In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).
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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.
A success story? Perhaps. But experts advise caution. For one thing, because Sweet Eze contains six different ingredients -- and because the severity of diabetes symptoms can fluctuate on their own -- it's hard to say what exactly is responsible for Cottingham's improvement. For another, supplements carry their own risks. Some products don't contain the ingredients listed on their labels. Others come mixed with dangerous -- and unlisted -- ingredients. And scientists are just beginning to verify which ones actually work.
Other research conducted at the same institute studied possible regeneration of the islets of langerhans in rats that were made diabetic for the study and then given gymnema sylvestre leaf extracts. The diabetic rats were able to double the number of their islets and beta cell numbers. Researchers felt that the herbal therapy was able to bring blood sugar stability by repairing the pancreas and increasing insulin secretion.
If you google “diabetes cure” you are directed to websites like WebMD and the Mayo Clinic where you find information on diet, exercise, medication, and insulin therapy, but nothing about the cure. This lack of information may have to do with the fact that Americans spend $322 billion a year to treat diabetes, $60 billion a year on weight-loss programs, and $124 billion a year on snack foods. This is about 3% of the US economy! Because so many peoples’ livelihoods are supported by diabetes and its main cause, obesity, the viral effect of people getting cured and telling others is greatly diminished.