Suppose your friend is diagnosed with type 2 diabetes, then works hard to lose 50 pounds. He takes himself off all his medications and his blood sugars are now normal. What would you say to him? Probably something like “Great job. You’re really taking care of yourself. Keep it up!” What you wouldn’t say is something like “You’re such a dirty, filthy liar. My doctor says this is a chronic and progressive disease so you must be lying ”. It seems perfectly obvious that diabetes reversed because your friend lost all that weight. And that’s the point. The disease is reversible.
The idea of “reversing” is describing the well managed type 2 diabetes that can be maintained without the outcome of complications (eye disease, kidney disease, etc.). And it is totally possible to have type 2 (or type 1 diabetes for that matter) and have no complications – however, this takes careful management and is largely driven by the patient and their access to quality healthcare.
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Like trials with any other supplement or herbal product, the primary question we must answer is “What exactly was studied?”. The cinnamon you have in your kitchen may be a single species of plant or a mix of different cultivars. Ceylon cinnamon (Cinnamommum verum) is more commonly found in the West. Cassia cinnamon (Cinnamomum aromaticum) is the version of cinnamon that’s been studied in trials. The chemical hydroxychalcone has been identified as a potential active ingredient, which is believed to modify the sensitivity of cells to insulin, enhancing their uptake. If that’s the true mechanism of action, then it would work in a manner similar to that of the drugs Avandia, Actos, and metformin (Glucophage). Given the active ingredient (or ingredients) have not yet been definitively isolated, the issue of studying cinnamon is problematic. There’s no way to assess the potency of any batch, which complicates any evaluation. And that may be a reason why the research with cinnamon is inconsistent and largely disappointing.
The physician can also make referrals to a wide variety of professionals for additional health care support. In the UK a patient training course is available for newly diagnosed diabetics (see DESMOND). In big cities, there may be diabetes centers where several specialists, such as diabetes educators and dietitians, work together as a team. In smaller towns, the health care team may come together a little differently depending on the types of practitioners in the area. By working together, doctors and patients can optimize the healthcare team to successfully manage diabetes over the long term.

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.

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).
There is no prescribed diet plan for diabetes and no single “diabetes diet”. Eating plans are tailored to fit each individual's needs, schedules, and eating habits. Each diabetes diet plan must be balanced with the intake of insulin and other diabetes medications. In general, the principles of a healthy diabetes diet are the same for everyone. Consumption of various foods in a healthy diet includes whole grains, fruits, non-fat dairy products, beans, lean meats, vegetarian substitutes, poultry, or fish.
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