Healing Molly — Part Two

Recently I (guest blogger Dennis Ferrill) posted a discussion of my young daughter’s experience with serious asthma (Healing Molly) and how we ultimately found an “alternative” treatment that helped her. The treatment came with a logical theory of onset—something that does not exist in the standard approaches—as well as a simple array of diagnostic tests and a clear plan for treatment. In short, while our experience represents a data set of one sample, my daughter is entirely well and our avid collection of data about her symptoms, medication, and peak flow readings from the time strongly support the hypothesis that the therapy was directly causal.

This experience raises an interesting question: How important is a theory of onset to the identification of effective treatment pathways? One comment on the posting suggested that “’how one gets there’ is not nearly as important as how one treats the asthmatic/atopic patient.” This is certainly true in the sense that symptom treatment—the only thing allopathic medicine has in its quiver of arrows, is often a necessary life saving response. But determination of a treatment that can result in real healing requires deeper understanding. In my daughter’s case, food sensitivities—allergies, really—to most of the foods in her diet, mediated by IgG and IgA, not the standard IgE, were likely behind her problems and would probably have persisted. Pharmacotherapy targeted at symptom control alone would have resulted in a long dependence on medications, ongoing illness, and a huge expense to the system. In my daughter’s case there is a chance that she might not have lived. Perhaps most important is the established view that medication is a sufficient response and that adherence to the textbook treatment plan is the best definition of the physician’s role. In a case such as ours, if the doc is following the book and the pharmaceutical companies don’t see potential for a silver bullet drug with a large revenue stream, who in the system has the job of looking more deeply for new approaches?

In the same comment on my initial posting, a physician defended allergists against my claim that they don’t work with IgA and IgG, but only look at IgE mediated reactions. I hold to my claim. When the allergic process was first documented it was due to the discovery of IgE, which could be found because it leads to fast reactions, unlike the other immunoglobulins which react slowly and are harder to identify. “Allergy” became defined by IgE. In our case, armed with clear test results showing serious food sensitivities based on IgA and IgG and with convincing evidence that an elimination diet had resulted almost immediately in symptom reversal we approached our well known pediatric allergy and asthma specialist in Boston for her view, only to be treated to a negative IgE based test and advice to our daughter that she could resume drinking her favorite milk. Of course we did not take that advice.

Every system has built in assumptions that are invisible to those inside it. These assumptions are ultimately the barriers that make new progress difficult. There is nothing surprising about that. The question remains: What has to be done to open up the new territory?

August 18, 2005

10 thoughts on “Healing Molly — Part Two”

  1. Mr. Ferrill,

    If I believed that symptomatic therapy was “all (I) had in (my) quiver of arrows”, I’d hang up my cleats and go into consulting.

    Indeed, prevention, or preventive medicine, if you prefer, occupies large amounts of my time and energy. I cannot speak for “allopathic medicine” (although I’m an allopath), but I hope I play as much offense as defense.

    If you read my last response carefully, I said that avoidance is the mainstay of allergy therapy. I chose the word “mainstay” deliberately. It is of paramount importance, and has nothing at all to do with pharmacotherapy!

    In defense of my colleagues the allergists, I did NOT say that they do not “work with IgA and IgG”, or that they only pay attention to IgE. But they don’t need me to defend them, they can defend themselves: please ask them.

    To the contrary, I said we generalists in the community start with IgE because it is a starting point, by which I meant it is a useful screening tool.

    Finally, I’m not trying to pull rank or make you look stupid, but I still don’t understand what you meant by “testing for permeability” or “reversal through treatment”.

  2. As a physician and scientist I think that it is helpful to know the mechanism of a therapy, but not necessary. If you find that eliminating milk or some other food from an individual’s diet removes asthma symptoms that is probably worth doing even if no one understands the mechanism. You will encounter skepticism because doctors will not know of other cases in which this worked on a non-IgE basis, but that doesn’t mean you are decieving yourself (presumably you have excluded other more common asthma triggers such as those listed at http://www.segal.org/asthma/).

    I’m aware of several generations of a family with IgG-based food sensitivities in which the symptoms are those exected from deposition of antigen-antibody complexes (abdominal and joint pain and fatigue). For that family, the availability of a plausible mechanism encouraged doctors to find the food mechanism convincing even before the recent work documenting some of the IgG association (Zar S et al. (2005) Am J Gastroenterology 100:1550).

    If you have found something that works, great, but doctors will urge you to be sure you have not latched onto a spurious association and ignored other possible explanations. But you may well be onto something, as were we with the other IgG symptoms.

    One of the problems with medical publishing is that is is not easy to share details of unexplained cases and encourage brainstorming. Hopefully blogging can change that in a positive way.

  3. Well said, Michael.

    I forgot to comment on David Ferrill’s last paragraph (the money paragraph?)

    A fish does not know he is wet, and doctors tend not to questions the assumptions under which they operate. The reasons are many but I may suggest one.

    Since I’ve been in solo practice, however, I’ve questioned ALL the assumptions under which I operate. I do so in part because I don’t need to answer to a boss or an administrator. These folks have agenda that have nothing to do with delivering caring, compassionate, evidence-based medicine.

  4. Dennis Ferrill here, original poster on this subject.

    Michael, avoidance is key in these cases as you suggest, but I am aiming for more. While knowledge of causality is not necessary for symptom avoidance for some period of time in some cases, that process alone may not eliminate the underlying problem and at best leaves a patient with a modified diet. In my daughter’s case, if our hypothesis is correct, she would probably have gone on to develop negative reactions to the new foods in her diet. Plus, the elimination diet she was on was pretty unsatisfactory. My hope and belief is that an understanding of the mechanism of onset, the initial cause of sensitization and activation of the immune reaction can result in a procedure for reversal of the whole process or, at least, a better idea about early avoidance. I wasn’t aware of the AJG paper you cite, but will look into it….thanks.

    Dr. Lindeman should go back to my posting to see that I didn’t say that he indicated that allergists don’t work with IgA or IgG. I am the one who made that claim. It is certainly true to the extent of my own experience and my informal sampling of physicians in practice.

    This gets back to the point of the fish not being aware of the water and docs not questioning their own assumptions. Dr. Lindeman gave one possible reason for this phenomenon, here are a few more: physicians are overwhelmed with information, that information is increasing exponentially, patient care comes first and there are only 24 hours in a day (except during early training when there may be more), there is an established system for accumulation, filtering, and dissemination of information (though it is broken), and it would be impossible to function in a clinical setting while doubting every accepted notion or technique. There are other, less flattering reasons out there, but I leave them aside for the moment. So there remains the question of how a clinical practitioner can stay on top of, and remain open to, new concepts while still doing his/her job? It may be that the job of finding out what’s new and exploring it is now in the hands of patients. That only works for the few who can a) do the research, b) understand it, c) trust their own judgment, often in the face of MD opposition, and d afford it. Besides that, it can be dangerous.

    Don’t worry about “pulling rank”, or making me “look stupid.” Rank is an archaic and dangerous concept and I, to a fault, rarely feel stupid. There are standard tests for intestinal permeability. My knowledge dates back several years now, so I won’t lean on that, but in those days the nature of the testing was to ingest two non-metabolized sugars and measure their appearance in urine as an indication of the extent of intracellular and transcellular passage through the intestinal wall. These tests appear in the literature and have been used in research.

    In my daughter’s case, permeability was high as was IgG and IgA sensitivity to most of the foods in her ordinary diet. We put her on a very extensive elimination diet and essentially fed her gut wall a cocktail of nutrients (probably a shotgun approach, much of which was unnecessary—a result of limited clinical trial and testing). Her permeability declined measurably into a normal range over a short period. We then continued to measure her food sensitivity and it, too declined, but over a longer period, perhaps a year. Her symptoms fell to near zero within two weeks of the elimination diet. While she had been on a full range of inhaled drugs and occasionally on systemic steroids, she was free of meds within a few months. After sensitivities were eliminated she went very gradually back to a full and unlimited range of foods. She has been completely healthy with no symptoms and no limitation of activity since.

    Assume just for a moment that this treatment is relevant and potentially successful for a meaningful percentage of asthmatics. Its adoption could result in health and enormous cost avoidance for many at very little cost, assuming the large issue of patient compliance could be dealt with. There is no drug for this. Big Pharma has no financial incentive to explore it, and in fact will suffer a large financial setback if it were to become a real part of practice. My question remains: how does a hypothesis with those characteristics get tested?

  5. The ability to patent a new medication adds incentives to solve problems that require new medications.

    The existence of “use patents” adds some incentives for re-using existing medications.

    Non-medication answers are often funded with taxpayer or foundation money.

    This funding mix builds in some bias towards patentable medications, but other solutions come out eventually.

    If you can convince other parents of children with asthma to have IgG testing you may be able to build a case for a pilot study. You will have to overcome the concern in the field that the IgG tests have lots of false positives, but the more studies that find real clinical entities with high IgG the more researchers will pay attention to stories such as yours.

    The asthma field is full of examples of inadequate study. If you ask doctors about the effect of perfume in triggering asthma, half will tell you that everyone knows of the perfume-asthma link (and many hospitals have perfume bans), but half will say there are no good studies to prove such a link. But who will do a study to prove something that most people know?

    Another discouraging asthma example is theophylline, a medication that used to be commonly used. The lore is that theophylline was used instead of caffeine because of intellectual property reasons, despite the superiority of caffeine. I don’t know if this is true, but it is not hard to imagine.

  6. Michael,

    Thank you again for the useful reference to the article in the Am. Jnl. of Gastroenterology. Unfortunately I can’t gain access to it because I am not a member of the society. While this brings to the surface my strong feelings about who owns the truth, I will set that aside and simply ask whether there is anyone out there who can point me to an ethical way to get access to this article, short of a trip to the library?

  7. If it makes you feel any better, Dennis, I can’t get the full-text of this article either. I suppose the conspiracy goes deeper than even I imagined.

    All is not lost, however. I have access to a thing called “Merck Medicus”, provided for me by a rep a few years back. I have access to full text of a whole bunch of GI and allergy journals. I’ll do a search and forward you the texts if you like.

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