I remember when doctors and nurses started telling me that they were using the Hexagen formula for patients with moderate to severe eczema. All I could ask was: “Why? What causes eczema? Is there a bacterial connection?” Missing: answer.
As a patient gone founder, I am particularly irked by drugs with package inserts that say “may work by xyz.” It has always been extremely important to me to be able to definitively explain why a medicine does what it does. So much so that I even waited some time before really pushing the envelope on the eczema program…I needed to know why it was working, not just that it was working.
Patients and doctors absolutely deserve that information so that they can make informed choices about their care. After finding this study by Johns Hopkins looking into the root cause of eczema, I finally got not just the answer to ‘what is eczema,’ but the answer to why our formula is reported to work so well as a symptom solution.
As it turns out, eczema, like so many diseases and/or conditions, is caused by an excess of microbes, in this case garden variety staph aureus, the most common skin-dwelling bacteria. In fact, research consistently shows ~90% of eczema sufferers have more staph aureus in their skin than non-eczema sufferers.
Why?
If you suffer from eczema, don’t take offense if someone ever says that you have ‘thin skin.’ It’s actually true, and it’s your parents’ fault, as it’s a genetic characteristic they were nice enough to pass on to you.
Imagine your skin as the roof on a house. It’s designed fundamentally to keep out elements: water, bugs, animals, etc. If the roof has cracks, bad stuff gets in, ultimately invading your house.
Everyone’s skin has some staph on/in it. But thin, eczema-prone skin simply lets more of the little buggers in. And once they’re in and have set up shop, staph replicates every 20 minutes.
Now, staph releases natural toxins called Delta Toxins, and these toxins attach to inflammatory receptors in the skin. At normal levels, the receptors don’t get overwhelmed by Delta Toxins. But too much? You guessed it.
The inundated receptors start a cascade of inflammatory events, ultimately leading to that red, scaly, itchy skin we call “eczema.”
Injectables on the market try to step in after this inflammatory cascade is triggered…steroids, even more so, long after symptoms have begun, in fact. It would be far preferable to patients to stop the inflammatory process before it starts by eliminating excess staph aureus colonization, thus halting downstream inflammatory signaling.
And oh do I love the simplicity: our active ingredient is a non-sensitizing antimicrobial (in English: it eliminates excess staph without irritating or sensitizing the skin).
We have kill data publicly available on our website, here. Reducing excess staph in eczema-prone skin logically reduces the volume of Delta Toxins. A reduction in these toxins gives inflammatory receptors a chance to cool off while our petrolatum carrier builds up the thin skin mantle…filling in the cracks, so to speak. And even though this reduction in excess staph and resulting Delta Toxins is as complete an explanation as one could usually hope for as far as mechanism of action, I’m taking things a step further: we’re running an in-vivo model as we speak to attempt to prove that IL-36, which research suggests is a primary receptor responsible for eczema symptoms, is inhibited by using our product during atopic dermatitis episodes.
This study could be very influential for the product and company, as a whole; if you search the most popular/profitable eczema products on the market, you’ll see terms like “IL-4 inhibitor” and “PDE4 inhibitor” in their descriptions.
So stay tuned! We’re advancing these programs all the time. Patience is not a Turn quality. But educating patients while providing affordable, safe, and effective medicines are core virtues.
