Cutting out the refined, processed starches and sugars, BG rebound into a normal range very quickly. My experience is when people begin to be more conscious of their food intake and physical activity, which happens immediately after being diagnosed with pre diabetes or diabetes, they begin to make better food choices and cut out the foods they know are not healthy.

Taylor and his colleagues observed that people who were unable to restart normal insulin production had lived with diabetes for a longer time. Individuals who had lived with diabetes for an average of 3.8 years could not correct their condition through weight loss, while those who had it for an average of 2.7 years were able to regain normal blood sugar control.


Type 2 diabetes is the most common form of diabetes, and unlike type 1 diabetes, it usually occurs in people over the age of 40, especially those who are overweight. Type 2 diabetes is caused by insulin resistance, which means that the hormone insulin is being released, but a person doesn’t respond to it appropriately. Type 2 diabetes is a metabolic disorder that’s caused by high blood sugar. The body can keep up for a period of time by producing more insulin, but over time the insulin receptor sites burn out. Eventually, diabetes can affect nearly every system in the body, impacting your energy, digestion, weight, sleep, vision and more. (5)

Although chromium does have an effect on insulin and on glucose metabolism, there is no evidence that taking chromium supplements can help in the treatment of diabetes. But chromium is found in many healthy foods, such as green vegetables, nuts, and grains. Studies have suggested that biotin, also called vitamin H, when used with chromium, may improve glucose metabolism in people with diabetes. But no studies have shown that biotin by itself is helpful.
"Perfect glycemic control" would mean that glucose levels were always normal (70–130 mg/dl, or 3.9–7.2 mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications.[17]

People with type 1 diabetes (T1D) can live long, happy lives with proper care and disease management. Advancements in medication types and delivery methods give people the freedom to choose which treatment options work best with their particular circumstance. T1D prognoses can be greatly improved with a combination of treatments and lifestyle choices.
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).

Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.
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