Cinnamon contains a bioactive compound that can help to fight and prevent diabetes. Cinnamon is known to stimulate the insulin activity and thus regulate the blood sugar level. As excess of anything is bad, likewise cinnamon if taken in excess can increase the risk of liver damage due to a compound called coumarin present in it. The true cinnamon, not the one buy from shops (Cassia cinnamon) is safer to have.

Control and outcomes of both types 1 and 2 diabetes may be improved by patients using home glucose meters to regularly measure their glucose levels.[citation needed] Glucose monitoring is both expensive (largely due to the cost of the consumable test strips) and requires significant commitment on the part of the patient. The effort and expense may be worthwhile for patients when they use the values to sensibly adjust food, exercise, and oral medications or insulin. These adjustments are generally made by the patients themselves following training by a clinician.

Magnesium deficiency is common in diabetic patients, as magnesium can be lost in the urine with hyperglycemia. A study in Diabetes Care reported that low magnesium status is common in Type 2 Diabetes Mellitus (T2DM) and showed that when low-magnesium Type 2 Diabetes Mellitus patients were given an oral dose of magnesium daily for sixteen weeks, the mineral reduced insulin resistance, fasting glucose, and A1C levels.

The first hint that type 2 diabetes is a fully reversible syndrome came from bariatric surgery. Almost a quarter century ago, Pories et al. (12) demonstrated that blood glucose levels normalized in obese people with type 2 diabetes undergoing bariatric surgery and that 10 years later, almost 90% remained free of diabetes. The phenomenon was more recently tested in a randomized prospective study comparing gastric banding with intensive medical therapy for type 2 diabetes (13). This least invasive type of surgery was most suitable for the randomized study, although it was associated with lower rates of diabetes reversal than other procedures. Mean fasting plasma glucose fell to normal levels in the surgically treated group but declined only modestly in the intensive medical treatment group despite oral agents and insulin (Fig. 1) (13). Remission of diabetes was related to the degree of weight loss rather than to group allocation and was achieved in 73% of the surgical group and 13% of the intensive medical treatment group because surgery was more effective in achieving weight loss as previously described (14). Type 2 diabetes can be reversed by applying a surgical procedure that diminishes fat mass.
Since the body functions as a whole, it is logical that when one hormone or part of the endocrine system is suffering, the other would be affected as well. This is the reason behind the recent research linking high stress levels to diabetes and other health problems. Most people think of stress only in the mental context (as in, “I’ve got a million things to do, I’m running late and I don’t have time to get anything done… I’m so stressed”) but stress can be physical, psychological, emotional, or mental and can be triggered by many factors including:
The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
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.[67] There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population.[68][69] Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms.[70] This suggests that it may be important to target mood in treatment.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Poor glycemic control refers to persistently elevated blood glucose and glycosylated hemoglobin levels, which may range from 200–500 mg/dl (11–28 mmol/L) and 9–15% or higher over months and years before severe complications occur. Meta-analysis of large studies done on the effects of tight vs. conventional, or more relaxed, glycemic control in type 2 diabetics have failed to demonstrate a difference in all-cause cardiovascular death, non-fatal stroke, or limb amputation, but decreased the risk of nonfatal heart attack by 15%. Additionally, tight glucose control decreased the risk of progression of retinopathy and nephropathy, and decreased the incidence peripheral neuropathy, but increased the risk of hypoglycemia 2.4 times.[21]
Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.
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