The gastric bypass that Benari got, for instance, resculpts the digestive system. Surgeons seal off a large part of the stomach using staples, leaving behind a small upper pouch, while rerouting part of the small intestine to the new pouch, bypassing the rest. The net result is that less food can fit in the stomach, and there’s much less time for that food to be turned into calories before it exits the body. The vertical sleeve gastrectomy, the most popular surgery in recent years, only tinkers with the stomach, using staples to turn it into a small banana-shaped organ. (There are less permanent procedures, such as the lap band, but these have fallen out of favor due to their ineffectiveness).
What’s critical is not necessarily the cutoff itself, but where someone falls within the ranges listed above. The level of risk of developing type 2 diabetes is closely related to A1c or FPG at diagnosis. Those in the higher ranges (A1c closer to 6.4%, FPG closer to 125 mg/dl) are much more likely to progress to type 2 diabetes, whereas those at lower ranges (A1c closer to 5.7%, FPG closer to 100 mg/dl) are relatively more likely to revert back to normal glucose levels or stay within the prediabetes range. Age of diagnosis and the level of insulin production still occurring at diagnosis also impact the chances of reverting to normoglycemia (normal blood sugar levels).

Initial clinical trial results, published in a 2012 PLOS One paper, reported that two doses of BCG spaced four weeks apart led to reductions in autoreactive T cells, an increase in Tregs and what turned out to be a transient increase in insulin production. But by the end of that short, 20-week trial, there was no reduction in HbA1c, the established measure of blood sugar levels over time. An extension and expansion of that trial with long term follow-up, the current results are based on data from 282 human study participants – 52 with type 1 diabetes who participated in the BCG clinical trials and 230 who contributed blood samples for mechanistic studies.
Treatment plans are designed around the pattern of insulin normally supplied by the pancreas throughout the day in someone without diabetes. In general, this involves providing a fairly steady "background" level of insulin to control blood sugar levels between meals and overnight, along with doses of rapid- or short-acting insulin to handle the fast rises in blood sugar that occur with meals.
Although the promises are big, these technologies are still far from the market. First, clinical trials will have to show they do work. Then, the price could be steep, as cell therapy precedents for other applications, such as oncology, come with price tags that reach the six figures and are finding difficulties to get reimbursed. Considering that compared to cancer, diabetes is not an immediately life-threatening disease, health insurers in some countries might be reluctant to cover the treatment.
If the patient were to gain weight back or scale back on their physical activity program, high blood glucose would return. If they were to overeat at a meal, their blood glucose probably would continue to go higher than someone without diabetes. Also, the decreased insulin production and/or increased insulin resistance that led to the initial diabetes diagnosis will gradually intensify over the years and during periods of stress. In time, the patient who could maintain normal blood glucose with diet and exercise alone may discover that he or she needs to add oral diabetes medications — or perhaps even insulin injections — to keep blood glucose in a healthy range.
The NIH National Institute of Diabetes and Digestive Diseases and Kidney Diseases says it, “currently supports studies that are working toward obtaining FDA licensure to reclassify islet allo-transplantation as therapeutic. In other countries, such as Canada and Scandinavia, islet allo-transplantation is no longer considered experimental and is an accepted therapy in certain patients.” It adds that “Some patient advocates and islet researchers feel that islet allo-transplantation is close to having a therapeutic label.”
If you have gestational diabetes, you should first try to control your blood glucose level by making healthy food choices and getting regular physical activity. If you can’t reach your blood glucose target, your health care team will talk with you about diabetes medicines, such as insulin or the diabetes pill metformin, that may be safe for you to take during pregnancy. Your health care team may start you on diabetes medicines right away if your blood glucose is very high.
In investigating how BCG administration produces its beneficial effects, the research team identified a mechanism never previously seen in humans in response to treatment with any drug – a shifting of the process of glucose metabolism from oxidative phosphorylation, the most common pathway by which cells convert glucose into energy, to aerobic glycolysis, a process that involves significantly greater glucose consumption by cells. The researchers also found that BCG could reduce blood sugar elevations in mice that were caused by means other than autoimmune attack, raising the possibility that BCG vaccines could also be beneficial against type 2 diabetes.”
Q. I have Type 2 diabetes, and I currently take 1,000 milligrams (mg) of metformin twice a day, 5 mg of Onglyza (saxagliptin) once a day, and 5 mg of glipizide once a day. Does it matter when I take the Onglyza and the glipizide? I used to take them both at breakfast, but I thought I might get better blood-glucose-lowering coverage if I took one of them with lunch and one with dinner.

The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).


Both type 1 and type 2 diabetes mellitus are chronic conditions that can only be managed using insulin, anti-diabetes medications, lifestyle changes, etc., but cannot be cured. Gestational diabetes generally resolves on itself after the delivery. If not managed properly, diabetes can cause several other complications, like hypoglycemia, diabetic ketoacidosis, nonketotic hyperosmolar coma, etc. Other serious and long-term complications include cardiovascular diseases, chronic renal failure, diabetic retinopathy, etc.
In type 2 diabetes the body has an increasingly harder time to handle all the sugar in the blood. Large amounts of the blood sugar-lowering hormone insulin are produced, but it’s still not enough, as insulin sensitivity decreases. At the time of being diagnosed with type 2 diabetes, diabetics usually have ten times more insulin in their bodies than normal. As a side effect, this insulin stores fat and causes weight gain, something that has often been in progress for many years before the disease was diagnosed.
Despite the encouraging findings, more research will be necessary to confirm that S. oblonga is an effective treatment for type 2 diabetes and to determine whether it offers any long-term health benefits. The researchers also want to look into the question of whether or not S. oblonga can prevent type 2 diabetes. They suggested that an extract could be added to a food or beverage for easy use.
Don’t let anyone discourage you! Your doctor may be skeptical and resist your efforts to cure yourself, but persevere! Worst case, put your doctor in touch with Dr. Jason Fung, a nephrologist who grew tired of simply controlling pain for his end stage kidney patients at the end of lives ravaged by diabetes, and decided to do something to help them thrive with the energy of a healthy life well-lived. Now follow the simple rules plainly and freely explained above and help yourself!
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