Diabetes is the major cause of blindness, kidney failure, heart attack and stroke. The number of people affected by all types of diabetic disorders is now over four times higher than just 40 years ago. This has led the World Health Organization (WHO) to consider diabetes an epidemic, predicting it will soon be the seventh biggest cause of death worldwide.

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Over the last century, advancements in new treatments aided by the remarkable developments in computer technology have helped many people better manage the disease, but achieving optimal glucose control remains an unattainable goal for the vast majority of those with diabetes, and particularly among young people. Despite patients' best attempts, managing diabetes remains a challenging, daily balancing act that requires constant vigilance. That's because insulin therapy cannot ideally mimic the exquisite biological function of a healthy pancreas. And that's why the Diabetes Research Institute and Foundation remain passionately committed to achieving this singular goal. Learn more about our progress toward a cure and the steps we are taking to turn our vision into reality.

Don’t let anyone discourage you! Your doctor may be skeptical and resist your efforts to cure yourself, but persevere! Worst case, put your doctor in touch with Dr. Jason Fung, a nephrologist who grew tired of simply controlling pain for his end stage kidney patients at the end of lives ravaged by diabetes, and decided to do something to help them thrive with the energy of a healthy life well-lived. Now follow the simple rules plainly and freely explained above and help yourself!

In some kids with diabetes, repeated insulin injections can cause a thickening or lumpiness of the fatty tissue beneath the skin, called lipodystrophy (or lipohypertrophy). This is more likely if injections are given in the same area again and again rather than in different injection sites as recommended. Usually, this is only a cosmetic problem. But in some cases, insulin injected in areas of skin with lipodystrophy may not be absorbed into the bloodstream as it should. This can make the insulin dose take longer than usual to work.

The study included 298 patients, aged 20 to 65, who had been diagnosed with type 2 diabetes within the previous six years. Half of the patients were put on a low-calorie diet and lost an average of 10 to 15 kg (22 to 33 pounds). The other half of patients, who served as a control group, received the best diabetes management available — but that did not include a weight loss program.

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.

Type 2 diabetes, the most common type, can start when the body doesn't use insulin as it should. If your body can't keep up with the need for insulin, you may need to take pills. Along with meal planning and physical activity, diabetes pills help people with type 2 diabetes or gestational diabetes keep their blood glucose levels on target. Several kinds of pills are available. Each works in a different way. Many people take two or three kinds of pills. Some people take combination pills. Combination pills contain two kinds of diabetes medicine in one tablet. Some people take pills and insulin.
In 1991, the National Institutes of Health issued a consensus statement, cautiously recommending surgery as a treatment for people living with morbid obesity, meaning they have a body mass index, or BMI, over 40. For people who have health complications connected to obesity, such as type 2 diabetes, the limit goes down to a BMI of 35. Relying on these guidelines, insurance companies and public payers like Medicaid and Medicare typically only cover surgery for people living with diabetes who fall into that category.
Glucose in the bloodstream passes through the kidneys, where it can either be excreted or reabsorbed.   Sodium-glucose transporter 2 (SGLT2) works in the kidney to reabsorb glucose, and a new class of medication, SGLT2 inhibitors, block this action, causing excess glucose to be eliminated in the urine. Canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance) are SGLT2 inhibitors that have been approved by the FDA to treat type 2 diabetes.  Because they increase glucose levels in the urine, side effects can include urinary tract and yeast infections.

Complications, which eventually lead to death, usually arise when the patient does not adhere to the advice of their doctor. Statistics show that sixty percent of patients are able to live long and productive lives; the rest suffer from a lot of complications including retinopathy (eye disease which can lead to blindness), gastroparesis (inability of the stomach to move food), neuropathy, and end-stage renal disease to name a few.
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.
With research funding, people managing this challenging disease have received tools that help them to live better lives. Every advancement or milestone has elevated our understanding of Type 1, achieved improved management and has gotten us one-step closer to an actual cure. That’s why donating to diabetes research is so important — it’s the only way we’ll eliminate this disease.
At Diabetes Daily, we prefer using the word remission over cure because far too often the state of diabetes returns even with people’s best efforts. Regardless of the definition of a cure, finding a way to live with little to know highs or lows is a worthwhile endeavor. Long-term studies show that even a few years of great blood sugars significantly reduces your long-term risk of complications.
Qi (pronounced “chi”) is translated into English as vital energy. It is defined in terms of function rather than as a discrete substance, and it is what animates us and allows us to move and maintain the activities of life. The origins of Qi include “congenital”’ (prenatal) Qi—that which is inherited from our parents—and “acquired” Qi—that which is incorporated from food and air.4
In investigating how BCG administration produces its beneficial effects, the research team identified a mechanism never previously seen in humans in response to treatment with any drug – a shifting of the process of glucose metabolism from oxidative phosphorylation, the most common pathway by which cells convert glucose into energy, to aerobic glycolysis, a process that involves significantly greater glucose consumption by cells. The researchers also found that BCG could reduce blood sugar elevations in mice that were caused by means other than autoimmune attack, raising the possibility that BCG vaccines could also be beneficial against type 2 diabetes.”
Researchers from Newcastle and Glasgow Universities believe they have found a way to effectively reverse type 2 diabetes, without requiring a new kind of drug or invasive surgery. Type 2 diabetes is a chronic condition that affects how a person’s body metabolizes sugar, either because they’ve developed resistance to the hormone insulin, or their pancreas fails to produce enough insulin.

Metformin: The DPP study found that metformin, the safest first-line therapy for type 2 diabetes, may help delay the onset of type 2 diabetes in people with prediabetes. Participants who took the low-cost generic drug had a 31% reduced risk of developing type 2 diabetes compared to the control group (those not on metformin or intensive lifestyle intervention). Again, 15-year follow up data showed that 17% of those on metformin continued to have a significant reduction in type 2 progression. At this time, metformin (or any other medication, for that matter) is not currently FDA approved for prediabetes, and it is sometimes prescribed “off-label” by a healthcare provider. Your healthcare provider can give you more information and determine whether metformin is a good option for you.
Chinese herbs have specific functions (i.e., warming, heat-clearing, eliminating dampness, and cooling) and can be classified according to those functions. They are also classified according to four natures (cool, cold, warm, and hot) and five tastes (sweet, pungent, bitter, sour, and salty).4 Herbs may be prescribed individually or as part of a formula.
Refined sugar: Refined sugar rapidly spikes blood glucose, and soda, fruit juice and other sugary beverages are the worst culprits. These forms of sugar enter the bloodstream rapidly and can cause extreme elevations in blood glucose. (7) Even though natural sweeteners like raw honey and maple syrup are better options, they can still affect blood sugar levels, so only use these foods on occasion. Your best option is to switch to stevia, a natural sweetener that won’t have as much of an impact.
Some herbal diabetes products have turned out to be downright dangerous. In February 2000, the FDA recalled five Chinese herbal products after discovering that they contained various amounts of two prescription diabetes drugs, phenformin and glyburide. (The products are listed at www.fda.gov/oc/po/firmrecalls/Herbal.html.) Phenformin was withdrawn from the U.S. market 20 years ago after it caused serious side effects, including several deaths.
Alternative: “I’m a fat-atarian,” says DeLaney, who tells her patients to avoid low-fat foods. She encourages them to eat whole-fat dairy products, egg yolks, butter, olive oil, and avocado. “Restoring healthful fats to our diets as well as eliminating trans fats and all refined oils that help deplete our fat and vitamin stores will help nourish the body and reduce the need for diabetes medication.”
Purdue and the IU School of Medicine collaborated on this patented work through the National Institute of Health T32 Indiana Bioengineering Interdisciplinary Training for Diabetes Research Program. The research was also supported by the National Science Foundation Graduate Research Fellowship; the Indiana University School of Medicine Center for Diabetes and Metabolic Diseases Pilot and Feasibility Program; and donations from the McKinley Family Foundation.

Although the promises are big, these technologies are still far from the market. First, clinical trials will have to show they do work. Then, the price could be steep, as cell therapy precedents for other applications, such as oncology, come with price tags that reach the six figures and are finding difficulties to get reimbursed. Considering that compared to cancer, diabetes is not an immediately life-threatening disease, health insurers in some countries might be reluctant to cover the treatment.