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Several prediabetes interventions exist based on evidence from the landmark Diabetes Prevention Program (DPP) study. The DPP study reported that moderate weight loss (5-7% of body weight, or ~10-15 lbs. for someone weighing 200 lbs.), counseling, and education on healthy eating and behavior reduced the risk of developing type 2 diabetes by 58%. Data presented at the ADA 2014 conference showed that after 15 years of follow-up of the DPP study groups, the results were still encouraging: 27% of those in the original lifestyle group had a significant reduction in type 2 diabetes progression compared to the control group.
In type 1 diabetes, the body produces none of the insulin that regulates our blood sugar levels. Very high glucose levels can damage the body's organs. Patients with type 2 diabetes, however, do produce insulin - just not enough to keep their glucose levels normal. Because I was fit and not overweight (obesity is a major risk factor in type 2 diabetes; however, a number of non-obese people, particularly members of south Asian communities, are also prone to it), my doctor told me I could control my condition with diet alone.
Hypoglycemia is also more likely in the first few weeks or months after someone develops type 1 diabetes. During this period — sometimes called a diabetic "honeymoon" — a child's pancreas may temporarily recover the ability to make insulin. If the insulin dose is not appropriately reduced, the combination of the child's own insulin and the injected insulin may be too much for the body, driving blood sugar levels down too low.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
Meanwhile, American Diabetes Scientist Zhen Gu, PhD, a professor in the Joint University of North Carolina/North Carolina State University Department of Biomedical Engineering, is working to develop a “smart insulin” patch that imitates the body's beta cells by both sensing blood glucose levels and releasing insulin using a nanotechnology that leverages bioengineering, biochemistry and materials science.
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).
"What is interesting is that some patients retain beta cell function for over 50 years," he said. "And, it seems if you retain some, that's a lot better." So, for Darkes to still have some functioning beta cells would not be impossible, but it wouldn't eliminate the disease, Von Herrath said. "Depending on how many beta cells he has, maybe his form of type 1 diabetes was not very severe."
Panax ginseng (Korean ginseng), which has a long history of use as a hypoglycemic agent. At least five constituents of this herb have been shown to exert hypoglycemic effects. In one study, treatment with ginseng lowered blood glucose levels and improved mood and psychological performance as compared with placebo. Recommended dosage is 100–200 mg/day.14
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Adams is the founder and publisher of the open source science journal Natural Science Journal, the author of numerous peer-reviewed science papers published by the journal, and the author of the world's first book that published ICP-MS heavy metals analysis results for foods, dietary supplements, pet food, spices and fast food. The book is entitled Food Forensics and is published by BenBella Books.
About the author:Mike Adams (aka the "Health Ranger") is a best selling author (#1 best selling science book on Amazon.com) and a globally recognized scientific researcher in clean foods. He serves as the founding editor of NaturalNews.com and the lab science director of an internationally accredited (ISO 17025) analytical laboratory known as CWC Labs. There, he was awarded a Certificate of Excellence for achieving extremely high accuracy in the analysis of toxic elements in unknown water samples using ICP-MS instrumentation. Adams is also highly proficient in running liquid chromatography, ion chromatography and mass spectrometry time-of-flight analytical instrumentation.
The bottom line is that diabetes can be bad news—but this doesn’t have to be the case. Interventions can prevent or delay the disease in people with prediabetes. The Diabetes Prevention Program (DPP), a large study of people at high risk of diabetes, has established a prevention plan that’s both feasible and cost-effective. The DPP showed that weight loss and increased physical activity reduced the development of type 2 diabetes by 58% during a three-year period.
The diet was strict: three litres of water a day, three 200-calorie food supplements (soups and shakes) and 200 calories of green vegetables. Thanks to my doctor's dietary guidance, and running three times a week, I had already lost a stone. Yet my glucose levels were still above 6mmol/L (millimols per litre), the upper limit for a healthy person without diabetes. According to Taylor, I had to lose a sixth of my pre-diagnosis bodyweight.
One easy way to increase your fat content and quit snacking is to begin your meal by eating an avocado. I and others I know have used this trick to easily quit snacking. Avocados protect you from one of the reasons some dietary research wrongly claims that high-fat diets are bad for you: the danger of gorging yourself on delicious, fatty foods. With plain avocados, there is little danger of gorging. Another danger is clogging your arteries and giving yourself heart disease. But it’s been amply shown that the blame for that falls squarely on trans fats, like margarine. If you see any product with the words “partially hydrogenated” or “hydrogenated” in the list of ingredients, put it back, it’s a trans fat. On the other hand, any fat that comes directly from an animal or plant is not a trans fat and can be safely consumed.