The bottom line is that diabetes can be bad news—but this doesn’t have to be the case. Interventions can prevent or delay the disease in people with prediabetes. The Diabetes Prevention Program (DPP), a large study of people at high risk of diabetes, has established a prevention plan that’s both feasible and cost-effective. The DPP showed that weight loss and increased physical activity reduced the development of type 2 diabetes by 58% during a three-year period.

When islet cells have been transplanted via the Edmonton protocol, insulin production (and glycemic control) was restored, but at the expense of continued immunosuppression drugs. Encapsulation of the islet cells in a protective coating has been developed to block the immune response to transplanted cells, which relieves the burden of immunosuppression and benefits the longevity of the transplant.[72]

The new research ties in with recent thinking among experts about what happens when type 2 diabetes develops, says Domenico Accili, MD, chief of endocrinology at Columbia University Vagelos College of Physicians and Surgeons. "We have been talking for some time, that in diabetes, primarily type 2, the insulin-producing [beta] cell is not dead but simply inactive," he says. "If you put patients with diabetes on a diet, you can do marvels with their beta cells."


Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars (the symptom) better, but not the diabetes (the actual disease). We’ve been pretending that the symptom is the disease.We can pretend the disease is better, but that doesn’t make it true. That’s the reason most doctors think type 2 diabetes a chronic and progressive disease. We’ve been using the wrong treatment. We’ve been prescribing drugs for a dietary disease. No wonder it doesn’t work.


Conventional: A dietary pattern that includes carbohydrates from fruits, vegetables, whole grains, legumes, and low-fat milk is encouraged for good health. Carbohydrate intake should be monitored using carbohydrate counting or experienced-based estimation. The Recommended Dietary Allowance for digestible carbohydrates is 130 g/day, which will provide a sufficient amount of glucose needed to fuel the central nervous system without reliance on glucose production from protein or fat. Using foods with a low glycemic index that are rich in fiber and other important nutrients is encouraged.
Your care team may recommend that you use a continuous glucose monitor (CGM). A CGM is a wearable device that can measure blood sugar every few minutes around the clock. It's measured by a thread-like sensor inserted under the skin and secured in place. The more frequent CGM blood sugar readings can help you and the care team do an even better job of troubleshooting and adjusting your insulin doses and diabetes management plan to improve blood sugar control.
Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
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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