scholarly journals Hypothesis on the glucose production’s communication model between thebrain and other internal organs, especially the stomach and liver

After reviewing the research results for six months, from September 2019 through February 2020, the author identified a probable internal communication model between the nervous system and certain vital internal organs, specifically the stomach and liver regarding postprandial plasma glucose (PPG) production. The author used a continuous glucose monitor device to collect 50,000 glucose data during the past 665 days. He focused on studying the relationships among different food nutritional contents, cooking methods, food material’s physical phases, and different characteristics and variants from his glucose waveform patterns. In this study, he focused on the three major meal groups based on food nutritional ingredients, meal’s preparation, and cooking methods of eggs, squash, and cabbage to create soup-based (liquid) meal and pan-fried (solid) meal. The PPG waveforms from these three meal groups demonstrated that soup-based liquid food produced a much lower glucose value than the pan-fried solid food. Although both liquid and solid meals have similar identical nutritional ingredients, he questions why did this occur? His hypothesis is that his PPG differences are due to specific physical phase of his finished meal either “liquid” or “solid”, which is his ready-to-eat meal’s final physical “phase” that determines his PPG characteristics and waveforms. The author utilized his GH-Method: math-physical medicine (MPM) approach to explore a T2D patient’s glucose production situation from a scientific view of the brain and nervous system’s functionalities. If this specific approach and above interpretation are accurate, we can then “trick” our brain into producing a “lesser” amount of glucose after food intake without altering or sacrificing the needed food nutritional balance. As a result, T2D patients can simply change their cooking method in order to lower both of their peak PPG values and their average PPG levels.

After reviewing the research results for six months, from September 2019 through February 2020, the author identified a probable internal communication model between the nervous system and certain vital internal organs, specifically the stomach and liver regarding postprandial plasma glucose (PPG) production. The author used a continuous glucose monitor device to collect 50,000 glucose data during the past 665 days. He focused on studying the relationships among different food nutritional contents, cooking methods, food material’s physical phases, and different characteristics and variants from his glucose waveform patterns. In this study, he focused on the three major meal groups based on food nutritional ingredients, meal’s preparation, and cooking methods of eggs, squash, and cabbage to create soup-based (liquid) meal and pan-fried (solid) meal. The PPG waveforms from these three meal groups demonstrated that soup-based liquid food produced a much lower glucose value than the pan-fried solid food. Although both liquid and solid meals have similar identical nutritional ingredients, he questions why did this occur? His hypothesis is that his PPG differences are due to specific physical phase of his finished meal either “liquid” or “solid”, which is his ready-to-eat meal’s final physical “phase” that determines his PPG characteristics and waveforms. The author utilized his GH-Method: math-physical medicine (MPM) approach to explore a T2D patient’s glucose production situation from a scientific view of the brain and nervous system’s functionalities. If this specific approach and above interpretation are accurate, we can then “trick” our brain into producing a “lesser” amount of glucose after food intake without altering or sacrificing the needed food nutritional balance. As a result, T2D patients can simply change their cooking method in order to lower both of their peak PPG values and their average PPG levels.


2020 ◽  
pp. 1-5
Author(s):  
Gerald C Hsu ◽  

In this paper, the author described the progress on his two-year long special research project, from 5/5/2018 through 8/13/2020, to identify a neural communication model between the brain’s cerebral cortex and certain internal organs such as the stomach, liver, and pancreas. He used a continuous glucose monitor (CGM) sensor collected postprandial plasma glucose (PPG) data to investigate the glucose production amount at different timing and waveform differences between 95 liquid egg meals and 110 solid egg meals


In this paper, the author presents the results of his national segmentation pattern analysis of the sensor PPG data based on both high-carb and low-carb intake amounts. It also verified his earlier findings on the communication model between the brain and internal organs such as the stomach, liver, and pancreas.


2020 ◽  
pp. 1-4
Author(s):  
Gerald C Hsu ◽  

In this paper, the author describes his 2+ years (801 days) research results, from 5/5/2018 through 7/14/2020, using his 171 special meals glucose data. Initially, he researched the detailed postprandial plasma glucose (PPG) data resulting from both food intake and post-meal exercise via 97 solid egg meals (74 pan-fried and 23 hard broiled) and 74 liquid egg meals (egg drop soup). Based on his findings, he adopted a statistical method of “decision making via elimination” to search and verify a hypothetical neural communication model between the brain’s cerebral cortex and internal organs, such as the stomach, intestines, liver, and pancreas


2020 ◽  
Vol 3 (3) ◽  

This article address the author’s hypothesis on the neurocommunication model existing between the brain and liver regarding production and glucose secretion in the early morning. This is based on the observation of the difference between glucose at wake up moment in the morning for the fasting plasma glucose (FPG), and glucose at the first bite of breakfast for the glucose at 0-minute or “open glucose” of postprandial plasma glucose (PPG). All of the eight identified glucoses of breakfast PPG are higher than the eight glucoses at time of wake up by a difference of an average of 8 mg/dL. The value difference using Method B of CGM sensor glucoses during the COVID-19 period offers the most accurate picture and credible glucose difference of 8 mg/dL between his FPG at wake-up moment and PPG at the first bite of breakfast. The author believes that the brain senses when a person wakes up due to different kinds of stimuli from many sources, including eye, environment, and even internal organs, which will alert the body to be in “active” mode requiring “energy” through glucose. Even though the person has not eaten anything or is not actively moving, the brain issues a marching order to the liver to produce or release glucose for the body to use in the forthcoming day. This hypothesis can currently explain why his glucose of eating his breakfast is ~8 mg/dL higher than his FPG at wakeup.


1993 ◽  
Vol 264 (5) ◽  
pp. G902-G909 ◽  
Author(s):  
G. R. Greenberg

Somatostatin-like immunoreactivity (SLI) released into the circulation after nutrients or secretagogues is heterogeneous. To determine whether similar neural pathways regulate secretion of SLI molecular forms, circulating somatostatin-28 (S-28) and somatostatin-14 (S-14) responses to ingestion of a solid meal, intraduodenal perfusion of a liquid defined formula meal, and intravenous infusion of cholecystokinin octapeptide (CCK-OP, 250 pmol.kg-1.h-1) were measured in four conscious dogs with and without cryogenic blockade of the cervical vagus nerves. SLI was separated by gel-filtration chromatography of extracted, acidified plasma and quantified by radioimmunoassay. Basal plasma concentrations of S-28 were 4.1 +/- 0.6 fmol/ml and of S-14 were 3.8 +/- 0.4 fmol/ml. Ingestion of the solid meal increased plasma SLI threefold, and elevations of S-28 and S-14 were equivalent. After the intraduodenal liquid meal or infusion of CCK-OP, plasma SLI rose twofold, but increments of S-28 exceeded S-14, comprising approximately 70% of SLI released. Vagal blockade by cooling reversibly inhibited both the S-28 and S-14 responses to the solid meal, intraduodenal liquid meal, and CCK-OP. In contrast, atropine (50 micrograms/kg iv), given after solid food, intraduodenal nutrients, and CCK-OP, suppressed S-28 but further increased S-14 responses. Atropine did not, however, alter the suppression of S-14 and S-28 by vagal cooling.(ABSTRACT TRUNCATED AT 250 WORDS)


2013 ◽  
Vol 58 (7) ◽  
pp. 2001-2006 ◽  
Author(s):  
Priyanka Sachdeva ◽  
Steven Kantor ◽  
Linda C. Knight ◽  
Alan H. Maurer ◽  
Robert S. Fisher ◽  
...  

1982 ◽  
Vol 60 (6) ◽  
pp. 769-776 ◽  
Author(s):  
Norman S. Track ◽  
Marilyn M. Cannon ◽  
Ann Flenniken ◽  
Stefa Katamay ◽  
Edward F. A. Woods

The effect of chronic consumption of diets containing either different sources of dietary fibre (8% guar, 8% pectin, or 8% multifibre) or low carbohydrate upon carbohydrate tolerance was examined in rats. Weight gain was significantly lower throughout the entire 28-day study period with the guar group and after 20 days with the multifibre group. When tested with a liquid meal (1 g sucrose/kg body weight) after 14 days on the diets, only the guar rats had significantly lower fasting and postprandial plasma glucose concentrations. After 28 days, the improved carbohydrate tolerance persisted in the guar rats and started to appear in the multifibre rats. Pectin and low carbohydrate diets had no effect upon either weight gain or carbohydrate tolerance. Consuming the fibre diets did not affect jejunal sucrase activities. Jejunal glucose uptake activity was significantly diminished when measured in fasting guar rats while postprandially activities were similar to controls. Jejunal Na-K-ATPase activities in fasting and postprandial guar rats were not related to changes in glucose uptake. These studies confirm that only certain types of dietary fibre improve carbohydrate tolerance and suggest that reduced weight gain and altered intestinal glucose uptake are factors involved in the chronic fibre effect.


1990 ◽  
Vol 63 (3) ◽  
pp. 447-455 ◽  
Author(s):  
Michael Horowitz ◽  
Anne Maddox ◽  
Judith Wishart ◽  
Jane Vernon-Roberts ◽  
Barry Chatterton ◽  
...  

Recent studies suggest that dexfenfluramine (D-fenfluramine), because of its pure serotonergic effect, may be a more potent anti-obesity agent, associated with fewer side-effects than the racemate DL-fenfluramine. The effect of dexfenfluramine on gastric emptying of a mixed solid and liquid meal was assessed with a double-isotope scintigraphic technique in eleven obese patients. Each subject took a placebo capsule on the morning and evening of the day before, and on the morning of the first gastric emptying measurement. Dexfenfluramine was then taken at a dose of 15 mg twice daily and gastric emptying measurements were performed at 5 and at 29 d after the initiation of active treatment. Dexfenfluramine significantly slowed gastric emptying of the solid meal at both 5 and 29d when compared with the placebo (P < 0.05) and also delayed emptying of solid food from the proximal stomach (P < 0.01), but no significant effect on liquid emptying was observed. No significant side-effects were reported and there was a marginal weight loss (P< 0.005) during treatment. We conclude that inhibition of gastric emptying may contribute to the efficacy of dexfenfluramine in the treatment of obesity.


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