Fruits and Vegetables Aren't Good for Every Body All the Time.
D) Autoinflammation and Autoimmunity
In autoinflammatory and autoimmune disorders, dysregulation of innate and acquired immune responses result in the excessive release of pro-inflammatory enzymes and autoantibodies. The secretion of these enzymes leads to a form of programmed cell death, damaging tissue and interfering with bodily functions.
Autoinflammatory diseases were discovered in 2000. They are characterized by acute systemic inflammatory flares not associated with infections, tumors or autoimmunity. "Though clinically similar to various infectious and rheumatologic diseases, neither distinct pathogens, nor specific autoantibodies, can be identified in [systemic autoinflammatory syndromes]: this group of disorders is mainly characterized by fluctuating topical signs of inflammation affecting skin, gastrointestinal tube, joints, serosal surfaces and central nervous system, with a variable modality of recurrence, alternating with periods of full well-being" (D. Rigante 2010).
Autoimmune diseases involve the body misidentifying normal tissue as unnatural and so attacks elements of one's own physiology. Inflammatory bowel diseases (e.g. Crohn's disease and colitis) are well known gastrointestinal autoimmune conditions.
Recurring inflammation of the gastrointestinal tract suggests that food digestion, nutrient absorption, microbiome health and epithelial barrier protection may be compromised. For example, the increase of a specific type of inflammatory enzyme, IL-1b, into the gastrointestinal tract increases epithelial permeability (L. Tesoriere+ 2014) by inducing the production of reactive oxygen species (Yu+2007) that can damage gastrointestinal tract lining.
Additionally affected tissues and systems in autoinflammation can include thermoregulation (periodic hyperthermia or hypothermia), abdominal, chest or muscle pain, swollen lymph nodes and headaches (Jeru+ 2011). Other symptoms may include brain fog, imbalance and lack of coordination.
Most autoinflammatory diseases occur rarely in the general population but a few types manifest more frequently among some groups. For example, Familial Cold Autoinflammatory Syndrome, Type 2 (FCAS2; NLRP12 gene), occurs with a somewhat higher frequency among individuals of northern European descent, e.g. British Islands, Scandinavia, Poland. Familial Mediterranean Fever (FMF; MEFV gene) manifests in communities genetically-originating near the Mediterranean sea in western Asia, southern Europe and northern Africa (Kanazawa+ 2013).
D. Rigante, The protean visage of systemic autoinflammatory syndromes: a challenge for inter-professional collaboration, European Review for Medical and Pharmacological Sciences, 2010; 14: 1-18.
Tesoriere, L., Attanzio, A., Allegra, M., Gentile, C. & Livrea, M. A. Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-kappaB-dependent release of inflammatory mediators and prevents the increase of epithelial permeability in IL-1beta-exposed Caco-2 cells. British Journal of Nutrition, 111, 415-423 (2014).
Yu, Y., Wang, Z., Liu, C., & Chen, C. (2007). Ellagic acid inhibits IL-1b-induced cell adhesion molecule expression in human umbilical vein endothelial cells. British Journal of Nutrition, 97(4), 692-698.
Isabelle Jéru, Gaëlle Le Borgne, Emmanuelle Cochet, Hasmik Hayrapetyan, Philippe Duquesnoy, Gilles Grateau, Alain Morali, Tamara Sarkisian, Serge Amselem, Identification and functional consequences of a recurrent NLRP12 missense mutation in periodic fever syndromes, Arthritis & Rheumatology, May 2011, Volume 63, Issue 5, Pages 1459-1464.
Kanazawa et al., Comprehensive Review of Rare Hereditary Autoinflammatory Disorders. Journal of Genetic Disorders and Genetic Reports,