When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs — the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.
All of the above contributing factors don’t usually happen by themselves. Since the body functions as a whole, a problem in one area will usually correlate to problems in others. A combination of the factors above can be the catalyst for a full blown case of diabetes (or a lot of other diseases). While researchers often look at a single variable when trying to discover a cure for a disease, often the best approach is one that addresses the body as a whole. As with all diseases, the best cure is good prevention, but certain measures can help reverse disease once it has occurred.
Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore, by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin-producing intestinal cells die off, they are boosted by additional oral medications.
But look closer. The results may be statistically significant, but they’re not that impressive compared to medication. Cinnamon lowered A1C by 0.09%, versus the usual 1% with medication. Give A1c reflects overall glucose trends, cinnamon doesn’t look that impressive. Even at the extreme of the confidence interval, cinnamon has, at best, 10% of the efficacy of drug treatments. At worst, it’s completely ineffective.
Schedule a yearly physical exam and regular eye exams. Your regular diabetes checkups aren't meant to replace regular physicals or routine eye exams. During the physical, your doctor will look for any diabetes-related complications, as well as screen for other medical problems. Your eye care specialist will check for signs of retinal damage, cataracts and glaucoma.
Chromium plays a vital role in binding to and activating the insulin receptor on body cells, reducing insulin resistance. Supplemental chromium has been shown to lower blood sugar levels, lipids, A1C, and insulin in diabetic patients. It can also help decrease one’s appetite, particularly for sweets. A dosage from 200 mcg to 2,000 mcg a day is safe. Higher doses are unnecessary and can cause acute kidney failure.
Vitamin C may make up for low blood levels of insulin, which normally works to help cells absorb the vitamin. Proper amounts of vitamin C may help the body maintain a good cholesterol level and keep blood sugar levels under control. But too much can cause kidney stones and other problems. Check with your doctor to see if a vitamin C supplement is right for you.
Some studies suggest that low magnesium levels may worsen blood glucose control in type 2 diabetes. There is also some evidence that magnesium supplementation may help with insulin resistance. For example, a study examined the effect of magnesium or placebo in 63 people with type 2 diabetes and low magnesium levels who were taking the medication glibenclamide. After 16 weeks, people who took magnesium had improved insulin sensitivity and lower fasting glucose levels.
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These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.