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.
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).
First, avoid the One-A-Day brand. All of the well-known One-A-Day products contain poor-quality products at low doses, and are full of unhealthy excipients, fillers, and preservatives. A high-quality multiple will require you to take three to six capsules a day, but will cover all the nutrients your body needs. For children, there are good liquid or powder multiples.
John’s naturopath, Susan DeLaney, ND, RN, from The Wellness Alliance in Carrboro, North Carolina, considers diabetes to be reversed when an individual is no longer dependent on medication to maintain blood glucose levels within a fairly normal range. Kathie Madonna Swift, MS, RD, LDN, owner of Swift Nutrition and author of The Inside Tract: Your Good Gut Guide to Great Digestive Health, describes reversal of diabetes as “restoring function and bringing the body back into glycemic balance.”
Now the question is, "what is the medicine that cures Diabetes?" The answer is, "Food is the medicine." Sounds interesting? Here in India, in the last 10 years we have seen a few thousands of them completely cured of Diabetes. All they have done is, they reversed the situation. To understand this, we first have to understand the bio-chemistry of Type-2 Diabetes. Type-2 Diabetes is caused either because our Pancreas not producing enough Insulin and/or our cells are not able to take the Insulin. Without the insulin accepted by the insulin receptors, the Glucose channel is not activated to take the Glucose. In most patients, even if Pancreas does not work well, Insulin units are given and then the insulin is slowly accepted by the Insulin receptors. But any food rich in Sugars, releases lot of Glucose instantly into the blood stream which cannot be absorbed by the cell at the same pace as the Insulin receptors are not capable/ready to accept the Insulin.
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
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).
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!