Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..
At his first visit, the naturopathic doctor told John he’d be “off medication and free of diabetes in three months.” John left the doctor’s office with instructions to eat a low-carb diet. He’d been on a low-fat diet for years because of heart problems, but while he’d cut the fat, his meals included many highly processed foods. His new diet included “a lot of salads and healthful, organic foods.” He was given several whole food supplements that he says were “simple to mix and tasted good.”
Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.[48] This new method autologous nonmyeloablative hematopoietic stem cell transplantation was developed by a research team composed by Brazilian and American scientists (Dr. Julio Voltarelli, Dr. Carlos Eduardo Couri, Dr Richard Burt, and colleagues) and it was the first study to use stem cell therapy in human diabetes mellitus This was initially tested in mice and in 2007 there was the first publication of stem cell therapy to treat this form of diabetes.[73] Until 2009, there was 23 patients included and followed for a mean period of 29.8 months (ranging from 7 to 58 months). In the trial, severe immunosuppression with high doses of cyclophosphamide and anti-thymocyte globulin is used with the aim of "turning off" the immunologic system", and then autologous hematopoietic stem cells are reinfused to regenerate a new one. In summary it is a kind of "immunologic reset" that blocks the autoimmune attack against residual pancreatic insulin-producing cells. Until December 2009, 12 patients remained continuously insulin-free for periods ranging from 14 to 52 months and 8 patients became transiently insulin-free for periods ranging from 6 to 47 months. Of these last 8 patients, 2 became insulin-free again after the use of sitagliptin, a DPP-4 inhibitor approved only to treat type 2 diabetic patients and this is also the first study to document the use and complete insulin-independendce in humans with type 1 diabetes with this medication. In parallel with insulin suspension, indirect measures of endogenous insulin secretion revealed that it significantly increased in the whole group of patients, regardless the need of daily exogenous insulin use.[74]

There are many promising studies suggesting chromium supplementation may be effective, but they are far from conclusive. For example, a small study published in the journal Diabetes Care compared the diabetes medication sulfonylurea taken with 1,000 mcg of chromium to sulfonylurea taken with a placebo. After 6 months, people who did not take chromium had a significant increase in body weight, body fat, and abdominal fat, whereas people taking the chromium had significant improvements in insulin sensitivity.
Sugars raise insulin levels, and over extended periods of time, damage the pancreas and cause insulin resistance, a precursor for diabetes. Fructose is the top offender in the sugar world, as it is recognized as a toxin the body and has no proven benefit to the body. Fructose is immediately taken to the liver, where it must be processed, and some doctors now suggest that this may be a large factor in development of fatty liver disease. Excess sugar in the bloodstream also increases the release of cortisol and adrenaline (more on those in a minute), slows the immune response, decreases necessary Leptin levels and promotes fat storage. There are various types of sugar and sweeteners, and while all should be limited, some are worse than others:
Knowing your blood-sugar levels and acting accordingly are among the most important ways to treat T1D. Monitoring lets a person know when insulin may be needed to correct high blood sugar or when carbohydrates may be needed to correct low blood sugar. Monitoring blood sugar can be done using traditional blood-sugar meters or continuous glucose monitors (CGMs).

Unfortunately, most people are not given the benefit of this approach. When diagnosed with diabetes, most people are told to avoid sugar (good step, not the solution). If the problem is bad enough, they are told to take medication to give the body insulin. The problem is, as we saw above, diabetes is a problem with the body’s regulation of insulin, caused by a resistance to insulin and an overproduction to remove toxic amounts of glucose in the bloodstream. Insulin is also dangerous if it is left circulating the the blood. Somehow, treating too much circulating glucose and insulin with more insulin doesn’t seem like the right approach…
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).
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Diabetics often find their bodies swinging wildly out of equilibrium. In Type 1 Diabetes, the body attacks insulin-producing cells in the pancreas, causing a rise in blood sugar levels. In Type 2 Diabetes there is insufficient insulin produced in the pancreas, which slows the metabolism and elevates blood sugar levels. Both conditions, if not treated correctly, can cause a host of unpleasant side effects including high blood pressure, neuropathy, kidney damage, and in extreme cases amputation and even death.

Alternative: “I’m a fat-atarian,” says DeLaney, who tells her patients to avoid low-fat foods. She encourages them to eat whole-fat dairy products, egg yolks, butter, olive oil, and avocado. “Restoring healthful fats to our diets as well as eliminating trans fats and all refined oils that help deplete our fat and vitamin stores will help nourish the body and reduce the need for diabetes medication.”
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FEED YOUR GUT BUGS, not just yourself. There are trillions of bugs that live in your gut – their health is critical in determining your health. Many studiesshow links between the state of your gut bugs (your microbiota) and type 2 diabetes. Start improving the health of your gut immediately by eating five servings of different coloured vegetables each day. The non digestible fibre in vegetables is the preferred food for your gut bacteria and when your gut bugs are happy, you will be happy. The wider the variety of colours, the more phytonutrients you will be getting.

Once you have diabetes, it is there for life. I help people to get their blood glucose levels back to or as near as possible the normal range. Firstly this will help you to feel better in the short term but it also helps to protect your blood vessels which can become very irritated and damaged by high glucose levels. Focussing on healthy eating, limiting unprocessed foods and getting a wide variety of fruits and vegetables in the diet helps.
Drugs of this class decrease the absorption of carbohydrates from the intestine. Before being absorbed into the bloodstream, enzymes in the small intestine must break down carbohydrates into smaller sugar particles, such as glucose. One of the enzymes involved in breaking down carbohydrates is called alpha-glucosidase. By inhibiting this enzyme, carbohydrates are not broken down as efficiently, and glucose absorption is delayed.
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