A further danger of insulin treatment is that while diabetic microangiopathy is usually explained as the result of hyperglycemia, studies in rats indicate that the higher than normal level of insulin diabetics inject to control their hyperglycemia may itself promote small blood vessel disease.[14] While there is no clear evidence that controlling hyperglycemia reduces diabetic macrovascular and cardiovascular disease, there are indications that intensive efforts to normalize blood glucose levels may worsen cardiovascular and cause diabetic mortality.[42]
Carbohydrate Spike Test-On one day of your blood sugar readings (after at least 2-3 days of testing) eat a food high in simple carbs at your test meal (a potato, rice, etc) along with any vegetables, but in the absence of any fats or proteins. This will test your basic glucose reaction to high levels of glucose not mitigated by fat. Record these numbers as usual. Important note: if you usually eat a low-carbohydrate diet, this number might seem higher than it should be. This is because of decreased tolerance to carbohydrates and is not a cause for concern.
The researchers followed the participants after they had completed an eight-week low-calorie-milkshake diet and returned to normal eating. Six months later, those who had gone into remission immediately after the diet were still diabetes-free. Though most of those who reversed the disease had had it for less than four years, some had been diabetic for more than eight years.

As self-management of diabetes typically involves lifestyle modifications, adherence may pose a significant self-management burden on many individuals.[65] For example, individuals with diabetes may find themselves faced with the need to self-monitor their blood glucose levels, adhere to healthier diets and maintain exercise regimens regularly in order to maintain metabolic control and reduce the risk of developing cardiovascular problems. Barriers to adherence have been associated with key psychological mechanisms: knowledge of self-management, beliefs about the efficacy of treatment and self-efficacy/perceived control.[65] Such mechanisms are inter-related, as one's thoughts (e.g. one's perception of diabetes, or one's appraisal of how helpful self-management is) is likely to relate to one's emotions (e.g. motivation to change), which in turn, affects one's self-efficacy (one's confidence in their ability to engage in a behaviour to achieve a desired outcome).[66]
Diabetes is an illness related to elevated blood sugar levels. When you stop releasing and responding to normal amounts of insulin after eating foods with carbohydrates, sugar and fats, you have diabetes. Insulin, a hormone that’s broken down and transported to cells to be used as energy, is released by the pancreas to help with the storage of sugar and fats. But people with diabetes don’t respond to insulin properly, which causes high blood sugar levels and diabetes symptoms.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
There has been a good amount of attention and time spent on discussing the “reversal” of diabetes, but there’s not been a lot of good facts to explain what this means. First, type 1 diabetes (an autoimmune disease) cannot be reversed, cured or avoided – period. It can be managed with insulin and made easier with good lifestyle choices like staying active and eating a healthy diet.
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.