Keeping close tabs on your diet is a major way to help manage type 2 diabetes. A healthy diet for people with type 2 diabetes includes fresh or frozen fruit and vegetables, whole grains, beans, lean meats, and low-fat or fat-free dairy. Focus on eating fruit and non-starchy vegetables, like broccoli, carrots, and lettuce, and having smaller portions of starchy foods, meats, and dairy products. Be especially careful about loading up on foods that are high on the glycemic index (GI) and especially the glycemic load (GL), systems that rank foods according to how they affect glucose levels.
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.

“Our findings suggest that even if you have had type 2 diabetes for six years, putting the disease into remission is feasible”, says Prof Michael Lean from the University of Glasgow who co-led the study. “In contrast to other approaches, we focus on the need for long-term maintenance of weight loss through diet and exercise and encourage flexibility to optimise individual results.”
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).
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Exercise– Even the mainstream medical community recognizes the advantage of exercise, as it increases the muscles ability to use insulin and over time can help fix insulin resistance. All exercise isn’t created equal though and fortunately, smaller amounts of high intensity exercise have been shown to have a better effect on insulin levels (and weight loss) than an hour of daily moderate cardio. According to the Healthy Skeptic: “A pair of studies done at McMaster University found that “6-minutes of pure, hard exercise once a week could be just as effective as an hour of daily moderate activity“, according to the June 6, 2005 CNN article reporting on the study.” I recommend high intensity exercise anyway for its various health advantages, and it is great for diabetes control. too.
As diabetes management is affected by an individual's emotional and cognitive state, there has been evidence suggesting the self-management of diabetes is negatively affected by diabetes-related distress and depression.[67] There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population.[68][69] Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms.[70] This suggests that it may be important to target mood in treatment.
In 2003, ephedrine -- also known as ma huang -- became the first herbal stimulant ever banned by the FDA. It was a popular component of over-the-counter weight loss drugs. Ephedrine had some benefits, but it could cause far more harm, especially in high doses: insomnia (difficulty falling and staying asleep), high blood pressure, glaucoma, and urinary retention. This herbal supplement has also been associated with numerous cases of stroke.
He emphasizes lifestyle changes and weight loss as a first step. "We give them a 3-month trial of diet and lifestyle [modification] before starting medications," he says. "A lot of times, for many patients newly diagnosed, we will see the sugars melt back into the normal range" after the weight loss and other changes. He has seen it happen after a weight loss of 7% to 10% of their starting weight.

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.
Big pharma are in the early stages of developing their own cell therapy approaches for diabetes. Novo Nordisk, one of the largest providers of diabetes treatments, is bidding for stem cells and an encapsulation device, stating that the first clinical trial could take place in the “next few years.” Sanofi, also a big name in diabetes, is working with the German Evotec in a beta cell replacement therapy for diabetics.
Most of those foods are refined, processed starches and sugars. Lots of diets place people on a restricted plan that doesn’t allow the refined, processed starches and sugars, and people lose weight, regain good BG control and feel better. However, in most cases, the weight comes back and weight creeps up and BG begins rising again due to the inability to sustain many of these diets.
Together with evidence of normalization of insulin secretion after bariatric surgery (84), insights into the behavior of the liver and pancreas during hypocaloric dieting lead to a hypothesis of the etiology and pathogenesis of type 2 diabetes (Fig. 6): The accumulation of fat in liver and secondarily in the pancreas will lead to self-reinforcing cycles that interact to bring about type 2 diabetes. Fatty liver leads to impaired fasting glucose metabolism and increases export of VLDL triacylglycerol (85), which increases fat delivery to all tissues, including the islets. The liver and pancreas cycles drive onward after diagnosis with steadily decreasing β-cell function. However, of note, observations of the reversal of type 2 diabetes confirm that if the primary influence of positive calorie balance is removed, then the processes are reversible (21).
When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs – the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.
Many manufacturers offer pen delivery systems. Such systems resemble the ink cartridge in a fountain pen. A small, pen-sized device holds an insulin cartridge (usually containing 300 units). Cartridges are available for the most widely used insulin formulations. The amount of insulin to be injected is dialed in, by turning the bottom of the pen until the required number of units is seen in the dose-viewing window. The tip of the pen consists of a needle that is replaced with each injection. A release mechanism allows the needle to penetrate just under the skin and deliver the required amount of insulin.
×