scholarly journals Sixty-Four Hour Changes in Oral-Intestinal, Extracellular, and Intracellular Redox Status After an All-Day Maillard-Coated Food Binge Followed by Two Days of Redox/Digestion-Balanced Culinary Medicine: A Pilot Single Case Analysis

2021 ◽  
Vol 6 (2) ◽  

Browned, melanoidin-coated, and Maillard reaction end-product-covered convenience and fast-foods are as addictive as street drugs. And drive overeating, systemic oxidative stress (SOS: pE- > pH+), and systemic reductive stress (SRS: pE- < pH+), overweight, and the leading causes of mortality and morbidity worldwide. Redox/digestion-balanced culinary medicine protocols are absent as healthcare professionals and the people they serve begin to recognize that Maillard abuse disorder is the main obstacle to self-actualization and a long, accomplished, and content energetically ambulatory extended lifespan. A PubMed search revealed no studies exhibiting sixty-four-hour changes in oral-intestinal, extracellular, and intracellular redox status after an all-day Maillard-coated food spree followed by two days of redox/digestion-balanced culinary medicine. The purpose of this single case study is to analyze changes, if any, in oral-intestinal, extracellular, and intracellular redox status after an all-day Maillard-coated binge followed by two days of redox/digestion-balanced culinary medicine and examine the feasibility of more extensive investigations. The participant met inclusion criteria, drank Maillard-rich colas for breakfast, a small pizza, a peanut butter shake for lunch, a double bacon cheeseburger, and a dozen chicken wings for dinner and provided blood and urine samples. The volunteer then underwent redox/digestion-balanced culinary medicine detoxification and provided laboratory samples. TSH, TG/HDL ratio, VLDL/HDL ratio, LDL/HDL ratio, and urine pH+ measured oral-intestinal and extracellular redox status. The neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios assessed intracellular redox status. It took sixty-four hours for the participant’s body and mind to neutralize the toxic manifestations of a day-long binge on Maillard reaction intermediate and end-products, melanoidins, advanced glycation end-products (AGEs), and advanced lipoxidation endproducts-coated and containing foods and beverages. More extensive investigations are needed to increase the Maillard abuse detoxification options. Healthcare professionals and the people they serve increasingly recognize that Maillard abuse is the main obstacle to self-actualization and a long, accomplished, and energetically ambulatory lifespan.

2008 ◽  
Vol 44 (4) ◽  
pp. 614-623 ◽  
Author(s):  
Damodar Gupta ◽  
Meredith E. Crosby ◽  
Alexandru Almasan ◽  
Roger M. Macklis

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Jong‐Sang Kim ◽  
Lesley Quintos ◽  
In Ae Lee ◽  
Ji Sun Lim ◽  
Ji Yeon Seo ◽  
...  

2019 ◽  
Vol 11 (3) ◽  
pp. e358
Author(s):  
Sabah Gheddouchi ◽  
Nassima Mokhtari-Soulimane ◽  
Hafida Merzouk ◽  
Fayçal Soulimane ◽  
Fadia Bekhti ◽  
...  

2012 ◽  
Vol 214 (3) ◽  
pp. 399-408 ◽  
Author(s):  
Gonzalo Alba ◽  
Consuelo Santa-María ◽  
María Edith Reyes-Quiroz ◽  
Rajaa El Bekay ◽  
Isabel Geniz ◽  
...  

Calcineurin (protein phosphatase 2B) (CN) comprises a family of serine/threonine phosphatases that play a pivotal role in signal transduction cascades in a variety of cells, including neutrophils. Angiotensin II (Ang II) increases both activity andde novosynthesis of CN in human neutrophils. This study focuses on the role that intracellular redox status plays in the induction of CN activity by Ang II. Bothde novosynthesis of CN and activity increase promoted by Ang II were downregulated when cells were treated withl-buthionine-(S,R)-sulfoximine, an inhibitor of synthesis of the antioxidant glutathione. We have also investigated the effect of pyrrolidine dithiocarbamate and phenazine methosulfate, which are antioxidant and oxidant compounds, respectively, and concluded that the intracellular redox status of neutrophils is highly critical for Ang II-induced increase of CN expression and activity. Results obtained in neutrophils from hypertensive patients were very similar to those obtained in these cells on treatment with Ang II. We have also addressed the possible functional implication of CN activation in the development of hypertension. Present findings indicate that downregulation of hemoxygenase-1 expression in neutrophils from hypertensive subjects is likely mediated by CN, which acts by hindering translocation to the nucleus of the transcription factorNRF2. These data support and extend our previous results and those from other authors on modulation of CN expression and activity levels by the intracellular redox status.


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