AUCTORES
Case Report
*Corresponding Author: Steve Yap, DSY Wellness and Longevity Center, Kuala Lumpur, Malaysia.
Citation: Steve Yap (2021) An Adjunct Treatment Reverses Chronic Insulin-dependent (Type 1) Diabetes in a Teenager. J, Biotechnology and Bioprocessing 2(9); DOI: 10.31579/2766-2314/061
Copyright: © 2021, Steve Yap, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 17 October 2021 | Accepted: 23 October 2021 | Published: 02 November 2021
Keywords: Type 1 diabetes mellitus, insulin-dependent diabetes, juvenile diabetes, autoimmune disorder, nutritional therapy
Globally, more than 30 million people suffer from diabetes mellitus type 1 (T1DM) characterized by pancreas producing little or no insulin hormone to facilitate glucose entering cells for energy production. T1DM patients tend to suffer a higher overall rate of atherosclerosis, cancer, and end-stage renal failure. No drug or surgical therapy seems to halt its annual upward trend amongst children and young adults. Consequently, a significant number of sufferers turn to complementary or alternative therapies for help to arrest this chronic endocrine condition. This paper discusses how a well-designed evidence-based dietary and nutritional therapy with some lifestyle modifications might offer a solution for this highly complex autoimmune disorder. The treatment outcome demonstrated a partial regeneration of pancreatic islet beta cells with substantial improvement for all relevant serum and urine markers tested.
Lee J., a slim 24-year old weighting 56kg, worked as an assistant chef at a restaurant serving local delicacies for a small town population in Peninsular Malaysia. He was on insulin injection for the past fifteen years after being diagnosed as suffering from juvenile diabetes (diabetes mellitus type I or T1DM) when he was eight years’ old. After been advised by his regular physician to reduce intake of refined starch and sugar during his initial years of administering his daily insulin, he felt that he was not gaining any weight like the rest of his school friends. Concerned about being laughed at as a ‘weakling’, he decided to resume his favourite noodles, buns, bread, biscuits, titbits, and sweet tropical fruits. He received no serious objections from his prescribing physician after raising this dietary issue with him. Worried about him developing early heart disease or hyperuricemia (elevated blood uric acid levels), his parents had discouraged him from consuming eggs, nuts, seeds, and beans. Over the past decade, the patient noticed that the amount of insulin prescribed for daily injection was raised on several occasions after tests confirmed his serum glucose gradual elevation. Being an insulin-dependent diabetic condition, he was instructed not to leave home without his insulin needle for which his parents paid. Having heard about complementary treatment for diabetes from a relative, he called on DSY Wellness Center to seek advice on how he could organise his diets while minimizing the use of insulin which often caused him to suffer from problems associated with hypoglycaemia (low blood glucose).
After reviewing his past and present medical records, the patient was advised to gradually make these dietary modifications with the objective of establishing a regular meal pattern with fairly consistent day-to-day caloric and carbohydrate intake:
The patient was also advised to initiate these lifestyle modifications with immediate effect:
Ceasing to cook protein food with sugary items under high temperatures. Formation in this manner of Advanced Glycated End-products (AGEs) in food could further damage his insulin-secreting beta cells. AGEs are accelerated in diabetes or during hyperglycaemic conditions, but their production also occurs in settings characterized by oxidative stress and chronic inflammation [37].
When the patient’s first set of blood and urine test results returned, he was advised to continue his insulin injection or any medication unless his regular physician ordered otherwise. As adjunct therapy, the following nutrients were prescribed to be taken after meals with the reasons explained to him:
Magnesium citrate (elemental value 16%): 1g TID. One in four diabetic patients [77] may suffer from hypomagnesemia, which can lead to poor diabetic control with higher HbA1c scores [78], early atherosclerosis [79] and microalbuminuria [80]. Its deficiency can cause retinopathy and hypertension [81], metabolic syndrome [82], and chronic diabetic complications [83] since it is a co-factor in more than 300 different enzyme systems in the body [84]. Insulin injection can enhance renal magnesium excretion [85]. Supplementation can improve insulin sensitivity and may stimulate insulin secretion [86].
T1DM is characterized by the infiltration of activated T-lymphocytes and monocytes into the islets of Langerhans of the pancreas, resulting in chronic inflammation and progressive destruction of the insulin-producing beta cells [87, 88]. Activated T-cells and cytokines secreted from immunocytes act synergistically to destroy these beta cells resulting in the development of this autoimmune disease [89]. Once islet auto-antibodies have developed, the progression to diabetes in antibody-positive individuals is determined by the age of antibody appearance and by the magnitude of the autoimmunity [90]. Globally, some 33 million people suffer from T1DM and its incidence increases by about 3% annually among children [91]. T1DM patients appear to face a higher overall incidence of cancer [92] and end-stage renal failure [93].
Vitamin D receptor (VDR) gene polymorphisms may determine risk of developing T1DM with the environment influencing the association between VDR genotype and T1DM risks [72]. The disorder commonly begins during childhood but may appear later in adulthood in a proportion of 30 to 40% of affected individuals [94].
Parent’s eating habits and the home food environment such as its accessibility and availability are important determinant of their children’s dietary intake [95, 96]. The likelihood of children making positive changes to their diets will be increased if their parents are involved and supportive. Vegetables and low-fructose citric fruits consumption should be raised [97] , while long-chain saturated fats intake should be lowered [98, 99] since atherosclerosis may be well-established when T1DM children reach adolescence [100, 101].
Increased intake of omega-3 fatty acids and fish oil is linked to reduced T1DM–associated autoantibody conversion [102]. Use of cod liver oil rich in vitamins A and D in the first year of life is associated with a significantly lower risk of T1DM [103]. Vitamin D3 supplementation in early childhood can offer protection against the development of T1DM [73, 104] as well as helping to reverse its increasing incidence [105].
A long list of environmental factors influences the risks for or progression to T1DM [87], which condition is on the rise globally [106] and especially in children [107]. The presence of multiple autoantibodies seems to have the highest positive predictive value for development of T1DM [108, 109]. Insulin autoantibodies, in contrast to the other autoimmune markers, are the only beta-cell specific antibodies [110].
There may be a link between viral infections and the first appearance or increase in islet antibodies [111-113] although the evidence is weak [114, 115]. However, viral infection of antigen presenting cells can locally raise inflammation and auto-reactive lymphocytes [116].
An early onset of T1DM can raise the child’s risk of learning disability [117]. Difficulties in diagnosing T1DM are a significant cause of diabetic ketoacidosis development in children with new-onset disease [118].
A cure for T1DM may require the provision or elicitation of new pancreatic islet beta cells as well as the reestablishment of immunological tolerance [119]. The limited regenerative ability of the endocrine pancreas may be linked to the defined number of pancreatic progenitors, which is generally incapable of compensatory growth in response to cell loss [120]. The inability to cure this chronic disorder is largely because of its highly complex pathophysiology [121].
Some 28% of the population in developed nations depends on complementary and alternatives modalities to treat their T1DM [28] although there seems to be insufficient research evidence to support differing nutritional needs for those with T1DM compared to type 2 diabetes [122].
The patient suffered from most of the major symptoms of juvenile diabetes such as polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss [123]. His dramatically reduced HbA1c score after three months’ therapy suggested a much lower level of glycated hemoglobin and a stronger diabetic control. Such a score could also be linked to his lower triglyceride levels [99]. The fasting insulin and glucose levels in November 2013 would suggest his pancreatic islet beta cells were releasing adequate insulin to meet his needs after some dietary modifications. This supports long-held belief that there would still be some functional beta cells in people with longstanding T1DM [124]. His chronic inflammatory conditions improved five-fold accompanied by much lower level urine microalbumin. The patient was delighted with the disappearance of any glucose from his urine sample taken at the end of the third month of therapy. This positive outcome was confirmed by the patient’s regular physician, who then advised a temporary halt to the administration of insulin pending further monitoring.
Although cytokines such as IL-1alpha, IL-1beta and IFN-gamma are widely implicated in the pathogenesis of autoimmune diabetes [125], local laboratories were unable to test these markers.
The patient was using the insulin pump and with flexible injection regimens designed for him to lead a normal lifestyle [126]. However, initial test results suggested his inability to benefit fully from these modern conventional therapie.
Extracts from the patient’s three months’ test results for 2013 were as follow:
The health outcome achieved by the patient suggested some form of pancreatic cell mass regeneration consequent upon undertaking this nutritional therapy which involved some lifestyle modifications. Further study involving a higher number of patients with similar conditions is warranted to elucidate its wider therapeutic benefits in the treatment of T1DM.
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