The problem, of course, has not been solved — the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). It’s putting a band-aid over a bullet hole. So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take medication to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of medication cannot force any more sugar into the body.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.
“The problem is we don’t treat diabetes as a dietary problem; we treat it with a lot of drugs, and that never addresses the root problem of the diabetes,” says principal investigator Jason Fung, MD, a kidney specialist at Scarborough and Rouge Hospital in Toronto, Canada, and author of The Complete Guide to Fasting,and The Obesity Code, a 2016 book thought to help popularize intermittent fasting.
Chromium plays a vital role in binding to and activating the insulin receptor on body cells, reducing insulin resistance. Supplemental chromium has been shown to lower blood sugar levels, lipids, A1C, and insulin in diabetic patients. It can also help decrease one’s appetite, particularly for sweets. A dosage from 200 mcg to 2,000 mcg a day is safe. Higher doses are unnecessary and can cause acute kidney failure.
A history of blood sugar level results is especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly.
Over a year ago I was diagnosed with DT2. I was devastated… I told that I needed to take medication and eat according to the ADA recommendations. I never did anything that I was told. I refused to take the medication and went to a LCHF diet. My A1C has never been above a 4.7 for an entire year and I lost 80 pounds with doing nothing but eating. I feel great and my labs are stellar…
Beware of claims that seem too good to be true. Look for scientific-based sources of information. The National Diabetes Information Clearinghouse collects resource information for the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Reference Collection, a service of the National Institutes of Health. To learn more about alternative therapies for diabetes treatment, contact the National Center for Complementary and Alternative Medicine Clearinghouse.
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
To make matters worse for the inactive, carb addict, when the body senses glucose in the bloodstream, the pancreas releases a hormone called insulin (perhaps you’ve heard of it?) to signal the body to store the glucose as glycogen. If the glycogen receptors are full and it can’t do this, the body thinks that the cells didn’t get the message and releases even more insulin.
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.