, and it’s not academic scientists.

    More to come.
    End Eczema

    2 Years Steroid Free

    So the day has arrived. I am now 2 years free from using topical steroid creams.

    I am however still suffering though. I’m just going to keep this post short and sweet as I have a lot to do today (see: cake), but I can say that even though I’m still having blips and flares (mostly due to infections!) it has still been the best decision I could have made. I was looking at some of my old photographs and even though I still get blotchy rashes from time to time they are no where near the same in their formation.

    That isn’t me any more. The rashes are completely different.
    I’m also pleased to say I’m no longer suffering from some of the unwanted side effects of topical steroid withdrawal either. For instance I no longer suffer from this:

    Elephant skin
    Nor this:
    Full body coverage
    Or this! 
    Red sleeve effect
    My allergies have distinctly diminished, though still exist only in a lesser form of severity. Life has been slightly easier to endure, though it would still be nice to be given an end point to this suffering. It would also be nice to stop getting so many bloody infections too. That is my main nemesis at present – not withdrawal but infections, both viral and bacterial.
    I hope everyone else is well, and I hope I have given others courage to partake in this wretched journey that we should never have to face to begin with.
    Best wishes,

    I Have Eczema