Depending on the severity of diabetes, an individual can keep control on his/her disease using diet alone, diet & oral hypoglycemic drugs, and diet & insulin. While a mild diabetic can practice disease control with diet alone, a severe diabetic might need to practice diet control along with insulin administration. Whatever the method of controlling diabetes, routine and reliability should be strictly pursued. A person suffering from diabetes should have limited amount of carbohydrates and fats along with moderate amount of protein in the diet. High-fiber diet like vegetables, whole wheat products, oats, whole legumes prove to be more beneficial. Let us have a look at what all should be had and what all should be avoided.
According to the Centers for Disease Control and Prevention (CDC), from 1980 through 2010, the number of American adults aged 18 and older with diagnosed diabetes more than tripled—soaring from 5.5 million to 20.7 million. Moreover, the diabetes epidemic shows no signs of slowing down, affecting 25.8 million people in 2011. Another 79 million adults have prediabetes, putting them at greater risk of developing type 2 diabetes down the road, according to the CDC.
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
We really can't blame anyone who says there's no cure for type-2 Diabetes. But there are 1000s of them who are completely cured of Diabetes and living normal life like us. The only problem here is, they are only in thousands who are completely cured of Diabetes while there are millions of them who are struggling with Diabetes forever. That's the reason, we feel Diabetes has no cure.

Type 2 diabetes is the most common form of diabetes, and unlike type 1 diabetes, it usually occurs in people over the age of 40, especially those who are overweight. Type 2 diabetes is caused by insulin resistance, which means that the hormone insulin is being released, but a person doesn’t respond to it appropriately. Type 2 diabetes is a metabolic disorder that’s caused by high blood sugar. The body can keep up for a period of time by producing more insulin, but over time the insulin receptor sites burn out. Eventually, diabetes can affect nearly every system in the body, impacting your energy, digestion, weight, sleep, vision and more. (5)
Not until I actually got this book into my hands could I see that its subtitle read "A medical approach that can slow, stop, even cure Type 2 Diabetes". If I'd known about the subtitle, I wouldn't have been interested in reading the book, since the "medical approach" bit indicated for me that it consisted of traditional precepts penned by a doctor, and also I am not particularly interested in Type 2 diabetes, only Type 1, which I myself have.
One can't, in spite of the initial reported success of following a 600 kcal vegetarian diet for 8 weeks cured all 11 participants of their diabetes, resulting in an enormous very beneficial weight loss of 15 kg and reversal of pancreatic fat infiltration that many think is the underlying defect causing type 2 diabetes, see this 2011 paper Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol only just 3 months afterwards diabetes had recurred in 5 out of the 11 see Diet reverses Type 2 Diabetes
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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 http://www.diabetesresearchclinicalpractice.com/article/S0168-8227(16)00070-X/abstract
The study, published in Diabetes Care, measured C-peptide, which is produced at the same time and in the same quantities as the insulin that regulates our blood sugar. By measuring C-peptide levels in blood or in urine, scientists can tell how much insulin a person is producing themselves, even if they are taking insulin injections as treatment. The team studied 1,549 people with Type 1 diabetes from Exeter, England and Tayside, Scotland in the UNITED study.
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).

Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
Diabetes is classically divided into three types: upper, middle, and lower Xiao-ke. Each has characteristic symptoms. The upper type is characterized by excessive thirst, the middle by excessive hunger, and the lower by excessive urination. These types are closely associated with the lungs, stomach, and kidneys, respectively, and all three are associated with Yin deficiency. At some point during the course of their illness, most people with diabetes manifest symptoms of all three types.

The ideas contained on this website are for educational purposes only, and are not intended to treat any disease, nor as a substitute for consulting with your physician. All matters regarding your health require medical supervision. The information provided is not intended to serve as health, medical, or other professional advice related to individual situations. No therapeutic or medical claims are either implied or made. No particular results are guaranteed. 
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.
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.
I was diabetic for 13 years and was taking metformin 1000 mg twice daily. Last A1C was 15. My symptoms have always been stomach and bowels. I am a 54 year old male. the metformin wasn’t really working so this year, our family doctor started me on Natural Herbal Gardens Diabetes Disease Herbal mixture, With the help of Natural Herbal Garden natural herbs I have been able to reverse my symptoms using herbs, my symptoms totally declined over a 7 weeks use of the Natural Herbal Gardens Diabetes disease natural herbal formula. My diabetes is totally reversed! Visit their website www . naturalherbalgardens . com I am thankful to nature
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