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Anorexia Nervosa (Physiological)

Anorexia nervosa (AN) is a serious health problem. Despite the highly destructive consequences of AN, the etiology of AN is still elusive. Illness/injury induced anorexia[1] may play a decisive role in triggering and developing AN. And AN is not purely a mental illness (eating disorder). As a physiological cause, the atrophy and dysfunction in gut mucosa, and the injury to the dysfunctional mucosa induced by improper food intake may also contribute to the triggering and developing of AN by repeatedly triggering illness/injury induced anorexia.

During illness induced anorexia, autophagy is upregulated to eliminate pathogens.[2][3][4] Autophagy is a highly regulated process in eukaryotes to maintain homoeostasis and deal with stress stimuli such as starvation and pathogen invasion. Illness induced anorexia as manifestation of upregulated autophagy.

The Luigi Cornaro diet of eat-but-little may be a feasible approach to restore gut homeostasis and healthy weight for an anorexia nervosa Patients.


References:

  1. ^ Exton, M. S. (1997-12). "Infection-induced anorexia: active host defence strategy". Appetite. 29 (3): 369–383. doi:10.1006/appe.1997.0116. ISSN 0195-6663. PMID 9468766. {{cite journal}}: Check date values in: |date= (help)
  2. ^ Jo, Eun-Kyeong; Yuk, Jae-Min; Shin, Dong-Min; Sasakawa, Chihiro (2013-05-06). "Roles of Autophagy in Elimination of Intracellular Bacterial Pathogens". Frontiers in immunology. 4: 97. doi:10.3389/fimmu.2013.00097.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ van Niekerk, Gustav; Isaacs, Ashwin W.; Nell, Theo; Engelbrecht, Anna-Mart (2016). "Sickness-Associated Anorexia: Mother Nature's Idea of Immunonutrition?". Mediators of Inflammation. 2016: 1–12. doi:10.1155/2016/8071539. ISSN 0962-9351.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ van Niekerk, Gustav; Loos, Ben; Nell, Theo; Engelbrecht, Anna-Mart (2016-04-02). "Autophagy-A free meal in sickness-associated anorexia". Autophagy. 12: 727–734. doi:10.1080/15548627.2016.1147672.

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