This question was such a good one and needed a more complete answer than I could give in a short blog post.  I will be rolling out the entire letter in 3 or 4 parts, and refining it as I go.  I will be asking more than one doctor I know for feedback, and revising as needed.  Here’s the link to Part 1 of the letter.  I hope the information is helpful. 


Question from a medical student:

“On your website, you write that detergents may be responsible for eczema 25-60% of the time. I was wondering if you wouldn’t mind sharing with me how you found this number. It is very interesting that so many people have had relief from eczema after eliminating detergents and I was wondering if you could direct me to any literature corroborating this finding so I can look into it further.”

My Answer — Part 2:

This is a good question, and the answer not a simple one. The estimate is not really equivalent to a traditional epidemiological statistic, but rather it encompasses circumstances related to outbreaks, per my empirical observations and ideas, and a view of the relevant medical literature through this new lens.

On my website, I wrote that detergent-reactive eczema “likely accounts for 25-60% of eczema, depending on the age group and locality, higher if other allergies and an inherited predisposition are factors.” I believe I can now propose a revision of the Hygiene Hypothesis that not only accounts for the rise in eczema and atopy, but can satisfy conditions of causality and leads to solutions consistent with the underlying basis. However, the issue is more complex than saying one thing underlies a certain percentage of cases and another thing underlies others.

Eczema as a Signal — “Normal” and “Abnormal” Eczema

First, I should point out that I do not see eczema as a “disease” that some people have and others do not, in the way that a person might have dysentery or chicken pox. I believe eczema (and other allergic symptoms), under normal environmental conditions (such as we evolved with), is a helpful signal from the immune system to the conscious brain, in the way that pain is an unpleasant but helpful signal from the nervous system to the conscious brain.   (I have a stack of research papers that I believe directly supports this contention, but that’s a discussion for another day.)

At any given time, some people may experience no pain, some may experience more pain than others under similar circumstances, others more chronic pain than others for a variety of reasons. The percentage of people experiencing pain depends on the circumstances. Some circumstances happen more frequently than others. Sometimes accident or disease processes that trigger pain unnaturally cause the pain itself to essentially be a “disease” problem. But fundamentally, pain in our bodies is a signal that everyone can express.

I believe eczema and allergies, too, are signals. The signal of eczema is triggered under certain conditions. Actually, let me be very careful in how I use the word “trigger” here. I believe the signal of eczema can be expressed when a certain threshold is crossed. That threshold depends on a number of factors having to do with the environment and the immune system, membrane health being intimately tied up with these. Once that threshold is crossed, outbreaks may happen continuously, or every time a traditional “trigger” is encountered, such as dust mite exposure or certain pollens, for example. If one is below that threshold, then exposure to the traditional triggers won’t cause eczema, or won’t cause it unless there is a very significant exposure. (I discuss this conceptually on my site as the bucket analogy of allergy.)

This is worth restating:   I see allergy, “normal” allergy — I consider anaphylactic allergy as different — as an adaptation, not disease pathology. Given the historic prevalence of allergy even before allergy rates saw such precipitous rise after WWII, this makes sense. As with pain, virtually anyone can develop an individual allergic response at some point in life under the right circumstances. For any inherited condition to maintain such significant prevalence in the population, there must be some compensating benefit. Given the rapid rise in eczema and atopy since WWII, the cause of this “abnormal” allergy must be primarily environmental. Per Klueken et al (review, from Schultz-Larsen et al) [1], “This continuously increasing frequency of [atopic dermatitis] during the past 30 to 40 years suggests that widespread environmental factors in the industrialized world are operating in genetically susceptible persons.”

Let me also be very clear by restating once again that I am differentiating historically “normal” allergy from the modern manifestation of eczema and allergy, which are not normal. If eczema is a signal, most eczema today is almost certainly the result of unnatural environmental conditions inappropriately triggering that signal — or, modulating down thresholds to reacting — with a genetic component to the susceptibility. I believe based on my present understanding that the people with naturally lower thresholds to reacting in normal environments would otherwise have a genetic advantage.

Allergens are similar to pathogens to the immune system. To the extent that harmless allergens take more energy to differentiate from pathogens, there is probably a survival advantage to people (or — speaking to possibly evolutionary roots — to migratory groups that have such people among them) whose immune systems can tell them to reduce exposure to certain benign substances that make the immune system’s job more difficult.  An interesting aspect of allergy is that “normal” allergy makes sufferers miserable in a way that often points to the source of the misery — aeroallergens relate to breathing symptoms, contact allergens to skin, etc. — but without incapacitating.  Allergy concurrently increases adrenaline, giving sufferers the ability to move away from what is making them miserable.

I believe there is probably a survival advantage in the more ready expression of this signal under normal environmental conditions, and that there is likely a way to support my overall perspective on allergy using genetic archeology.

Restore more normal environmental conditions, and the signal is still triggered under the right conditions, only far less often and in a more “normal” and helpful way (giving the conscious brain important feedback). But the signal can be triggered in anyone, I believe, under the right conditions.

The ISAAC studies (I’m remembering off the top of my head, please correct me if it was another source — after I post this, I will go back and put in the citations in a few days anyway) (Feb 2017 update – I am not sure this is the original paper I meant but it’s close [2]), showed a roughly linear relationship between atopy rates and eczema rates by nation. If you accept that the expression of atopy is mainly the result of abnormal modern environmental conditions in recent decades — given the rapid rise, significant prevalence, and genetic aspect, most serious researchers take that perspective — then nations with the lowest rates of atopy would be most likely to demonstrate historically natural rates of eczema.  Off the top of my head, rates of eczema might be low single-digit percentages, or even a fraction of a percent.

I think there is a relatively short list of threshold modulators and a longer, well-known list of triggers. Threshold modulators are where I believe the solution to the eczema problem lies; they seem at first glance to be unrelated, but I think they can be tied together in a simple and logical way. (Also a long discussion for another day.) Detergents — which my site deals with at length because their role is as yet poorly recognized and they are a relatively new environmental issue — abnormally modulate that threshold. I believe high levels of environment mold exposure (to be more precise, dampness-related exposure), or abnormal internal fungal involvement, is one of the more significant normal modulators of the threshold, in fact, may be primarily responsible for the adaptation.

The World Health Organization report on Dampness and Mould/Guidelines for Indoor Air Quality notes that atopic individuals experience increased susceptibility to dampness-related health effects, and according to NIOSH, “a more recent epidemiologic review published in 2011 reported that indoor dampness or mold was consistently associated with bronchitis and eczema [Mendell et al. 2011][3].”

In other words, eczema is more readily expressed in the presence of increased indoor dampness/mold, and atopic individuals are more susceptible under the circumstances. In regard to internal fungal involvement, much research has been published over the years in regards to the use of antifungals with eczema. (Again, big topic for another time.) Some viral illnesses can, in the short-term, do the same. (I discuss this on the blog, I think.)

Certain protein foods associated with full-body eczema outbreaks, too, can modulate that threshold, or be both modulator and trigger, under different circumstances. As I said, I believe there is a connection between these and detergent effects, but that’s a complex discussion for another day.   (Discussed briefly in several posts on the blog.) Basically, I suspect compromised gut barrier leading to proteins in the blood stream — and consequently increased levels of circulating endogenous detergents to denature them — has a similar impact to abnormal environmental detergent exposures. Associated outbreaks could run the gamut between normal and abnormal and/or amplified by other abnormal threshold modulators.

Abnormal environmental conditions today lead to abnormally lowered thresholds to reacting, especially in those with a certain genetic susceptibility. Abnormal environmental conditions also effectively amplify traditional triggers (for example, detergents are known to increase antigen penetration).   Again, this isn’t necessarily a topic I can cover in this letter, but I believe all of these seemingly unrelated factors tie together.

There is a proportionality to the reaction to detergents — a proportionality to the impact on permeability — but the reaction itself is not a simple irritant or an IgE-mediated allergy to detergents, as I discuss on my site. The eczema, I believe, in its abnormal manifestation resulting from abnormal environmental influences today, is an amplified, unnatural triggering of a normal signal.

So when I say 25-60% of cases result from detergents, I’m really considering the commonality of circumstances under which detergents would likely be the overwhelming factor in the outbreaks. These circumstances vary.


To be Continued in Part 3:

“… — I think generally it’s possible to estimate how often the different major modulators dominate.”


[1] Klüken, H., Wienker, T. and Bieber, T. (2003), Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution. Allergy, 58: 5–12. doi:10.1034/j.1398-9995.2003.02162.x

[2] Flohr, C, et al. The role of atopic sensitization in flexural eczema: findings from the International Study of Asthma and Allergies in Childhood Phase Two. The Journal of Allergy and Clinical Immunology. 2008; 121(1):  141147.e4. doi:  10.1016/j.jaci.2007.08.066

[3] Mendell, Mark J. et al. “Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness-Related Agents: A Review of the Epidemiologic Evidence.” Environmental Health Perspectives 119.6 (2011): 748–756. PMC. Web. 17 Feb. 2017.



This work by A.J. Lumsdaine is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License