A patient diagnosed with type 2 diabetes (HbA1c of 6.5% or above) will always have type 2 diabetes. Interventions such as medication (including insulin), staying active and making good diet choices must be maintained to prevent the disease from progressing further. However, even if the patient undergoes strict medication, diet and exercise adherence and manages to lower the HbA1c they will still have type 2 diabetes.
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.
Take about 200 gms. of Curds (dahi)(Yogurt) blend it in a mixer. Cut two full ripe tomatoes in small pieces and add to the curds, with black pepper powder and salt as per taste. Keep aside for 10 minutes and have the same for breakfast. Dont use Refined Oils for preparation of foods. Use only filtered oils. Reduce your intake of food to 75%. Whenever you feel hungry in beteen meals take this mix of curds and tomatoes. Besides your morning exercise take a brisk walk of 30 minutes before dinner. Your sugar levels however high will drop to normal within 3-4 weeks. This is the best natural remedy which has given me relief from diabetes.
A couple of studies have found that cinnamon improves blood glucose control in people with type 2 diabetes. In the first study, 60 people with type 2 diabetes were divided into six groups. Three groups took 1, 3 or 6 g of cinnamon a day and the remaining three groups consumed 1, 3 or 6 g of placebo capsules. After 40 days, all three doses of cinnamon significantly reduced fasting blood glucose, triglycerides, LDL cholesterol, and total cholesterol.

A history of blood sugar level results is especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly.
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.
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.
Sage can have metformin-like effects, according to a study published in the British Journal of Nutrition. So you may want to consider cooking with this herb often. It has been used on traditional medicine for centuries, as one of the important herbs to reduce blood sugar. A word of warning – taking high doses of sage along with diabetes medications might cause your blood sugar to go too low, a condition called hypoglycemia. Monitor your blood sugar closely.
The most detrimental thing sugar does is cause inflammation, and inflammation is the root of almost everything that misfires in your body. There is a direct link between inflammation and diabetes,[6] and a lower carb diet reduces C-reactive protein, a marker of inflammation.[7] In addition to sugar, it’s a good idea to keep an eye on your toxic load and keep your omega-3 to omega-6 ratio low to keep inflammation down.

It is also known as insulin-dependent diabetes mellitus (IDDM) and results from body's inability to produce insulin. Usually, it occurs in childhood or adolescence, but can surface up at any age. In this, the patient needs to take insulin injections on regular intervals (generally daily) in order to absorb glucose in the body. Type 1 diabetes mellitus is also referred to as juvenile diabetes, at times.

The information on this website is provided as general health guidelines and may not be applicable to your particular health condition. Your individual health status and any required medical treatments can only be properly addressed by a professional healthcare provider of your choice. Remember: There is no adequate substitution for a personal consultation with your physician. Neither Desert Springs Hospital Medical Center, or any of their affiliates, nor any contributors shall have any liability for the content or any errors or omissions in the information provided by this website.            


Indian gooseberry is one of the richest sources of vitamin C. When mixed with bitter gourd juice, its efficacy manifolds, and it can prove to be a highly effective concoction against diabetes. The mixture arouses the islets of Langerhans, that is, the isolated group of cells that secrete the hormone insulin in the pancreas. Just consume one tablespoon of Indian gooseberry juice mixed with one cup of bitter gourd juice daily for 8 to 12 weeks. It is recommended to take it first thing in the morning, if possible. The mixture has also been found to trigger insulin production. All in all, a great herbal remedy for diabetes.

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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