Free movement of people was only one aspect of why people voted to leave the eu. There is another even more pressing, that of regaining sovereignty given away by those who thought nothing of betraying it in the first place. Yes the Gov. could be brought down by the latest betrayal of sovereignty, not only the Gov but the Tory Party itself, with no chance of a come back for decades to come, if ever.
As of this writing, new and exciting research is being done to prevent and cure Diabetes. JDRF Australia is working on a cure that aims to allow the body to produce insulin and for the body to stop attacking its own B-cells. Another cure that is being worked on is enhancing the survival of B-cells so that they can be transplanted to diagnosed patients. In terms of prevention, since testing can now be done for an individual’s genetic risk, diet modifications have been found to delay the onset of diabetes to at least five years.
This 2013 paper http://www.ncbi.nlm.nih.gov/pmc/... on page 5 reported that after the 8 weeks on that 600 kcal diet 10 out of the 11 participants, so not all, of the Counterpoint study, as the study is now known, regained normal glucose metabolism, 3 months after resuming a normal diet 4 out of the 10 still had a normal glucose metabolism, 3 had an impaired glucose tolerance, 3 had better controlled diabetes, no more recent figures published in spite of the first publication had been published in Octobre 2011, which doesn't bode well for the long term outcome I'd say, I'd have expected them would to have reported the longer term results by now were they positive.
Momordica Charantia goes under a variety of names and is native to some areas of Asia, India, Africa and South America. Marketed as charantia, it is also known as karela or karolla and bitter melon. The herb may be prepared in a variety of different ways, and may be able to help diabetics with insulin secretion, glucose oxidation and other processes.
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.
The earliest oral diabetes drugs were the sulfonylureas. These work by stimulating the pancreas to produce more insulin. The oldest of these drugs still on the market is chlorpropamide (Diabinese), which has been used for more than 50 years. The second-generation sulfonylureas are taken once or twice a day. They include glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta, Glynase), and glimepiride (Amaryl).
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).
Treatment plans are designed around the pattern of insulin normally supplied by the pancreas throughout the day in someone without diabetes. In general, this involves providing a fairly steady "background" level of insulin to control blood sugar levels between meals and overnight, along with doses of rapid- or short-acting insulin to handle the fast rises in blood sugar that occur with meals.
The above two rules are the only dietary rules you need to maintain ideal weight for the rest of your life, assuming you apply common sense and avoid extremes. The diet works by building in regular periods of insulin relief, keeping your body from becoming resistant to insulin. Following these two rules, you will maintain your weight and health by never entering the vicious cycle of increasing insulin resistance.