Nutritional interventions to reverse Type 2 diabetes has accelerated with relevance to the global Type 2 diabetes epidemic. The recent interest in Type 3 diabetes has now linked the reversal of Type 2 diabetes to Type 3 diabetes. Type 3 diabetes involves brain dysfunction with complete loss brain regulation of blood plasma glucose levels. The stabilization of Type 3 diabetes is critical to prevent the Type 2 diabetes complications that are irreversible such as myocardial infarction, non alcoholic fatty liver disease and pancreas programmed cell death. Nutritional therapy is essential to activate the brain and to control the brain function that is linked to accelerated aging and the severity of Type 2 diabetes. Compounds such as caffeine, Indian spices, magnesium, xenobiotics and LPS should be carefully assessed to prevent the induction of Type 3 diabetes that will lead to accelerated Type 2 diabetes and multiple organ disease in the developing and developed world.
RELEVANT REFERENCES:
1. Caffeine consumption with Relevance to Type 3 diabetes and accelerated brain aging. Research and Reveiws: Neuroscience. 1,1, December, 2016.
2. Nutrition Therapy Regulates Caffeine Metabolism with Relevance to NAFLD and Induction of Type 3 Diabetes. J Diabetes Metab Disord. 2017; 4: 019.
3. Type 3 diabetes with links to NAFLD and Other Chronic Diseases in the Western World. International Journal of Diabetes. 2016; 1:1-5.
4. Diet and Nutrition reverse Type 3 Diabetes and Accelerated Aging linked to Global chronic diseases. J Diab Res Ther. 2016; 2(2). 5. Insulin Therapy and Autoimmune Disease with Relevance to Nonalcoholic Fatty Liver Disease. Non Alcoholic Fatty Liver Disease. An Update. IntechOpen. October, 2018
6. Nutrition increases Survival and Reverses NAFLD and Alzheimer's disease Ian J Martins ·First Edition edited by Alina Berdos, 01/2015; LAP LAMBERT., ISBN: 978-3-659-78371-5. Printed/Ebook Release
Ian,
The first question to be addressed is what does type 2 and type 3 diabetes have in common? The answer, hypothesized, is insulin resistance. Hyperglycemia produces glycated RBC (HbA1c), glycated proteins, that produced Advanced Glycation End products (AGEs); and what still needs to be developed are analyte testing for glycated albumin and, most importantly, glycated insulin, the etiology of insulin resistance. Glycated protein, I hypothesize, is what stimulates aggregation of protein into amyloid plaques.
Insulin resistance is a progressive disease, not because of glucose. Hyperinsulinemia produces type 2 diabetes and, a study we conducted showed that all the comorbid diseases associated with diabetes 2 develop before a diagnosis of diabetes. Insulin is the problem. Most comorbid diseases are reversible when insulin is reigned in.
Nutritional interventions to reverse Type 2 diabetes and your listed supplements are still “downstream” treatments that are not treating liver function and hepatic immune system. All comorbid diseases can be traced back to the liver function and its related digestion problems. What is not appreciated, by other than clinical nutritionists, is the immense impact of digestive problems.
Liver dysfunction, not producing bile, sets up digestive problems leading to digestive fermentation [this problem can be exacerbated by H. pylori infections] producing alcohol and gas = acid reflux. This is the foundation of nonalcoholic fatty liver disease; which is, actually, “brewery syndrome” alcohol.
Unable to digest and adsorb amino acids from the food [because of bile deficiency] the body needing to replenish its amino acid pool, start catabolizing muscle, leading to sarcopenia [seen in woman’s “bat wings” and men’s calves getting thinner] Muscles and bones cross- talk constantly, and when muscles get smaller, the bones start loosing minerals.
It is free, ionized calcium from bones that produce arteriosclerosis, plugging the arteries that produce myocardial infarction.
The pancreas programmed cell death, apoptosis, is triggered by its mitochondria. When adenine triphosphate is not being produced and deposited on the brush border of the cell, the mitochondria commit suicide. In the pancreas, conversion of glucose increase into insulin secretion involves mitochondria.
Let’s first correct liver dysfunction and improve digestion, to support the body’s metabolism
Dear Dr Viana,
Thank you for your mail.
Yours sincerely, Ian Martins (Ph D)
Fellow of International Agency for Standards and Ratings (IASR) https://sites.google.com/site/internationalindexing/advisory-board Centre of Excellence for Alzheimer's Disease Research and Care Sarich Neuroscience Research Institute
Edith Cowan University 8 Verdun Street, Nedlands 6009. Western Australia, Australia
From my point of view, this is an extremely interesting question. That type 3 and type 2 are related has been published repeatedly in the meantime. Article Alzheimer's disease and Type 2 Diabetes mellitus are distinc...
It is also known that type 3 is associated with an increase in glucose levels in the brain which could also be an indicator that both diseases are closely linked to each other.Article Evidence for brain glucose dysregulation in Alzheimer's disease
Some papers examine metabolic connections after both diseases have developed. So I searched for papers that try to identify the causes a little earlier. I came across a paper that also points to the dysfunction of mitchondria.Article Etiology of type 2 diabetes and Alzheimer's disease: Explori...
The next logical step was to find a connection between nutrition and the positive effects on both diseases and I also found it here.Article Feeding mitochondria: Potential role of nutritional componen...
To answer the question, I would say that both diseases are highly entangled and that the intensity of one gives an indication of the other. Based on what I have read so far, I would not see type 3 as the cause for type 2. My suggestion would be to investigate the common causes at earlier stages and that is, for example, the onset and prevention of mitchondria malfunction. In my opinion, your nutrition findings provide an indication that perhaps it could go that way.
Dear Ruediger Buchkremer,
THANK YOU for your mail.
Yours sincerely, Ian Martins (Ph D)
Fellow of International Agency for Standards and Ratings (IASR) https://sites.google.com/site/internationalindexing/advisory-board Centre of Excellence for Alzheimer's Disease Research and Care Sarich Neuroscience Research Institute
Edith Cowan University
8 Verdun Street, Nedlands 6009.
Western Australia, Australia
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