Diabetes Testimonial & Okra (Part 3)

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[i] Department of Internal Medicine, Overlook Hospital, Summit, NJ, USA.
Hypomagnesemia has long been known to be associated with diabetes mellitus. Mather et al confirmed the presence of hypomagnesemia in nearly 25% of their diabetic out-patients. Low serum magnesium level has been reported in children with insulin-dependent diabetes and through the entire spectrum of adult type I and type II diabetics regardless of the type of therapy. Hypomagnesemia has been correlated with both poor diabetic control and insulin resistance in nondiabetic elderly patients.
Hypomagnesemia and diabetes mellitus. A review of clinical implications. Tosiello L;  Arch Intern Med. 1996 Jun 10;156(11):1143-8.  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=
[ii] Barbagallo, Mario et al. Effects of Vitamin E and Glutathione on Glucose Metabolism:  Role of Magnesium; (Hypertension. 1999;34:1002-1006.) American Heart Association http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&l
[iii] v57, Better Nutrition for Today’s Living, March ’95, p34.  http://www.mgwater.com/articles.shtml
[iv] Barbagallo, Mario et al. Effects of Vitamin E and Glutathione on Glucose Metabolism:  Role of Magnesium; (Hypertension. 1999;34:1002-1006.) American Heart Association http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=
[v] Hua H. et al: Magnesium transport induced ex vivo by a pharmacological dose of insulin is impaired in non-insulin-dependent diabetes mellitus.Magnes Res. 1995, Dec;   Magnes Res. 1995 Dec;8(4):359-66. PMID: 8861135 [PubMed – indexed for MEDLINE]  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display&DB=pubmed
[vi] A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure. Magnesium in Diabetes Mellitus; de Valk HW.   Neth J Med. 1999 Apr;54(4):139-46.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstr
[vii] Lower serum magnesium levels are associated with more rapid decline of renal function in patients with diabetes mellitus type 2.Clin Nephrol. 2005 Jun;63(6):429-36. PMID: 15960144  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&li
[viii] Diabetic ketoacidosis (DKA) is a dangerous condition that can cause you to lose consciousness. If untreated, it can be fatal. This is a diabetic crisis state, and can quickly lead to fatality, including cerebral edema, most often seen in children. It is also common in DKA to have severe dehydration and significant alterations of the body’s blood chemistry. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia. (ketones and acid in the bloodstream) Major components of the pathogenesis of diabetic ketoacidosis are reductions in effective concentrations of circulating insulin and concomitant elevations of counterregulatory hormones (catecholamines, glucagon, growth hormone and cortisol). These hormonal alterations bring about three major metabolic events: (1) hyperglycemia resulting from accelerated gluconeogenesis and decreased glucose utilization, (2) increased proteolysis and decreased protein synthesis and (3) increased lipolysis and ketone production.
[ix] Diabetic ketoacidosis: Check your ketones; From MayoClinic.com  Special to CNN.com  http://www.cnn.com/HEALTH/library/DA/00064.html
[x] This article exemplifies the AAFP 1999 Annual Clinical Focus on management and prevention of the complications of diabetes. Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non­insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. (Am Fam Physician 1999;60:455-64.)ABBAS E. KITABCHI, PH.D., M.D., and BARRY M. WALL, M.D. University of Tennessee, Memphis, College of Medicine Memphis, Tennessee   http://www.aafp.org/afp/990800ap/455.html
[xi] Chronic Renal Failure (Chronic Renal Insufficiency, Kidney Failure, Renal Insufficiency)  (CRF) Irreversible, progressive impaired kidney function. The early stage, when the kidneys no longer function properly but do not yet require dialysis, is known as Chronic Renal Insufficiency (CRI). CRI can be difficult to diagnose, as symptoms are not usually apparent until kidney disease has progressed significantly. Common symptoms include a frequent need to urinate and swelling, as well as possible anemia, fatigue, weakness, headaches and loss of appetite. As the disease progresses, other symptoms such as nausea, vomiting, bad breath and itchy skin may develop as toxic metabolites, normally filtered out of the blood by the kidneys, build up to harmful levels. Over time (up to 10 or 20 years), CRF generally progresses from CRI to End-Stage Renal Disease (ESRD, also known as Kidney Failure). Patients with ESRD no longer have kidney function adequate to sustain life and require dialysis or kidney transplantation. Without proper treatment, ESRD is fatal.
[xii] Sloan Kettering Health Care Information for Professionals: http://www.mskcc.org/mskcc/html/11571.cfm?RecordID=481&tab=HC

 

 

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