Problem Solving Eczema – The Big Picture

Here’s an edited question and an edited version of an email I wrote in response. It covers a lot of topics I’ve been meaning to post anyway, so I have inserted headers to make it more readable. —A.J.

Dear A.J.

Just wanted to touch base to see if you had achieved any success in finding someone to do a scientific study of the effects of detergents on skin? I was also intrigued by some recent research finding a very strong genetic link with eczema. The University of Dundee found a strong link with a mutant gene that prevents normal amount of “filaggrin” protein being produced by the outer layers of the skin. Several other studies with other population samples around the world, have confirmed the significance of this link. Apparently 1/10 of the total population has this mutant gene and therefore a disposition to eczema type conditions. Could it be that the recent use of detergents in combination with this mutant gene that 1/10 of the population could be the cause of such huge increase in number of people with eczema/ asthma?

Interested to hear your thoughts? Please also let me know, if financial contributions towards some kind of research study would help. If so, I would gladly like to help out. I now see your point, that some rigourous scientific evidence needs to be produced to give the theory a solid foundation.

Thanks,
A. Ranade

My Response:

Eczema Genes?
I have seen the University of Dundee findings as well [Pubmed link], but as you might imagine, I have something of a different take. Unfortunately, the type of genetic association that is being made is not the same as finding a gene that underlies a disease. It is interesting work, and important science. In fact, I think it provides strong support for my own theories about what allergy is and isn’t, and I plan to cite their work as I write more. From a problem solving standpoint, the work is significant for proving eczema as a barrier function problem rather than primarily immunologic (other work is proving this as well). It’s good science; I’d hate to see it serve bad problem solving through a typical confusion of correlation with causality.

Let me explain. My favorite analogy (and this unfortunately works for a lot of genetic associations being made today) is this: Let’s say the standard door opening allows 80% of the population to pass through easily, but the rest do not, so that 20% of the population over time experiences injury, especially head injury, through the normal course of life.

Now, it would be possible to find genetic associations, especially related to height. So it would be possible to then conclude that people with certain genes or gene combinations are more likely to get a particular type of head injury, say, and have a compromised door-passing functionality. And, oh yeah, since HEIGHT has something to do with their door-passing functionality, we must be on the right track with the height-associated genes, right?

The next steps usually run along the lines of: 1) identifying people with the genes in order to make adaptive devices for them to minimize their chance of injury, or 2) working toward future genetic therapies to correct these abnormal height genes. Or, one could take a different approach and simply enlarge the doors.

Whether one chooses to go with the first two steps or the last depends on one’s standards for results and to a great extent, how one defines what is normal. In some perspectives, everyone must fit through the door to be normal, everyone who doesn’t has something wrong with them; others would find conforming all people to recently developed, arbitrary environmental factors as wrong, preferring to look at what is causing the problem externally first (especially since addressing these external factors is easier from a problem solving standpoint). At least for eczema, I happen to have the latter perspective.

Learning From History: Ulcers
For a relevant example from medicine, one could look at ulcers, which can be cured with antibiotics because Dr. Barry Marshall illuminated their underlying cause as H. pylori bacteria (for which he recently won the Nobel Prize in medicine). Certainly, one could correlate stomach acid levels, susceptibility to stress, and diet with severity of symptoms, but addressing those factors never satisfactorily solved the problem because they were not the root cause. Read the following quote from a typical 22-year-old paper on ulcers with the current conversations about eczema in mind:

Recent advances in the medical therapy of duodenal ulcer support the long held concept that hyperacidity is an important physiological abnormality in the majority of patients with duodenal ulcer. It can also be shown that the origin of hyperacidity is heterogeneous. Certain specific physiological abnormalities that lead to hyperacidity may have a genetic basis. The various physiological abnormalities, alone or in combination, may lead to two final common pathways: abnormally large meal-stimulated acid secretion, and nocturnal acid hypersecretion. Indeed, success of medical therapy aiming at the control of postprandial acid secretion or of nocturnal acid secretion strongly supports their significance. It is possible that hyperacidity occurs as a temporary phenomenon and is associated with stressful life events. However, it is also possible that it occurs as a constant abnormality, bestowed perhaps genetically on the duodenal ulcer patient. In the presence of hyperacidity, mucosal repair may be affected adversely. In either situation, an acute ulcer, such as that associated with stress, is allowed to develop into a full-blown ulcer. Healing takes place if the hyperacidity recedes or is reduced therapeutically, allowing normal mucosal repair to take place.” [SK Lam, Pathogenesis and pathophysiology of duodenal ulcer, Clin Gastroenterol, 1984 May; 13(2):447-72.]

Controlling acid secretions was never a satisfactory cure from a patient standpoint. It was a logical step from correlations that were made, and did help temporarily, but it wasn’t the best answer from a problem-solving standpoint. It never made any sense that some people were so susceptible to diet, stress, etc., unless one assigned a pathological weakness to those patients. (As ultimately happened to millions of patients, at quite a burden to individual lives, health, and psyches.) If one could see the obvious, that there wasn’t a proportional correlation between ulcer occurrence and such apparent weaknesses in the population, then the next step (if one believes the problem stems from an inherent weakness) is to define a genetically susceptible population by making genetic correlations with hyperacidity. And in such a problem, given the conditions, one would likely find them.

But from a problem solving standpoint, such a perspective and line of inquiry would never lead to a satisfactory solution, it never did lead to a satisfactory solution. If one takes a different perspective, that perhaps something external like a microbe causes ulcers — knowing that hyperacidity can be a defense mechanism against gastrointestinal pathogens — the interpretation of the information changes, the place of those hyperacidity genes in the problem solving picture changes. And it just so happened, this line of inquiry led to a more satisfactory cure and understanding of related diseases.

My point is, correlation is not causality. And, one can be entirely right yet not on the best track to solve a problem.

Environment or Genes?
There is a very good book called Plague Time by biology professor Paul Ewald. In my opinion, it has one of the more useful and accurate perspectives on what disease is and isn’t. (He goes into detail about Dr. Marshall’s story, by the way.) Dr. Ewald points out that many so-called genetic diseases occur or increase at a rate that is much too high to be accounted for by ordinary mutation rates. If you read a lot of literature about eczema, many researchers acknowledge that, given the astronomical rates of increase in recent decades, the underlying cause of most eczema and asthma has to be primarily environmental.

Ewald points out that “Only if a genetic instruction provides some compensating benefit can the disease it causes persist as a common ailment.” And “Without a compensating benefit, harmful genetic instructions can be maintained only at a frequency that is set by their generation through mutation; at equilibrium, the loss in the harmful genetic instruction that results from their harmful effects must match the rate at which the instructions are being generated by mutation. If a genetic instruction is even moderately harmful, then it can be maintained in the population only as a very uncommon instruction. Even if a disease reduced reproductive success by as little as one tenth of 1 percent when averaged over the entire population, the genetic instructions responsible for the disease would dwindle over time.”

My Allergy Worldview: Allergic Advantage
Now here’s the thing: my perspective on allergy actually fits naturally with the work of the group in Dundee, because I believe “normal” (non-anaphylactic) allergic symptoms are an adaptation, that the effect of the genes the Dundee group discussed does confer an advantage.

That discussion is much longer and more detailed than I can go into here, but here’s the gist of it: As human beings living in the world, we are extremely porous. We take in all kinds of tiny substances, through our lungs, our guts, our skin. Our bodies have to do something with all of those substances, the useful, the harmless and the harmful. The amount of energy and resources available to accomplish internal tasks is finite — variable from one person to the next, dependant on circumstances, and optimizable, but nevertheless, finite.

If a given body is overwhelmed by harmless substances, especially substances that may be similar to the harmful substances, the body would then be expending enormous resources sorting between the harmless and the harmful, making the success of the harmful more likely. It is known that allergens are similar to pathogens to the immune system. The classic interpretation then of an allergic response is that the body becomes confused. I think this is not correct. I think the body has to expend more energy to differentiate between substances that are similar, a critical process if some of those substances are harmful. To the extent that the body, especially the immune system, can communicate to the conscious brain that the environment is filled with invisible substances that are unnaturally loading it so that it cannot optimally do its job, there is a survival advantage. Particularly for our human ancestors, as they emerged from Africa and traveled across very different landscapes, having an optimally functioning immune system would have conferred a survival advantage.

When you think about it, our allergen sensors are quite sophisticated. When the offending substance is touched, we have skin reactions, when it is breathed, we react in the nose or lungs, when ingested … well, that’s a little more complicated, but befitting the greater load on that system, we typically have gastrointestinal and/or skin responses that give us a great deal of information for identification of the antigen. Normal allergic responses allow the conscious brain to make decisions about what is best in the short-term, even to ignore the warning, while remaining enough of a burden to persuade avoidance of the problematic environmental influence over the long-term.

Anaphylactic Allergies are Different
Parenthetically, I believe anaphylactic allergies are different and are not just an extreme extension of “normal” allergy. If you would ever like my theories on those, please ask, I believe there may be a more complete solution to those as well.

Detergents: Environmental Compromise of Skin Barrier Function
Detergents compromise skin barrier function. They increase antigen penetration and load. Their use has increased precisely in step with the increases in eczema and asthma worldwide, over time and geography. In modern households, they are a major component of household dust and are in contact with skin and lung tissue almost constantly. They change the permeability and quality of the skin barrier, especially in people with certain skin type. (And if one factors in this issue in the research studies used to support the so-called hygiene hypothesis, one gets a more consistent picture. )

I have said all along that skin type is a factor in susceptibility to detergent-reactive eczema. In fact, atopy seems strongly correlated with this type of eczema. I have heard from numerous families where eliminating the eczema of a child by going detergent-free in the household also eliminated a parent’s eczema or allergies. But the expression of this type of eczema isn’t limited to just some people with certain genes, it’s a continuum. If detergents were strong enough, I believe eventually the entire population would be affected.

More importantly, when people with this type of eczema live in a detergent-free environment, over time, the appearance and quality of the skin changes. Typically, the skin becomes more substantial and supple. It normalizes and becomes less dry. After two months in a detergent-free environment, the skin of affected patients would look entirely different under a microscope. Babies, with naturally more permeable skin, are most affected.

So, to make a long story short, I personally think of the eczema and asthma increases in the latter half of the last century as entirely environmental. The genetic associations are interesting, but I don’t think it’s reasonable to think of them as a “defect” just because they are more frequently associated with an unhappy reaction to a new and artificial environmental influence that didn’t exist 100 years ago. Removing the environmental cause is a more logical and more productive perspective to take for problem solving.

Naturally, I have my theories about those environmental causes, and I don’t think it’s very complicated. It seems to me from everything I have observed, that the two biggest environmental reasons for eczema in the 20th century are detergents and antibiotics/diet (yeast), in that order. My web site has a discussion of what I believe are the more common types of eczema — despite how different they may seem, I think now I can tie all of them together in a very simple and logical way.

Banking Healthy Germs
Parenthetically, I feel I should defend antibiotics since antibiotics do a great deal of good, but I think we need to be more intelligent in how we use them to avoid problems like eczema, for example, by more rigorously restoring natural bacteria head to toe after treatment.

I strongly believe that we ought as a species to bank the natural germs from the guts, lungs, sinuses, eyes, etc., of the healthiest people who have never had antibiotics and whose predecessors never had antibiotics. We should do this for people of different geographical regions, of different genetic profiles. Such people are going to be harder and harder to find as time passes. We’ll never be able to restore the most favorable evolved balance of microorganisms in healthy people unless we do this. Our dairy animals have the same problem, many have been treated with antibiotics and no longer pass along the balance of healthy flora to both their offspring and humans who drink their milk.

Universal Theory of Eczema
At any rate, back to the issue: I think I can describe an underlying biological basis that ties together all the seemingly unrelated types of eczema. It has to do with the way our bodies use biological detergents. Please note that when I write “biological detergent,” I am referring to the detergents made by the human body, not to detergent products with enzymes added, a more common way the term is used. I believe the more standard term for what I am referring to may be bio-surfactant, but here I feel I need to be specific about relationship to detergents as outlined on my web site.

It turns out that our bodies make detergents, of which sodium lauryl sulfate is an analog (one reason SLS may in particular be such a problematic detergent). One of the roles of biological detergents is in regulating membrane permeability (no surprise there). Another role is in denaturing proteins in the blood stream. So, for example, this could explain full body eczema in infants from certain ingested proteins (which end up in the blood stream when the gut is immature), and why this particular eczema is truly outgrown when the gut matures. Biological detergents are increased in the wake of certain microbial illnesses — probably as an aid to immunity by increasing permeability of microbial membranes — coincidentally, some people, especially children who have more permeable skin, get eczema outbreaks during and/or following certain microbial illnesses. Interestingly, gut lactobacillus (I am remembering off the top of my head, a dangerous thing for me to do, but write if I’m wrong) produce a biosurfactant that restores normal gut membrane permeability function. [I’ll add the citation on my blog.]

Anyway, I’m getting into too much detail. The point is that our bodies produce detergents for various functions, and our skin has to have some tolerance for increases that would simultaneously increase skin membrane permeability. There is an efficiency, an elegance to the idea that if the body is dealing with some immunological challenge that necessitates release of biological detergent, that the increased permeability of the skin would come with a visible warning of excessive antigen load. To the extent that one would then reduce antigen load, the immune system could more efficiently deal with whatever short-term disease challenge it faces. To that end, there may be survival and immunological advantages in a lower set point, i.e., skin that expresses eczema from a relatively lower antigen load.

When we cover ourselves head to toe with detergents, breathe significant amount of it in dust daily, eat it daily, we lower our natural setpoint, reduce our tolerance to increases in membrane permeability, hence abnormal expressions of eczema in some people.

Everyone, Not Just Patients With Eczema at Risk
Even people who do not express eczema experience some level of increased antigen load. Their immune systems have to bear a greater load on a daily basis, which may not directly result in a disease in the short-term, but would almost certainly compromise one’s ability to deal with disease in the longer term. I would point out that because of the exponential increase in membrane permeability from increases in local moisture, such as with sweating, being covered in detergents would amplify the negative effects of stress on the immune system and eczema (if one has eczema).

Solving Eczema and Asthma
I believe it would be possible with very simple steps to bring levels of eczema to near pre-WWII levels within a short period of time, and to drastically reduce the incidence of asthma. As we discussed, it would just take a very convincing study to start the whole medical community on the optimal track. I think it’s really just pointing to a more optimal problem-solving direction — the science is there already.

As I said, it may seem at first blush that environmental detergents and fungal/yeast loads in the gut have very little to do with each other, and other types of eczema even less, but I see a very simple, elegant way to tie it all together. Since it almost doesn’t get any simpler than that — by Occam’s razor — and more importantly, this line of thinking leads to a simple and lasting solution, I feel it’s the most productive problem solving approach.

I want to be very clear that I no longer see the problem as restricted to people who express eczema. I’ve heard from people who eliminated asthma, other food allergies, and even ameliorated hayfever and symptoms of autoimmune diseases when they went detergent free, whether they had eczema or not.

The effect on the lungs is especially a concern. Detergents increase healing times and antigen penetration. In everyone, not just people with eczema. Several studies — and admittedly, I could quibble over the rigorousness — have demonstrated a significantly lower rate of lung cancer in people with a self-reported history of eczema. Now, one possible perspective is that an overactive immune system produces this benefit, though I find that hard to fit logically into the worldview of damaging autoimmunity. (I’m not a fan of the whole autoimmunity interpretation anyway, but that’s a whole book in itself.)

Here’s another possibility: in anyone old enough to develop lung cancer, who has had bad enough eczema to remember it or continue to have it at that age, there would be a history of years of significantly reduced levels of detergent in the home environment. Such people likely haven’t solved the problem — hence the eczema — but from what I know of this population, it’s absolutely a given that overall there is a reduced use of surfactants and a preference for weaker surfactants. Over time, especially if viruses (for example) are an aspect of asthma or lung cancer, having that decreased antigen load and improved healing time in the lungs could increase the likelihood that a person is able to take care of whatever underlying problem turns into lung cancer.

I must sound like a broken record. I’ve gotten a tremendous amount of moral support from local doctors who have read my web site (and some who are now referring patients to the information). One recently mentioned in passing that it just wouldn’t be that difficult to do a study to prove what I am saying. He’s right, of course. Since this whole endeavor is more or less a hobby for me (and I have no time for hobbies!), my direction right now is to get a scientific paper published this year, then try to establish a 501(c)(3) organization so that I can take donations for a study and apply for a grant through either the government or a foundation like Robert Woods Johnson. If I can work things to where I can offer direction to someone else who can conduct a study professionally, things could happen pretty quickly. That has been my intention all along — I only put up the web site in the first place because I wanted to at least help however many people I could until I could get a scientific paper finished. The cover story that Asthma and Allergy Today Magazine did this year got the message out to another order of magnitude of people with allergies, and doctors as well.

Thank you for offering to help financially, other people have written offering as well, I’m just not at the stage where I can do much. I will try to keep you abreast of any news on that front, I appreciate your offer of help. If you have the time or expertise to set up a 501(c)(3), that would help tremendously (though I realize that’s a huge time commitment for anyone — which I why I haven’t done it yet — I don’t even know from where in the world you are writing and if you even know why I’m bringing it up!)

Practical Tips on Trying Detergent Free
If you haven’t done a whole switch to soap for your eczema, you might consider it. My site is geared to parents with babies who have ultra-permeable skin and need really dramatic results fast. The transition seems like a lot of work, but it doesn’t have to be. For adults, especially if you’re willing to judge the results over seasons rather than days, you could just look at the switch as a change in washing products. It really doesn’t have to be anything more than that, except for the laundry. I’m concerned because of what I observed in that transitional stage, and because I don’t know the health implications of the dust, I have to recommend the superwashing to everyone, not just for infants. However, it would probably be possible to circumvent the superwashing by simply switching to a laundry conditioner (only, no surfactant at all) like Oxo-brite for a month or so, then switching to soap in the laundry. And possibly vacuuming with the well-filtered vac a little extra in the meantime. I personally never thought this would have any health benefits to me because I did not think of myself as sensitive to detergents. Yet when our household dust became detergent free, my own typical seasonal reactions to pollens and dust dropped dramatically.

Kind Regards,
A.J. Lumsdaine
www.solveeczema.org

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