Type 2 diabetes is generally very easy to get rid of.
Type 2 diabetes is the most common form of the various forms of diabetes, which literally means excessive urination. This is why there are also 2 forms of non-sugar diabetes, diabetes insipidus type 1 and 2 that are due to lack of vasopressin (antidiuretic hormone) or an inability to utilize vasopressin.
In the early stages of type 2 diabetes the pancreas works fine and actually secretes too much insulin as pancreatic beta cells respond directly to blood sugar levels. Insulin in normal levels is a vasodilator, but in the higher levels from type 2 diabetes it becomes a potent vasoconstrictor damaging blood vessels. This is what leads to the diabetic retinopathy, nephropathy (kidney damage), gangrene, high blood pressure, and much of the heart disease in type 2 diabetes. The elevated blood glucose leads to diabetic cataracts, elevated triglycerides and the excessive urination. The elevated blood sugar is also responsible for the immune suppression in diabetes. This is due to the fact that insulin is also responsible for the transport of vitamin C to cells including immune cells. When there is an excess of glucose, the insulin is busy trying to get the glucose down at the expense of the vitamin C, which reduces white blood cell activity leading to immune suppression.
In the long run, both the elevated glucose of the oral hypoglycemic drugs used to "treat" type 2 diabetes can damage the insulin producing beta cells leading to a lack or absence of insulin, and thus a requirement for external insulin. This can still be reversed, but is more difficult.
In the early stages of type 2 diabetes, the insulin receptors are either closed or plugged by fats, which prevents insulin from doing its job. Normally, when blood sugar rises insulin is secreted that latches on to the insulin receptors on cells. This sensitizes the cells to uptake glucose. If the insulin receptors are closed or plugged, the insulin cannot dock on the receptor to sensitize the cells and the glucose remains high, and the beta cells secrete more insulin in an attempt to force the blood sugar down.
The most common cause of type 2 diabetes is a lack of chromium and/or magnesium that both play important roles in keeping insulin receptors open. There are different forms of chromium and magnesium, some better absorbed and more effective than others. For chromium, chromium polynicotinate (not picolinate) is the safest and most effective. For magnesium, magnesium malate is the best absorbed and provides the most benefits including preventing insulin damage also by dilating blood vessels, and increasing cellular ATP levels.
Chromium and blood sugar abstracts
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"In conclusion, chromium supplementation seems to improve glycaemic control in type 2 diabetic patients, which appears to be due to an increase in insulin action rather than stimulation of insulin secretion."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"Chromium is an essential dietary trace mineral involved in carbohydrate and lipid metabolism. Chromium is required for cellular uptake of glucose, and chromium deficiency causes insulin resistance. Chromium supplementation may improve insulin sensitivity and has been used as adjunct treatment of diabetes mellitus in humans."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"CONCLUSION: Chromium supplementation gives better control of glucose and lipid variables while decreasing drug dosage in type 2 diabetes patients."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"CONCLUSIONS: These data demonstrate that corticosteroid treatment increases chromium losses and that steroid-induced diabetes can be reversed by chromium supplementation."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"Chromium (Cr3+) is an essential micronutrient for humans. Its main action is thought to be the regulation of blood sugar, because chromium deficiency is associated with diabetic-like symptoms, and chromium supplementation is correlated with increased glucose tolerance and insulin sensitivity."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"These data demonstrate that supplemental chromium had significant beneficial effects on HbA1c, glucose, insulin, and cholesterol variables in subjects with type 2 diabetes. The beneficial effects of chromium in individuals with diabetes were observed at levels higher than the upper limit of the Estimated Safe and Adequate Daily Dietary Intake."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"Chromium is an essential nutrient required for sugar and fat metabolism. Normal dietary intake of Cr for humans is suboptimal. The estimated safe and adequate daily dietary intake for Cr is 50 to 200 microg. However, most diets contain less than 60% of the minimum suggested intake of 50 microg. Insufficient dietary intake of Cr leads to signs and symptoms that are similar to those observed for diabetes and cardiovascular diseases. Supplemental Cr given to people with impaired glucose tolerance or diabetes leads to improved blood glucose, insulin, and lipid variables. Chromium has also been shown to improve lean body mass in humans and swine. Response to Cr is dependent upon form and amount of supplemental Cr. Chromium is a nutrient; therefore, it will only be of benefit to those who are marginally or overtly Cr deficient. Trivalent Cr has a very large safety range and there have been no documented signs of Cr toxicity in any of the nutritional studies at levels up to 1 mg per day. "
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"The influences that age-related decreases in chromium levels might have on increasing the risk to develop age-related impaired glucose metabolism, disordered lipid metabolism, coronary heart disease, arteriosclerosis, and type II diabetes mellitus are outlined, and the role that refined carbohydrates play in the development of compromised chromium status is presented."
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract"CONCLUSIONS--Ours is the first report of a significant reduction in serum TGs in a group of NIDDM patients treated with chromium. The low cost and excellent safety profile of chromium make it an attractive lipid-lowering agent for this population.
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract[Is chromium an essential or a toxic element?]
"Chromium holds a frequent and important place in toxicological literature. The large number of more or less important toxicological facts (e.g. allergic dermatoses, ulcer, perforations of the nasal septum, bronchitis, cancerogenity etc.) are the reason why chromium is conceived rather as a toxic element. On the other hand in the non-toxicological literature favourable actions of chromium are described (its relationship to carbohydrate utilization, the glucose tolerance factor, diabetes etc.) which may induce us to consider chromium an essential element. Is chromium toxic or essential? It is both. The concept of essential or toxic cannot be conceived statically, these terms are relative and depend on a number of other facts and data (dose, time, chemical form, individuality of the organism, interaction with other substances in the environment etc). This relative view has a more general validity not only for chromium but for trace elements in general and it is very important in particular with regard to prevention of health damage caused by deficiency or excess of a substance."
Chromium and magnesium effects on blood sugar-abstracts
www.ncbi.nlm.nih.gov/entrez/query...t=Abstract[Chromium: physiologic role and implications in human pathology]
[Article in French]
Dubois F, Belleville F.
Laboratoire de Biochimie B, CHU Nancy-Brabois, France.
Reported values for total body stores of chromium vary between 0.4 mg and 6 mg. Chromium stores may be higher in neonates than in adults, relative to body size, whereas tissular chromium may be depleted in the elderly. The recommended daily allowance for chromium is 50 to 200 micrograms/day but actual needs are poorly known. Digestive absorption is better for organic chromium, which is part of the "glucose tolerance factor" (GTF), than for inorganic chromium. Furthermore, chromium (VI) is better absorbed than chromium (III). In the body, chromium (VI) is rapidly reduced to chromium (III) by a number of metabolic pathways. Absorbed chromium binds to proteins, mainly to transferrin which exhibits a high affinity for chromium (III). Most absorbed chromium is eliminated through the kidneys. Renal excretion occurs according to a two or more-compartment model. Current methods used to assay chromium, i.e., atomic absorption spectrometry using a graphite furnace or neutron activation, are sufficiently sensitive and specific to evaluate chromium levels in blood, urine or hair. However, none of these levels accurately reflects chromium body stores. Chromium is part of the GTF molecule. This factor has no effect per se but may facilitate binding of insulin to insulin receptors and amplify the effects of insulin on carbohydrate and lipid metabolism. Chromium deficiency may play a role in a development of some forms of adult diabetes mellitus and of arteriosclerosis. Partial chromium deficiencies seem to be common, especially in individuals with high intakes of refined foods. Acute chromium poisoning is usually due to an excess of chromium (VI) and is sometimes seen in the chromium industry.(ABSTRACT TRUNCATED AT 250 WORDS)
www.ncbi.nlm.nih.gov/entrez/query...t=AbstractThe therapeutic potential of glucose tolerance factor.
McCarty MF.
Glucose Tolerance Factor (GTF) is synthesized in vivo from absorbed dietary chromium, and acts as a physiological enhancer of insulin activity, binding to insulin and potentiating its action about three-fold. Since GTF is well absorbed orally, the development of sufficiently concentrated and stable supplementary sources of this agent may enable convenient and physiologically appropriate pharmacological modulation of insulin activity. A review of the numerous physiological actions of insulin suggests a number of therapeutic applications for GTF, in such diverse ailments as diabetes mellitus, hyperlipidemia, reactive hypoglycemia, obesity, cancer, protein malnutrition or malabsorption, endogenous depression, Parkinsonism, hypertension and cardiac arrhythmias. GTF supplementation may also have value in preventive medicine.
www.ncbi.nlm.nih.gov/entrez/query...t=AbstractMagnesium Intake and Risk of Type 2 Diabetes in Men and Women.
Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, Manson JE, Hu FB.
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts. Division of Preventive Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts.
OBJECTIVE:-To examine the association between magnesium intake and risk of type 2 diabetes. RESEARCH DESIGN AND METHODS-We followed 85,060 women and 42,872 men who had no history of diabetes, cardiovascular disease, or cancer at baseline. Magnesium intake was evaluated using a validated food frequency questionnaire every 2-4 years. After 18 years of follow-up in women and 12 years in men, we documented 4,085 and 1,333 incident cases of type 2 diabetes, respectively. RESULTS:-After adjusting for age, BMI, physical activity, family history of diabetes, smoking, alcohol consumption, and history of hypertension and hypercholesterolemia at baseline, the relative risk (RR) of type 2 diabetes was 0.66 (95% CI 0.60-0.73; P for trend <0.001) in women and 0.67 (0.56-0.80; P for trend <0.001) in men, comparing the highest with the lowest quintile of total magnesium intake. The RRs remained significant after additional adjustment for dietary variables, including glycemic load, polyunsaturated fat, trans fat, cereal fiber, and processed meat in the multivariate models. The inverse association persisted in subgroup analyses according to BMI, physical activity, and family history of diabetes. CONCLUSIONS:-Our findings suggest a significant inverse association between magnesium intake and diabetes risk. This study supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables.
www.ncbi.nlm.nih.gov/entrez/query...t=AbstractDietary Magnesium Intake in Relation to Plasma Insulin Levels and Risk of Type 2 Diabetes in Women.
Song Y, Manson JE, Buring JE, Liu S.
Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, Massachusetts.
OBJECTIVE:-Higher intake of magnesium appears to improve glucose and insulin homeostasis; however, there are sparse prospective data on the association between magnesium intake and incidence of type 2 diabetes. RESEARCH DESIGN AND METHODS-In the Women's Health Study, a cohort of 39,345 U.S. women aged >/==" BORDER="0">45 years with no previous history of cardiovascular disease, cancer, or type 2 diabetes completed validated semiquantitative food frequency questionnaires in 1993 and were followed for an average of 6 years. We used Cox proportional hazard models to estimate multivariate relative risks (RRs) of type 2 diabetes across quintiles of magnesium intake compared with the lowest quintile. In a sample of 349 apparently healthy women from this study, we measured plasma fasting insulin levels to examine their relation to magnesium intake. RESULTS:-During 222,523 person-years of follow-up, we documented 918 confirmed incident cases of type 2 diabetes. There was a significant inverse association between magnesium intake and risk of type 2 diabetes, independent of age and BMI (P = 0.007 for trend). After further adjustment for physical activity, alcohol intake, smoking, family history of diabetes, and total calorie intake, the multivariate-adjusted RRs of diabetes from the lowest to highest quintiles of magnesium intake were attenuated at 1.0, 1.06, 0.81, 0.86, and 0.89 (P = 0.05 for trend). Among women with BMI >/==" BORDER="0">25 kg/m(2), the inverse trend was significant; multivariate-adjusted RRs were 1.0, 0.96, 0.76, 0.84, and 0.78 (P = 0.02 for trend). Multivariate-adjusted geometric mean insulin levels for overweight women in the lowest quartile of magnesium intake was 53.5 compared with 41.5 pmol/l among those at the highest quartile (P = 0.03 for trend). CONCLUSIONS:-These findings support a protective role of higher intake of magnesium in reducing the risk of developing type 2 diabetes, especially in overweight women.
www.ncbi.nlm.nih.gov/entrez/query...t=AbstractLow plasma magnesium in type 2 diabetes.
Walti MK, Zimmermann MB, Spinas GA, Hurrell RF.
Laboratory for Human Nutrition, Institute of Food Science and Nutrition, Swiss Federal Institute of Technology, Zurich, Switzerland. monika.waelti@ilw.agrl.ethz.ch
QUESTIONS UNDER STUDY/PRINCIPLES: Magnesium depletion has a negative impact on glucose homeostasis and insulin sensitivity in type 2 diabetic patients. Low plasma magnesium concentration is a highly specific indicator of poor magnesium status. In the USA and some European countries, plasma magnesium concentrations have been found to be decreased in diabetics. The aim of this study was to compare plasma magnesium concentrations of type 2 diabetics and healthy controls in Switzerland. METHODS: Plasma magnesium concentrations were determined in 109 type 2 diabetics and 156 age- and sex-matched healthy controls. RESULTS: Mean (+/- SD) plasma magnesium concentrations of the diabetics and controls were 0.77 +/- 0.08 and 0.83 +/- 0.07 mmol/L, respectively (p <0.001). Plasma magnesium concentrations were below the normal reference range in 37.6% of the diabetic patients and 10.9% of the control subjects (p <0.001). Plasma magnesium was not correlated with glycemic control as measured by HbA1c. CONCLUSIONS: Lower plasma magnesium concentrations and poor magnesium status are common in type 2 diabetics in Zurich, Switzerland.
www.ncbi.nlm.nih.gov/pubmed/15319146Intracellular magnesium and insulin resistance.
Magnesium, the second most abundant intracellular divalent cation, is a cofactor of many enzymes involved in glucose metabolism. Magnesium has an important role in insulin action, and insulin stimulates magnesium uptake in insulin-sensitive tissues. Impaired biological responses to insulin is referred to as insulin resistance. This review was designed to reach a better understanding of the mechanism involved in the correlation between magnesium and insulin resistance. Intracellular magnesium concentration is low in type 2 diabetes mellitus and in hypertensive patients. In patients with type 2 diabetes an inverse association exists between the plasma magnesium and insulin resistance due to intracellular changes. The suppressed intracellular magnesium concentration may result in defective tyrosine kinase activity and modify insulin sensitivity by influencing receptor activity after binding or by influencing intracellular signaling and processing. Intracellular magnesium deficiency may affect the development of insulin resistance and alter the glucose entry into the cell. CONCLUSIONS: Magnesium is required for both proper glucose utilization and insulin signaling. Metabolic alterations in cellular magnesium, which may play the role of a second messenger for insulin action, contribute to insulin resistance.
www.ncbi.nlm.nih.gov/pubmed/12537988Role of magnesium in insulin action, diabetes and cardio-metabolic syndrome X.
Magnesium (Mg) is one of the most abundant ions present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular Mg concentrations are tightly regulated by several factors. Among them, insulin seems to be one of the most important. In vitro and in vivo studies have demonstrated that insulin may modulate the shift of Mg from extracellular to intracellular space. Intracellular Mg concentration has also been shown to be effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli. A poor intracellular Mg concentration, as found in noninsulin-dependent diabetes mellitus (NIDDM) and in hypertensive patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in noninsulin-dependent diabetic and hypertensive patients. By contrast, in NIDDM patients daily Mg administration, restoring a more appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. The benefits deriving- from daily Mg supplementation in NIDDM patients are further supported by epidemiological studies showing that high daily Mg intake are predictive of a lower incidence of NIDDM. In conclusion, a growing body of studies suggest that intracellular Mg may play a key role in modulating insulin-mediated glucose uptake and vascular tone. We further suggest that a reduced intracellular Mg concentration might be the missing link helping to explain the epidemiological association between NIDDM and hypertension.
The herb Gymnema sylvestre is also great for opening insulin receptors, and has been sown to aid in the regeneration of beta cells. Taken before eating, it is also a very effective sugar blocker, blocking around 80% of the sugar ingested afterward for around 2 hours.
The supplement vanadyl sulfate functions like insulin, but can lower blood sugar bypassing the insulin receptors. It is also effective in opening insulin receptors.
The other cause is plugging of the insulin receptors, which is most often from excess body fat, In this case, losing weight often gets rid of the diabetes.