The public health hazards associated with Maillard end-products such as melanoidins and advanced lipoxidation end-products (ALEs) and advanced glycation end-products (AGEs), intermediary Maillard reaction creations, include most of the leading causes of morbidity and mortality globally. At the same time, only a few clinicians understand the intricacies linking redox biophysics and disease to humans and animals, explained here and in companion articles in simple to conceptualize terms.
Maillard abuse causes increased systemic oxidative stress (SOS: pE-> pH+), an accelerant to the fatal vascular complications of type 1 diabetes. Maillard abuse-induced SOS (pE-> pH+) is also linked to type 2 diabetes, thyroid disorders, polycystic ovary syndrome, low testosterone, and osteoporosis.
Many studies have shed light on exotic, intricate, and pricey markers to test extracellular and intracellular Maillard reaction-induced redox imbalance. And their corresponding influence on soluble and cell receptor signaling and the Maillard-induced redox-based diseases and deaths they cause. Inconclusive and pricey new markers for measuring extracellular and intracellular redox balance and imbalance cost thousands of US Dollars (USD) per in vivo assay. The author presents seven extracellular and intracellular redox markers costing less than 150 USD per in vivo assay, using standard laboratory tests available to medical centers worldwide.
A PubMed search revealed no studies testing colas, pizza, burgers, and wings-specific intra-day Maillard-rich food binges on TSH, TG/HDL ratio (THR), VLDL/HDL ratio (VHR), LDL/HDL ratio (LHR), and urine pH+ extracellular redox markers, and neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) intracellular redox indicators.
The objective of this pilot single case study is to test the feasibility of replication on a much larger scale. The second objective is to analyze the potential influence or lack of impact of Maillard intermediate and end-products on oral-intestine, corporal extracellular, and intracellular redox biophysics, soluble and cell receptor signaling, immunosuppression, inflammation, and risk for developing one or more of the leading causes of morbidity and mortality worldwide at three targeted intraday-pH+ points.
The participant met inclusion criteria and drank acidic tide-inducing Maillard-rich colas to prompt an intra-oral-intestinal and the body’s extracellular systemic oxidative stress (SOS: pE-> pH+)-associated plasma acidic-tide. And had blood drawn for CBC with differential and platelet count, comprehensive metabolic panel, lipid panel, and TSH, and provided a sample for a routine urinalysis after an at-home confirmation of extracellular acidic-tide using ‘Just Fitter pH Test Strips pH 4.5 – pH 9.0.’ In a concerted attempt to reach an at-home urine pH+ strip value of 5.5, the top of the 4.5 to 5.5 urine and 7.35 to 7.38 blood systemic oxidative stress range (SOS: pE-> pH+). Before driving to the lab to give blood and urine samples for CBC with differential, comprehensive metabolic panel, lipid panel, TSH, and routine urinalysis. A similar procedure occurred to consuming mainly alkaline-botanical pizza, peanut butter shake, stronger alkaline tide-inducing acidic bacon double cheeseburgers and twelve fried chicken wings.
The move from cola-associated urine pH+ 6 to pizza-associated pH+ 6.5 within the prime systemic energy PSE (pE- = pH+) urine pH+ range increased oral-intestinal, extracellular, and intracellular SOS by a factor of 50. The move from pizza-associated urine pH+ 6.5 to burgers and wings-associated pH+ 7.0 within the systemic reductive stress (SRS: pE-< pH+) urine pH+ range of 6.7 to 7.7, increased oral-intestinal, extracellular, and intracellular SOS (SOS: pE- > pH+) by a massive score of 556.
This pilot study warrants reproduction on a larger scale with similarly healthy participants with elevated antioxidant tone. Such Maillard-intense trials require safe inclusionary criteria that limit initial subject sample pools to the equivalent of less than 25% of healthy females and males 8 to 80 years of age within or close to their ideal body mass indices and waist-to-height ratios.
Circulating uromodulin inhibits systemic oxidative stress by inactivating the TRPM2 channel