the remedies you have mentioned has given me heart ,as i am having half cup of of karela juice....but i have not taken my blood test as i am fed up and my finger tips are also fed i take my dose of insulin and also the juice.;-)...and hope it works. or is working . i do my daily morning and evening walk of half nothing sweet.or starchy 15th july 08

Alternative: “The reason I use food-based supplements is because they most closely help correct what I see as the problem: The food we’re eating is lacking in nutrients,” DeLaney says. “If their vitamin D is low, it tells me all their fat-soluble vitamins are low.” She uses cod liver oil along with high-vitamin butter oil to restore these deficiencies.
“Type 1 diabetes affects about one in every 100 companion animals in the U.S., including dogs and cats, and approximately 1.25 million American children and adults,” Purdue University reports. “Because diabetes in dogs happens similarly in humans, treatment has so far been largely the same: Both need their glucose to be monitored throughout the day and insulin to be administered after meals.”
This class of medicines includes rosiglitazone and pioglitazone. These medicines help your body respond better to insulin. Rosiglitazone and pioglitazone can be used alone or in combination with other diabetes medicines. Side effects may include weight gain, fluid retention, and an increase in LDL (“bad”) cholesterol. People taking rosiglitazone and pioglitazone also need periodic liver tests.
High doses of magnesium may cause diarrhea, nausea, loss of appetite, muscle weakness, difficulty breathing, low blood pressure, irregular heart rate, and confusion. It can interact with certain medications, such as those for osteoporosis, high blood pressure (calcium channel blockers), as well as some antibiotics, muscle relaxants, and diuretics.​
High doses of magnesium may cause diarrhea, nausea, loss of appetite, muscle weakness, difficulty breathing, low blood pressure, irregular heart rate, and confusion. It can interact with certain medications, such as those for osteoporosis, high blood pressure (calcium channel blockers), as well as some antibiotics, muscle relaxants, and diuretics.​
Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
Steve Vincent, 58, from Southampton, England, was diagnosed with type 2 in December 2010. He was told there was no known cure and he had an increased risk of heart attack, stroke, blindness and limb loss. He had a BMI of 29, weighed 93kg and showed an HbA1c of 10.7%. In summer 2011 he read the reversal story and went on a daily 600 calories green vegetable diet and three litres of water, for two months. At the end he was and remains diabetes-free. In December 2012 he told me: "All my blood test levels are within the normal range, and my cholesterol and blood pressure levels are now normal." When he came off the diet he weighed just 72kg, although he has put on weight since then as he admits he has not been eating as healthily as he might, but his BMI remains at a healthy 24, and his HbA1c level is 5.5%.
In 2017 the results of the DIRECT study were published, where obese type 2 diabetic were put on a 830 Cal diet for 6 month by their GPs (the two former studies were led by medical specialists), mean weight loss 15% ≈ 15 kg Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The more weight one lost, the higher the success rates
The fact these improvements can happen independently of weight loss should also signify a shift in how we conceptualize both obesity and diabetes, according to Peter Billings, the Seattle bariatric surgeon who operated on Benari. Billings, a nearly 20-year veteran in the field, has started to perform surgery on other lower-BMI patients similar to Benari, though they often pay out of pocket.
First, speak with your doctor — you should not start relying on plants or stop your medicines on your own. You’ll need to work closely with your diabetes health-care provider, and you’ll need to do some research and monitor yourself. Still, millions of people are using plant medicines, and a number of them have written to Diabetes Self-Management to tell us that they’re working.
Khodneva, Y., Shalev, A., Frank, S. J., Carson, A. P., & Safford, M. M. (2016, May). Calcium channel blocker use is associated with lower fasting serum glucose among adults with diabetes from the REGARDS study. Diabetes Research and Clinical Practice, 115, 115-121. Retrieved from

How to use basal insulin: Benefits, types, and dosage Basal, or background, insulin helps regulate blood sugar levels in people diagnosed with diabetes. It keeps glucose levels steady throughout the day and night. It is taken as injections, once a day or more often. The type of insulin and number of daily injections varies. Find out more about the options available. Read now
Benari, an Ashkenazi Jew, doesn’t fall into that category. But Cummings and other bariatric experts I spoke to said that surgery should be a possible option for any person whose diabetes isn’t improving. Cummings himself is currently working on a clinical trial in India of bariatric patients with BMIs as low as 25. And he expects similar trials will come down the pipeline.
So, let's understand why a cell does not accept the Insulin fast enough. A healthy cell has a Sodium:Potassium ratio of 1:8. This varies a little from person to person depending on the amount of activity he/she does. A diabetic cell on the other hand has a very bad ratio. Any naturally available food always has more Potassium and less Sodium. When heated, Potassium is lost but Sodium is retained. And we add more Sodium to the food in the form of salt. We only require about 500mg of Sodium per day for normal activities which is naturally available in all types of food even without adding in the form of salt. A person who does more physical activity as part of his job or is an athlete etc. will require more Sodium not exceeding 2000mg. On the other hand, Potassium requirement is around 4700mg.

Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
It would be a mistake to assume that the diabetes has gone away, however. Basically, type 1 diabetes occurs when about 90 percent of the body's insulin-producing cells have been destroyed. At the time that type 1 diabetes is diagnosed, most patients still are producing some insulin. If obvious symptoms of type 1 diabetes emerge when the patient has an illness, virus or cold, for example, once the illness subsides the body's insulin needs may decrease. At this point, the number of insulin-producing cells remaining may be enough — for the moment — to meet the person's insulin needs again.

Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
Aside from the financial costs of diabetes, the more frightening findings are the complications and co-existing conditions. In 2014, 7.2 million hospital discharges were reported with diabetes as a listed diagnosis. Patients with diabetes were treated for major cardiovascular diseases, ischemic heart disease, stroke, lower-extremity amputation and diabetic ketoacidosis.
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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.

An unbalanced microbiome composition, known as dysbiosis, has been found in patients with diabetes, for whom the diversity of the gut microbiome is often reduced as compared to healthy people. Researchers from the University of Amsterdam recently showed that fecal transplants, used to transfer the microbiome of a healthy person to the gut of one with diabetes, can result in a short-term improvement of the insulin resistance found in obese patients with type 2 diabetes.