Detox with Chelation Therapy — Help Your Heart & Brain. “…Some chelating agents (e.g. L-Carnosine), including peptides like glutathione (e.g. bone broth) and metallothionein, have been well-researched and proven to transport and excrete toxins from the body, all without the need for expensive surgeries and risky medications. …”
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Trace Elements in Diabetes Mellitus “…Conclusion: The cause of diabetic hypomagnesaemia is multifactorial. An altered metabolism, a poor glycaemic control and osmotic diuresis may be contributory factors. Decreased serum zinc levels in diabetes may be caused by an increase in urinary loss. These decreased levels of trace elements cause disturbances in glucose transport across cell membrane lead to insufficient formation and secretion of insulin by pancreas which compromise in the antioxidant defense mechanisms. …” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809622/
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Variation in Macro and Trace Elements in Progression of Type 2 Diabetes “…4. Conclusion
Micro-/macronutrients play an important role in glucose metabolism, so understanding the impact of micronutrient deficiencies and the potential utility of supplementation is relevant to the prevention and/or management of type 2 diabetes mellitus. Macro elements are the natural elements of which the body needs more amounts and are more important than any other minerals. Trace elements are required in minute amounts to maintain a healthy body. They are required mainly as components of enzymes and hormones or are involved in the activation of enzymes. Electrolyte imbalance in diabetes is primarily a result of elevated blood glucose. With hyperglycemia, the body tries to rid itself of the excess blood glucose by increasing urinary output. Increased urination produces water and electrolyte loss, which then upsets the body’s balance of electrolytes. The balance is especially disturbed between sodium and potassium. Hypomagnesemia in diabetes is usually observed in patients with deficient metabolic control or is associated with the DM chronic complications, according to clinical and epidemiological studies. The responsible mechanisms for Mg deficiency in patients with diabetes have still not been clarified, mainly about the impact in the insulin resistance and in the development of diabetes and its chronic complications. Any alterations in calcium flux can have adverse effects on β-cell secretory function. The elevated cytosolic calcium will lead to the pathogenesis of complications of T2D. Chromium is required for normal carbohydrate metabolism and plays a role in glucose homeostasis. The effect of cobalt in diabetes causes decreases in systemic glucose production and increased tissue glucose uptake. A deficiency of copper results in glucose intolerance, decreased insulin response, and increased glucose response. Copper possesses an insulin-like activity and promotes lipogenesis. The role of iodine is correlated with thyroid hormone and it is clear that insulin resistance and β-cell function are inversely correlated with thyroid stimulating hormone which may be explained by insulin-antagonistic effects of thyroid hormones along with an increase in thyroid stimulating hormone (TSH). Elevated iron stores may induce diabetes through a variety of mechanisms, including oxidative damage to pancreatic β cells, impairment of hepatic insulin extraction by the liver, and interference with insulin’s ability to suppress hepatic glucose production. The effect of selenium in diabetes has contradictory effects; the antioxidant property of selenium prevents the development of complications in diabetic patients. While in other studies higher serum selenium concentrations were associated with a higher prevalence of diabetes. Manganese activated enzymes plays an important role in the metabolism of carbohydrates, aminoacids, and cholesterol and it is required for normal synthesis and secretion of insulin. Many of the complications of diabetes may relate to an increase in intracellular oxidant and free radicals associated with decrease in intracellular zinc and zinc dependent antioxidant enzymes. The vanadium salt was shown to induce a mechanism to reduce hyperglycemia and improve insulin action by increasing the glucose transporters activity via insulin receptor substrates 1 and 2 (IRS1/2) and phosphatidylinositol 3-kinase (PI 3-kinase). Nutrition management aims to improve health quality maintaining blood glucose levels in normal range so as to reduce the risk for diabetes complications. A well-balanced diet will maintain the impairment of essential macro- and micronutrients in patient with diabetes. In this paper, micronutrients recommendations have been displayed for the management of T2D and the prevention of its complications. …”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138889/
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Trace elements, oxidative stress and glycemic control in young people with type 1 diabetes mellitus. “…Our results suggest that high serum copper levels and oxidative stress correlate with glycemic control. Therefore, strict glycemic control, decreased oxidative stress, and a lower copper concentration might prevent diabetic complications in patients with type 1 diabetes mellitus. …” https://www.ncbi.nlm.nih.gov/m/pubmed/24315963/
SERUM NUTRIENT STUDIES
Zinc: Serum levels of zinc are usually found low in diabetic patients. Insulin is stored in a crystalline form and zinc is a constituent of crystalline insulin. Zinc affects the antigenic properties of insulin and the binding of insulin to hepatocyte membranes and a deficiency can lead to increased insulin resistance and hyperglycemia. Elevated glucose in turn produces hyperzincuria. Low zinc leads to poor or slowed wound-healing common in diabetic patients. Zinc has a biphasic effect, in that it is required for insulin storage and cellular binding, although high concentrations can lead to a reduction in insulin release.
Chromium: Chromium is a well-known component of the glucose tolerance factor (GTF). Other components include nicotinic acid, glycine, cystine, and glutamic acid. As a constituent of a metalo-enzyme, chromium is involved as a cellular receptor for insulin. A deficiency of chromium can result in elevated glucose, triglycerides, and cholesterol levels
Calcium: Calcium in a sufficient concentration is necessary for insulin release. In juvenile diabetic patients, serum calcium and magnesium are low with increased urinary excretion, along with decreased parathyroid hormone activity. These conditions are not present in adult onset diabetic (AOD) patients.
Copper: A deficiency of copper results in glucose intolerance, decreased insulin response, increased glucose response and is associated with hypercholesterolemia and atherosclerosis. Copper possesses an insulin-like activity and promotes lipogenesis. Serum copper is elevated in AOD patients.
Manganese: Manganese deficiency can impair glucose utilization. Intra-uterine deficiency produces islet cell atrophy. Hepatic manganese is elevated in some forms of diabetes, and may be related to increased arginase activity.
Iron: Excess iron accumulates in the pancreas and causes tissue injury. Excess iron relative to copper results in increased lipid peroxidation.
Selenium: Insulin reserves are diminished with deficiency of selenium and can contribute to glucose intolerance. Selenium deficiency results in decreased glutathione peroxidase activity.
Vitamin A: Vitamin A aids in the stimulation of insulin release from the pancreas. However, vitamin A is required in low concentrations and can inhibit insulin release at high concentrations.
Thiamin: Vitamin B1 is low in the serum of diabetic patients, and is related to reduced transketolase activity. Deficiency of B1 may be related to the development of diabetic neuropathy.
Pyridoxine, B12: Plasma vitamin B6 and pyridoxal 5-phosphate (P5P) activity is reduced in AOD patients. B12 deficiency is common in insulin dependent diabetics (IDD) and may result in pernicious anemia.
Ascorbic Acid: Plasma ascorbate is low in diabetic patients with increased dehydroascorbate levels. AOD patients have a higher turnover of ascorbic acid.
Vitamin D: Vitamin D is decreased in juvenile and elevated in AOD individuals. Vitamin D enhances insulin production, and is synergistic to, calcium, copper, PTH, insulin, and estrogen.
Vitamin E: Vitamin E requirements are increased in diabetic patients. High intake can reduce oxidative stress and improve the action of insulin. http://www.traceelements.com/Docs/News%20May-June%2099.pdf
