Thank you for including me in the forum. We all agree that a low-glycemic, nutrient-packed diet—coupled with a healthful lifestyle—is the best way to treat and prevent type 2 diabetes. One of the easiest ways to start is by moving colorful plant-based foods to the center of the plate. If you’re interested in learning more about or test-driving a healthful vegan diet, please visit http://www.PhysiciansCommittee.org/diabetes.
Thank you for explaining just how things work. I have just (2months ago)gone off Diabetes Type 2 medication. BGLs around 7-10 now. It looks like I replace the rolled oats for cauliflower for breakfast and the three slices of wholegrain sourdough bread for veggies. Those two items were the continued delaying function. I’ll be on my way to decreasing the BGLs to normal, now. I have lots of fat from cold pressed virgin olive oil in my home-made hummus and over the veggies. I can look forward to the soya coffee with no guilt.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.