Papadopoulos NG, Konstantinou GN
Biomed Pharmacother61p21-8(2007 Jan)
Papadopoulos et al. have written that atopy should be treated as a suboptimal innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease..1) Consistent with that thinking, the Marshall Protocol is a treatment for allergies. Other treatments (some of which are contraindicated) include the following.
vitamin D supplementation can cause allergies2)
Hyppönen et al. performed a retrospective cohort study of 7,648 Finnish infants born in 1967. The prevalence of atopy and allergic rhinitis at age 31 years was 46% higher in participants who had received vitamin D supplementation regularly during the first year compared to others.3)
The word allergy is often misused. An allergy is an acquired hypersensitivity to a substance (allergen) that does not normally cause a reaction. It is essentially an antibody-antigen reaction. The reaction is due to the release of histamine or histamine-like substances from injured cells.
Manifestations most commonly involve the respiratory tract (most serious is anaphylactic shock) or the skin because this is what the histamine reaction affects. Other types of reactions such as gastric disturbances or side effects of medications are more correctly labeled intolerances. True allergies are a Th2 response of the immune system. Many patients on the MP have found that their long-term 'allergies' disappeared. This is not surprising since Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. is often not recognized as the cause of allergy-type symptoms.
…Review my presentation on antibiotics at Chicago, where I argued that the size of antibiotic molecules is too small for true allergy to develop, as they are too small to catalyze the formation of antibodies? Consequently they are typically recognized by innate immunity, and not by acquired immmunity.Now, my arguments can (of course) be challenged. But nobody has done that yet.
~Trevor Marshall, PhD
Asthma is a chronic or recurring inflammatory condition in which the airway develops increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, inflammation , increased mucus production, and intermittent airway obstruction. Only a minority of asthma sufferers have an identifiable allergy trigger. Sounds a lot like Th1 disease, doesn't it? The Marshall Protocol will resolve your asthma. 4)
Symptoms may include trouble breathing through the nose, headache, aching behind the eye area, tenderness in the cheeks, sinus congestion, nasal discharge, or post nasal drip.
Nasal irrigation or a steam inhaler may relieve some symptoms.
Sinus symptoms are often an expression of trigeminal nerve dysfunction and will respond to the MP, albeit in the later stages of the therapy.
~Greg Blaney, MD
The issue of pollen allergies is a difficult one. I cannot personally suggest anything, as all the allergies (which I used to have aplenty) slowly disappeared as therapy progressed. I would suspect that the pollen will be less of a problem for you this year, and virtually no problem next year, but I may be wrong. Be careful to not confuse the signs of sinus due to immunopathology and sinus due to allergies.
~Trevor Marshall, PhD
Reactions to foods are due to inflammation and immunopathology. Many members report resolution of their food intolerances on the MP.
My food allergies are totally gone. For the first time in years, I am not having reactions to trigger foods like corn, milk, sugar, wine, etc.
If your 'allergy' symptoms are intolerable, first reduce immunopathology by using the strategies suggested in My immune response / symptoms are too strong. What should I do? to see if they improve. If they do, then you know you are dealing with a Th1 response, also known as Immunopathology.
If you do not achieve relief from the MP meds adjustments, you may use palliative meds (Rx or OTC) orderd by your Dr and not listed in the Medication To Avoid While on the Marshall Protocol
It is okay to take antihistamines to treat intolerable symptoms. Try to use short-acting antihistamines, such as Benadryl (diphenhydramine) which can be taken as needed only, to reduce the amount of medication used.
The use of allergy medications such as Singulair tablets, which is a bronchodilator, preventive for allergic (Th2 immune system) responses and anti-inflammatory agent, are not so benign. They affect the immune system and may interfere with the MP meds so their use should be avoided unless you are sure that the source of your symptoms is a true allergic response. If your breathing feels okay without it, perhaps you do not need it. An short-acting, nonsteroid inhaler may be a better choice.
Sample PubMed cite5)
Last updated: January 4, 2009
Marshall Protocol member comments
We've found that hypersensitivity, whether skin reactions to metals or reactions to fumes, dust, odors, smoke, etc., resolves with recovery on the MP. Evidently when the Th1 inflammation is under control, normal homeostasis is reached. I know this will be hard to believe. I myself find it astonishing that I can wear jewelry without rashes, touching and eating certain foods no longer bothers me, and I pay little attention to smoke, orders and fumes. It's quite a change in my life after 40+ years.
I think it's just experience that tells us things are herx. We nearly all start by arguing that something 'couldn't be herx because…' and we all end up saying 'ok, you were right, it was herx' when we see what a limited timescale it has, and how its coming and going relates to the medication programme.
Anyway, it doesn't make any practical difference to what you do, does it? I mean, the MP is the way forward, no matter what's causing your symptoms. And you'll gradually see them fading, or going altogether. Keep a good record of daily symptoms, so that you track your progress.
I had a lot of true allergies before I started the MP; I had no idea they could be sarc-related. Now they've gone - except that sometimes I get a few hours or even a day or two of returned allergy, on the same days of my Z cycle each time. Allergies are an over-reaction of our distressed immune system; it stands to reason that some herxes will be allergy-like symptoms.
I can be certain it is herx and not “allergy” to the antibiotics because so many of us took larger doses of antibiotics many times pre-MP with no adverse reactions at all; but it knocked us on the ground once we avoided light, D and got the 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. down with the Benicar. I can see no other logical explanation for why I could take large doses every day before, and then a 'crumb' will now hit me like a freight train on MP. Others have noticed this too, and it is no group hallucination. I am certain if you looked for antibodies to the antibiotic in your system you would find none.
One thing I wanted to mention is on Christmas, the wind was blowing and the dust was kicking up. This often happens in Arizona and there are days when you can't see the mountains because of the dust. On Christmas day, I had some pleurisy like symptoms, dizziness, brain fogThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning., fatigue and sinus problems. Since I started the Marshall Protocol, I haven't needed steriods for my allergy / asthma problems. In the past, I would often need steriods and/or emergency care when this happened.
* Legacy content
Allergy Asthma Clin Immunol. 2009 Nov 19;5(1):8.
Introduction of oral vitamin D supplementation and the rise of the allergy pandemic.6)
Wjst M. Institute of Genetic Medicine, EURAC research, Drususallee 1, I-39100 Bozen, Italy. email@example.com Abstract The history of the allergy pandemic is well documented, enabling us to put the vitamin D hypothesis into its historical context. The purpose of this study is to compare the prevalence of rickets, vitamin D supply, and allergy prevalence at 50-year intervals by means of a retrospective analysis of the literature since 1880. English cities in 1880 were characterized by an extremely high rickets prevalence, the beginning of commercial cod liver oil production, and the near absence of any allergic diseases. By 1930 hay fever prevalence had risen to about 3% in English-speaking countries where cod liver oil was preferentially used for the treatment of rickets. In 1980 vitamin D was used nation-wide in all industrialized countries as supplement to industrial baby food, thus eradicating nearly all cases of rickets. At the same time the allergy prevalence reached an all-time high, affecting about 30% of the population. Time trends are therefore compatible with the vitamin D hypothesis although direct conclusions cannot be drawn. It is interesting, however, to note that there are at least two earlier research papers linking synthesized vitamin D intake and allergy (Reed 1930 and Selye 1962) published prior to the modern vitamin D hypothesis first proposed in 1999. PMID: 20016691
Allergy Asthma Clin Immunol. 2010 Jan 18;6(1):1.
Panallergens and their impact on the allergic patient.
Hauser M, Roulias A, Ferreira F, Egger M. Christian Doppler Laboratory for Allergy Diagnosis and Therapy, Department of Molecular Biology, University of Salzburg, Hellbrunnerstrasse 34, A-5020 Salzburg, Austria. Abstract The panallergen concept encompasses families of related proteins, which are involved in general vital processes and thus, widely distributed throughout nature. Plant panallergens share highly conserved sequence regions, structure, and function. They are responsible for many IgE cross-reactions even between unrelated pollen and plant food allergen sources. Although usually considered as minor allergens, sensitization to panallergens might be problematic as it bears the risk of developing multiple sensitizations. Clinical manifestations seem to be tightly connected with geographical and exposure factors. Future population- and disease-based screenings should provide new insights on panallergens and their contribution to disease manifestations. Such information requires molecule-based diagnostics and will be valuable for developing patient-tailored prophylactic and therapeutic approaches. In this article, we focus on profilins, non-specific lipid transfer proteins, polcalcins, and Bet v 1-related proteins and discuss possible consequences of panallergen sensitization for the allergic patient. Based on their pattern of IgE cross-reactivity, which is reflected by their distribution in the plant kingdom, we propose a novel classification of panallergens into ubiquitously spread “real panallergens” (e.g. profilins) and widespread “eurallergens” (e.g. polcalcins). “Stenallergens” display more limited distribution and cross-reactivity patterns, and “monallergens” are restricted to a single allergen source. PMID: 20298513
Antimicrobials May Compromise Immune SystemDECEMBER 3, 2010 | ISSUE 46•48 Researchers at the University of Michigan School of Public Health found that young people with high levels of triclosan, an antimicrobial agent commonly found in soaps, were at greater risk for allergies
Exp Dermatol. 2010 Jul 1;19(7):661-6. Epub 2010 Feb 25.Anti-inflammatory effects of the GABA(B) receptor agonist baclofen in allergic contact dermatitis. Duthey B, Hübner A, Diehl S, Boehncke S, Pfeffer J, Boehncke WH. Department of Dermatology, Clinic of the Johann Wolfgang Goethe-University, Theodor-Stern-Kai, Frankfurt, Germany. Abstract The gamma amino butyric acid B (GABA(B)) receptor is a G protein-coupled receptor (GPCR) involved in synaptic transmissionAn incident in which an infectious disease is transmitted.. Recent data indicate it to be also expressed on immune cells, along with chemokine receptors, which are also GPCRs. As GPCRs can undergo heterologous desensitization, we have examined the ability of baclofen, a GABA(B) receptor selective agonist, to interfere with the function of pro-inflammatory chemokine receptors known to be upregulated in cutaneous inflammation. In vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory., baclofen reduces chemotaxis of human peripheral blood mononuclear cells towards CCL2, CCL5, CXCL10, CXCL2 and CX3CL1 in a dose-dependant manner. Protein kinase C inhibitors calphostin C and G0 6976 could reverse this effect, pointing towards the involvement of both calcium-dependent and -independent protein kinase C in baclofen-induced inhibition of chemokine receptors. In an in vivoA type of scientific study that analyzes an organism in its natural living environment. model of contact hypersensitivity in C57BL/6 mice, intraperitoneal injection of baclofen markedly alleviated signs of inflammation as well as recruitment of neutrophils, monocytes and lymphocytes into the skin. This study demonstrates a new role for the GABA(B) receptor in inflammation, making it a potential new therapeutic target to treat inflammatory skin diseases. PMID: 20201957
Scand J Gastroenterol. 2011 Jun 17. [Epub ahead of print] Perceived food hypersensitivity: A review of 10 years of interdisciplinary research at a reference center. Lied GA, Lillestøl K, Lind R, Valeur J, Morken MH, Vaali K, Gregersen K, Florvaag E, Tangen T, Berstad A. Source Institute of Medicine , University of Bergen, Bergen , Norway. Abstract Abstract Perceived food hypersensitivity is a prevalent, but poorly understood condition. In this review article, we summarize narratively recent literature including results of our 10 years' interdisciplinary research program dealing with such patients. The patients (more than 400) included in our studies were all adults referred to a university hospital because of gastrointestinal complaints self-attributed to food hypersensitivity. Despite extensive examinations, food allergy was seldom diagnosed. The majority of the patients fulfilled the diagnostic criteria for irritable bowel syndrome. In addition, most suffered from several extra-intestinal health complaints and had considerably impaired quality of life. However, psychological factors could explain only approximately 10% of the variance in the patients' symptom severity and 90% of the variance thus remained unexplained. Intolerance to low-digestible carbohydrates was a common problem and abdominal symptoms were replicated by carbohydrate ingestion. A considerable number of patients showed evidence of immune activation by analyses of B-cell activating factor, dendritic cells and “IgE-armed” mast cells. Multiple factors such as immune activation, disturbed intestinal fermentation, enteric dysmotility, post-infectious changes and “local” allergy in the gut as well as psychological disturbances may play a role in the pathophysiology of perceived food hypersensitivity. Hence, our results support the view that management of these patients should be interdisciplinary.
I think this article (abstract below) that Trevor brought up may be one of the means that immune function improves when food allergies are reduced.
TNF alpha is also elevated in celiac disease and improves when the Gluten free diet is followed:
The following abstract shows that reducing TNF alpha (olmesartan does that at least some and food allergy reduction should do it), then the VDR will be more active against bacteria.