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.

A OGTT glucose of less than 140 ml/dl is considered normal, with 141-199 being pre-diabetic and levels above 200 mg/dL considered full-blown diabetes. From my research, I believe that  OGTT blood sugar levels above 140 mg/dL , especially regularly, can increase risk of vision problems, cancer, stroke and cardiovascular disease, even without an official diabetes diagnosis.
Effect of an 8-week very-low-calorie diet in type 2 diabetes on arginine-induced maximal insulin secretion (A), first phase insulin response to a 2.8 mmol/L increase in plasma glucose (B), and pancreas triacylglycerol (TG) content (C). For comparison, data for a matched nondiabetic control group are shown as ○. Replotted with permission from Lim et al. (21).
Carbohydrates break down into glucose in the small intestine which is then absorbed into the bloodstream. Spices like Cayenne pepper stimulate glucose absorption from the small intestine, according to a Hungarian study published in the March 18, 2006 issue of the “European Journal of Pharmacology”. Add a bit to cayenne pepper to your home-cooked meals to stabilize your blood sugar levels naturally. The entire pepper family – including bell peppers, chilli peppers, and cayenne are known to help fight inflammation. That is why they are prized in several Asian culinary traditions. Use Cayenne wisely to get its anti-inflammatory benefits as well.

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Recently i been diagnosed with diabetes..doctor want me to take medicine i tried it for 10 days but that made me so dizzy.so i stop that medicine..i am following the fenugreek method but what i do is i soak it and i eat few of them two times a day.. i dont know how far that is working..can you anyone tell me the best way it work.and do you know if it cause any effects with eye sight????? thanks alot..
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
Low blood sugar (hypoglycemia). If your blood sugar level drops below your target range, it's known as low blood sugar (hypoglycemia). Your blood sugar level can drop for many reasons, including skipping a meal, inadvertently taking more medication than usual or getting more physical activity than normal. Low blood sugar is most likely if you take glucose-lowering medications that promote the secretion of insulin or if you're taking insulin.

This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.


Before making any fiber recommendations, Dean has her patients tested for “pancreatic insufficiency.” She believes people with pancreatic insufficiency should be given digestive enzymes along with fiber, “otherwise the fiber will just bloat them up, and they’ll be quite unhappy,” she says. Dean uses a glucomannan fiber supplement for her patients with type 2 diabetes.
Type 1 diabetes is commonly called “juvenile diabetes” because it tends to develop at a younger age, typically before a person turns 20 years old. Type 1 diabetes is an autoimmune disease where the immune system attacks the insulin-producing beta cells in the pancreas. The damage to the pancreatic cells leads to a reduced ability or complete inability to create insulin. Some of the common causes that trigger this autoimmune response may include a virus, genetically modified organisms, heavy metals, vaccines, or foods like wheat, cow’s milk and soy. (4)
Metformin is a biguanide drug that increases the sensitivity of the body’s cells to insulin. It also decreases the amount of glucose produced by the liver.. In 1994, the FDA approved the use of the biguanide called metformin (Glucophage) for the treatment of type 2 diabetes. Today, this is still typically the first drug prescribed for type 2 diabetes.
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