So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.
High blood sugar (hyperglycemia). Your blood sugar level can rise for many reasons, including eating too much, being sick or not taking enough glucose-lowering medication. Check your blood sugar level often, and watch for signs and symptoms of high blood sugar — frequent urination, increased thirst, dry mouth, blurred vision, fatigue and nausea. If you have hyperglycemia, you'll need to adjust your meal plan, medications or both.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Given the prevalence of diabetes and the chronic nature of the disease, it’s no surprise that CAM is a popular treatment option. I don’t see a lot of CAM use in Type 1 diabetics. Insulin is the primary treatment, it works well, and patients can objectively measure their own blood sugar. Type 1 diabetics don’t seem to experiment with supplements that might alter their blood sugars. Those patients end up hospitalized or dead.