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Eosinophilic esophagitis

It is an autoimmune disorder, which immediately makes me believe it is linked to Poison/"Vitamin A" toxicity.  Scientists and conventional physicians have NO IDEA what causes it.  It is often abbreviated as EoE:

Eosinophilic esophagitis: an autoimmune esophageal disorder.

Eosinophilic esophagitis (EoE) represents a chronic, immune/antigen-mediated esophageal inflammatory disease associated with esophageal dysfunction resulting from severe inflammation. The incidence and prevalence of EoE have been increasing in the past decade; however, the reason for this increase is unclear. There is a chronic inflammatory infiltrate that is present in EoE which promotes inflammation, symptoms, and dysfunction. In addition to eosinophils, interleukin (IL)-5 expressing T cells, B cells, eotaxin-3, IL-13, and IgE-bearing mast cells are present in EoE and are thought to contribute to the disease process. Eosinophils are pro-inflammatory and modulate multiple aspects of the immune response. Eosinophils produce a wide range of inflammatory cytokines, chemokines, granulocyte-monocyte colony-stimulating factors, and tumor necrosis factors. Once activated, eosinophils release granule components, which are toxic to a variety of tissues. Transforming growth factor β1 is a pro-fibrotic molecule produced by epithelial and inflammatory cells, is overexpressed in EoE, and plays a role in esophageal remodeling. Fibrous remodeling in EoE could be associated with symptoms of dysphagia and may explain and predict future esophageal strictures and dysmotility. EoE is a complex disease involving multiple activation pathways, a large number of cells, and various inflammatory molecules. It, along with other atopic disease, is becoming increasingly prevalent and has an important genetic load and may represent as an immunological tolerance disorder of the GI tract.

Before we go further, we should talk about apoptosis.  Apoptosis is the death of cells which occurs as a normal and controlled part of an organism's growth or development.

What major disease group is associated with problems (lack of) apoptosis happening as it should?  CANCER.

Apoptosis in the development and treatment of cancer

Inhibition of apoptosis can lead to cancer

The evidence that inhibition of cell death can lead to cancer comes mainly through accidents of nature, such as translocations in lymphomas and leukemias. For some cell death genes knockout and transgenic mice have provided evidence confirming that failure of cell death can cause cancer. Although there have been a very large number of studies determining the levels of expression of genes for cell death inhibitors in various types of cancer, these studies only provide correlative evidence.

To bring this theory to a close, we have to tie it all together.  Once you understand that EoE is too many eosinophils (eosinophilia) running amok, and that inhibiting apoptosis can lead to very serious diseases, and that retinoic acid is Poison/"Vitamin A"...I give you this study:

Retinoic Acids Are Potent Inhibitors of Spontaneous Human Eosinophil Apoptosis

Retinoic acids (RAs), which are active metabolites of vitamin A, are known to enhance Th2-type immune responses in vitro, but the role of RAs in allergic inflammatory cells remains unclear.

Unclear...sort of like how conventional medicine has no clue about what causes EoE.  Go on...

In this study, we demonstrated that purified peripheral blood eosinophils expressed nuclear receptors for RAs at the mRNA and protein levels. Eosinophils cultured with all-trans RA (ATRA) and 9-cis-RA showed dramatically induced cell survival and nuclear hypersegmentation, and the efficacy of RAs (10−6M) was similar to that of IL-5 (1 ng/ml), the most critical cytokine for eosinophil activation. Pharmacological manipulation with receptor-specific agonists and antagonists indicated that the antiapoptotic effect of RAs was mediated through ligand-dependent activation of both retinoid acid receptors and retinoid X receptors (mainly retinoid acid receptors). Furthermore, using a gene microarray and a cytokine Ab array, we discovered that RAs induced vascular endothelial growth factor, M-CSF, and MCP-1 secretion, although they were not involved in eosinophil survival. RA-induced eosinophil survival appears to be associated with down-regulation of caspase 3 and inhibition of its enzymatic activity. These findings indicate an important role of RAs in homeostasis of granulocytes and provide further insight into the cellular and molecular pathogenesis of allergic reactions.

It is Poison/"Vitamin A" toxicity (aggravated by glyphosate) that is behind the recent epidemic of allergic disease, that's what this study is really showing.

Tissue eosinophilia is one of the hallmarks of allergic diseases and Th2-type immune responses. Eosinophils contribute to tissue injury, vascular leakage, mucus secretion, and airway contraction by releasing cytotoxic granule proteins, reactive oxygen species, and lipid mediators (1). In addition, eosinophils can produce several chemokines, growth factors, and Th2-type cytokines such as IL-4 and IL-13 (2). The evidence suggests the potential of eosinophils to not only act as terminal effecter cells but also to possess immunoregulatory activities.

If eosinophils didn't "die" when they are normally supposed to, wouldn't that be a great way to get TOO MANY of them causing TOO MUCH INFLAMMATION?  Makes sense to me.

Prolonged eosinophil survival at an allergic inflammatory site is essential for them to exert their function sufficiently and is associated with pathological conditions. IL-5 is one of the key regulators of eosinophil differentiation and survival. Eosinophils cultured in the absence of IL-5 undergo rapid apoptosis, which is physiological cell death characterized by morphological changes (3). However, treating patients with anti-IL-5 mAb only partially reduced eosinophilia in airway tissue and bone marrow, suggesting that other factors contributed to eosinophil survival in these tissues (45). Therefore, investigation of the mechanism and factors involved in the survival prolongation of eosinophils would be beneficial in the treatment of allergic diseases.
Despite these results that suggest that vitamin A biases the response in a Th2 direction, the influence of RA on allergic disease is limited and appears contradictory. For instance, supplementation with a natural source of vitamin A had a protective effect against exercise-induced asthma in some patients (17). Several epidemiological studies suggested that vitamin A intake had no association with or protective effect on asthma (18). In contrast, RA can induce eosinophilia and exacerbation of asthma under certain conditions (19). Therefore, it is of paramount importance to clarify the regulation of immune responses by RA and its underlying cellular and molecular mechanisms.

The direct effect of RA on allergic inflammatory cells, especially eosinophils, is less well understood. In the present study, we investigated the functional roles of RA on purified human eosinophils. We found that peripheral blood eosinophils expressed receptors for RAs and, interestingly, ATRA and 9-cis-RA dramatically inhibited spontaneous eosinophil apoptosis. The effect exerted by RA was parallel with the down-regulation of caspase 3 transcription and its enzymatic activity. Together, our experiments showed that RAs activated eosinophils to produce several proinflammatory cytokines.

Poison/"Vitamin A" induces eosinophilia (too many eosinophils), prevents them from dying in their normal time (they "live" longer than they are supposed to).  Sounds a lot like the process of cancer cells, doesn't it?  I think we have the mechanism of EoE, and it is Poison/"Vitamin A" toxicity.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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