Momordica Charantia goes under a variety of names and is native to some areas of Asia, India, Africa and South America. Marketed as charantia, it is also known as karela or karolla and bitter melon. The herb may be prepared in a variety of different ways, and may be able to help diabetics with insulin secretion, glucose oxidation and other processes.
Mr. Tutty, who weighed about 213 pounds before the trial, lost a little more than 30 pounds, the average weight loss in the trial. The people in the study most likely to respond to the treatment were in their early 50s on average and younger than the nonresponders, and they had had diabetes for fewer years. The responders were also healthier before the trial: They had been taking fewer medications than nonresponders, had lower fasting glucose and hemoglobin A1c before the trial, and had higher baseline serum insulin levels. Three of those who went into remission had lived with diabetes for more than eight years.
I was diagnosed with Type 2 diabetes and started with a nutritionist two years ago. I was losing weight (20 lbs) and doing well on her prescribes diet. She reviewed my food log and comment that I was cutting down too low on my carbs. She said that it would damage my kidneys. I was concerned and slightly increased my carbs — which led to cravings and weight gain. Why was that the advice given? It failed.
“I have many ways to help patients manage diabetes, but it’s very hard to reverse,” says Dr. Rita Louard, director of the Clinical Diabetes Program at Montefiore Health System in Bronx, New York. Still, some diabetes experts will use the word “reverse” when talking about this topic, Louard says, acknowledging the controversy that exists when discussing diabetes reversal.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
There are many studies showing that by initialing lose 5% of current body weight and getting 150 minutes of exercise weekly can and do return many folks’ blood glucose levels back into a normal range. However we must continue these actions as lifestyle changes, not just a means to an end. The human body is incredible forgiving and will always move towards health when given the opportunity to do so.
Many studies show that lifestyle changes, such as losing weight, eating healthy and increasing physical activity, can dramatically reduce the progression of Type 2 diabetes and may control Type 1 diabetes. These lifestyle changes can also help minimize other risk factors such as high blood pressure and blood cholesterol, which can have a negative impact on people with diabetes.

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.
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.