Is Asthma A Bowel Problem?

Majid Ali, M.D.

Is asthma a bowel problem? The answer: yes. How do I know this? My true teachers taught me. Who are my true teachers? My patients. How can I be sure that they told me the truth? Because they don’t lie to me. How about my clinical judgement? Don’t I use it? Yes, I do. When they stop wheezing and prevent asthma attacks without drugs, then I know that I am on the right track? Where does the bowel come into the picture? My patients do not control asthma until they get their bowel ecology restored. Does the bowel approach also work for steroid-dependent asthma? Yes, it takes much longer when the steroids have suppressed the immune system for long periods of time.

Can I control my asthma by working on my bowel on my own? Yes, but only after you have discovered the best asthma doctor in your mirror. How long does that take? Only you can answer this question. This is making asthma control too simple. How would lung specialists look at it? For them, I describe my Oxygen Model of Asthma with technical details later this article. Can you say something about this model here in simple words for general readership? Yes. Here it is:

Oxygen Model of Asthma

My Oxygen Model of Asthma is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of bronchial asthma—causes, clinical course, consequences, and control—on the basis of disturbed oxygen functions. The most important among there are: (1) impaired or blocked oxygen signaling; (2) interrupted oxygen’s ATP energy generation; (3) diminished oxygen’s detergent functions; (4) interrupted oxygen’s cellular detox functions; (5) impeded oxygen-governed cellular repair mechanisms; and (5) oxygen-regulated cell membrane and matrix functions. These abnormalities usually begin in early life but asthma can develop at any time during life.

How Do I Discover My Asthma Doctor in My Mirror?

You can start by taking “Dr. Ali’s Course on Healing.” It is a self-learning course based on 8 video seminars. I suggest you download the first four seminar from my website http://www.AliAcademy.Org (links for the Course appear on the top of the home page). View them, then review them five days or so later. From each seminar, you will learn to do some simple natural remedy. Then download seminars 5-8 and view them twice. Again, from each seminar, you will learn to do some simple natural remedy. Finally two weeks later, you should review all eight seminars for the third. Why three times? I think you will give the best answer yourself after taking the Course.

Oxygen Model of Asthma for Professional and Advanced Readers

In 2000, I published my Oxygen Model of model of allergy and hypersensitivity in Current Opinion in Otolaryngology.11 That model of atopy is a unifying model that integrates diverse clinical, biochemical, morphologic, and experimental observations in the following three areas: (1) classical studies of IgE-mediated atopic response and, to a lesser degree, the other three types of Gell and Coombs hypersensitivity responses; (2) an ecologic view of clinical allergy that includes sensitivity to environmental agents independent of the dose of the excitant; (3) an expanded, integrative perspective of hypersensitivity responses that focuses on oxidative-dysoxygenative dysfunction, which profoundly influences sensitivity reactions included in the first two categories. In 2000, one of the authors (MA) also proposed that oxidative coagulopathy is a major pathogenetic mechanism of hypersensitivity disorders in an article published in Environmental Management and Health.12 Our focus in the management of asthma patients was on elements in the bowel, blood, and liver ecosystems that cumulatively add to the total oxidative stress and eventually disrupt cellular energetics. The existence of the dysox state — impaired oxygen homeostasis with respiratory-to-fermentative shift — was documented by establishing increased urinary excretion of metabolites of Krebs cycle and gkycolytic pathways. This subject is discussed at length in Dysoxygenosis and Oxystatic Therapies, the third volume of The Principles and Practice of Integrative Medicine.13

Particulate Matter (PM), Diesel exhaust particles (DEP) , Pollutants, and Hypersensitivity

The issues of particulate matter (PM), industrial pollutants, and hypersensitivity are crucial in both understanding the pathogenesis of asthma and for designing rational plans for the prevention and treatment of asthma. PM in ambient air inflicts oxidative injury and induces inflammation in microecologic cellular and organ-system macroecologic systems. Such injury involves myriad prooxidant and proinflammatory pathways, as well as antioxidant and antiinflammatory systems.14-22 Examples of the former include cellular heme oxygenase-1 (HO-1), NADPH cytochrome P-450 reductase (P-450 reductase), nitric synthase, sulfates, nitrates, organic hydrocarbons, metallic compounds, and prooxidant transition metals, such as copper, vanadium, chromium, nickel, cobalt, and iron. The counteractive antioxidant and antiinflammatory responses evoked include superoxide dismutase, catalase, glutathione peroxidase, and antioxidants.

The redox phemonena occurring in the pulmonary and cardiovascular system in patients with asthma have been investigated.23,24 The uptake of PM in macrophages and epithelial cells and induction of oxidative stress is affected by differences in the size of particles — characterized as coarse particles (2.5-10 microns), fine particles (< 2.5 microns), and ultrafine particles (UFP, < 0.1 micron) — and composition of such matter. UFPs are the most potent inducer of cellular heme oxygenase-1 (HO-1) expression and depletion of intracellular glutathione. Furthermore, HO-1 expression is directly correlated with the high organic carbon and polycyclic aromatic hydrocarbon (PAH) content of UFPs.22 What increases the biological potency to UFPs markedly is their localization in mitochondria.33 For all citations and full text of The Oxygen Model of Astma, please see my article in Current Opinion in Otolaryngology.


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