For my diabetes control, I researched indepth true cinammon (Ceylon) and not the fake supermarket cinammon (cassia) with it's dangerous side effects. I had tried the supermarket varity for two months and noticed very little change in my blood sugar levels. After trying Ceylon cinammon in just two days my sugar readings had dropped approx 30 points. So for me...it's works. Will try it for a month and report back.
The problem is, glucose is actually toxic if it is just floating around in your bloodstream, so that body has a defense mechanism. Any glucose that is not immediately used is stored as glycogen in the liver and the muscles. This would be all well and good except that your body has a limited number of glycogen receptors. When these are full, as they almost always are in inactive people, the body only has one option left: to store all the excess glucose as saturated fat within the body.
Green tea contains the bioflavinoid epigallocatechin gallate (EGCG), which has been shown to be a safe and effective antioxidant. In a study in Japan, green tea was shown to reduce the risk for Type 2 Diabetes Mellitus onset. It has been shown to improve glucose tolerance in patients, and decrease blood sugar production and over-secretion in Type 2 Diabetes Mellitus  patients. Green tea has also been shown to have an effective anti-angiogenesis factor, that is, it reduces problematic overgrowth of blood vessels, which may have a significant effect on preventing diabetic retinopathy. It has also been shown to promote fat oxidation and thermogenesis. Last, green tea can provide antioxidant protection for the pancreas and the fatty liver. A good dose is 200 to 400 mg a day. It’s also beneficial to drink organic green tea.
Until the findings are reproduced consistently, and cinnamon has been show to provide a meaningful improvement in relevant measures, there is no persuasive evidence to suggest that cinnamon has potential as a useful treatment option. Drugs that work, work consistently and provide meaningful improvements in measures of the disease. Why doesn’t cinnamon work?  There may be an active ingredient, but it’s present in low concentrations, and varies in content between the different batches of cinnamon used in the different trials. In that case, the active ingredient needs to be standardized and possibly isolated, which would make it a drug treatment.  Or this could be yet another example of a supplement that looks promising in early studies, only to see the effect disappear as the trials get larger and control for bias more effectively.
Effect of an 8-week very-low-calorie diet in type 2 diabetes on arginine-induced maximal insulin secretion (A), first phase insulin response to a 2.8 mmol/L increase in plasma glucose (B), and pancreas triacylglycerol (TG) content (C). For comparison, data for a matched nondiabetic control group are shown as ○. Replotted with permission from Lim et al. (21).
Data from the Swedish randomized study of gastric banding showed that a loss of 20% body weight was associated with long-term remission in 73% of a bariatric surgery group, with weight change itself being the principal determinant of glucose control (13). Dietary weight loss of 15 kg allowed for reversal of diabetes in a small group of individuals recently receiving a diagnosis (21). In individuals strongly motivated to regain normal health, substantial weight loss is entirely possible by decreasing food consumption (88). This information should be made available to all people with type 2 diabetes, even though with present methods of changing eating habits, it is unlikely that weight loss can be achieved in those not strongly motivated to escape from diabetes. Some genetic predictors, especially the Ala12 allele at PPARG, of successful long-term weight loss have been identified (89), and use of such markers could guide future therapy. It must be noted that involuntary food shortage, such as a result of war, results in a sharp fall in type 2 diabetes prevalence (90,91).
Efforts to cure or stop type 1 diabetes are still in the early stages, and these approaches will also not be suitable for people that have already lost their insulin-producing cells. A solution could be the creation of an “artificial pancreas” — a fully automated system that can measure glucose levels and inject the right amount of insulin into the bloodstream, just like a healthy pancreas would.
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 drop pounds, Galati emphasizes using portion control, avoiding processed foods, and eating fresh vegetables, fruits, and fresh lean meat, poultry, and fish. Regular exercise should also be part of the program. Typically, he talks to patients about first targeting a weight loss goal of 10 percent. Once that is achieved, they typically strive for increments of 5 percent to 7 percent on a 6- to 12-month basis.
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.
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