Cinnamon has the ability to lower blood sugar levels and improve your sensitivity to insulin. A study conducted at Western University of Health Sciences in Pomona, Calif. found that the consumption of cinnamon is associated with a statistically significant decrease in plasma glucose levels, LDL cholesterol and triglyceride levels. Cinnamon consumption also helped increase HDL cholesterol levels. (15)
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. There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population. Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms. This suggests that it may be important to target mood in treatment.
Mr. Tutty said he jumped at the chance, becoming one of 30 men and women ages 25 to 80 to sign up. Mr. Tutty was one of 13 participants whose fasting plasma glucose dropped, and during the six-month follow-up remained below the seven millimole per liter (or 126 milligrams per deciliter) that defines diabetes. Although Mr. Tutty completed the study nearly three years ago, his fasting blood sugars continue to range from 5.2 to 5.6 mmol/L, he said.
Alternative: “I’m a fat-atarian,” says DeLaney, who tells her patients to avoid low-fat foods. She encourages them to eat whole-fat dairy products, egg yolks, butter, olive oil, and avocado. “Restoring healthful fats to our diets as well as eliminating trans fats and all refined oils that help deplete our fat and vitamin stores will help nourish the body and reduce the need for diabetes medication.”
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.
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.
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.