Formal recommendations on how to reverse type 2 diabetes in clinical practice must await further studies. In the meantime, it will be helpful for all individuals with newly diagnosed type 2 diabetes to know that they have a metabolic syndrome that is reversible. They should know that if it is not reversed, the consequences for future health and cost of life insurance are dire, although these serious adverse effects must be balanced against the difficulties and privations associated with a substantial and sustained change in eating patterns. For many people, this may prove to be too high a price to pay, but for those who are strongly motivated to escape from type 2 diabetes, the new understanding gives clear direction. Physicians need to accept that long-term weight loss is achievable for a worthwhile proportion of patients (96). In the United States, diabetes costs $174 billion annually (97), and in the United Kingdom, it accounts for 10% of National Health Service expenditure. Even if only a small proportion of patients with type 2 diabetes return to normal glucose control, the savings in disease burden and economic cost will be enormous.
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
Low glycemic index foods also may be helpful. The glycemic index is a measure of how quickly a food causes a rise in your blood sugar. Foods with a high glycemic index raise your blood sugar quickly. Low glycemic index foods may help you achieve a more stable blood sugar. Foods with a low glycemic index typically are foods that are higher in fiber.
This article is great, it combines all of the info I have found, not only putting it into a well written article but adds info I had not found yet. I have struggled with type 2 and losing weight, starting an aggressive weight cardio plan in 2016 with an A1C level of 9.7%. Even after three months of an hour or more of weight lifting and 30-50 mins of hard hilly terrain bike riding, my bets A1C was 7.7% with lowering my carb count to the recommended range. After an injury caused me to have to stop many of the exercises for a bit my A1C went up to the 9% range. July this year my A1C was 9.9% and my Dr was talking about insulin shots, which I hate needles. One last ditch effort to find a solution and avoid the shots, I found an article about the benefits of intermittent fasting. I did a lot of research on the matter before creating my own version of a Keto diet, and went on a strict diet of 5-8 servings of green leafy vegetables a day, around 45g of carbs a day, 3oz of lean or healthy fat protein a meal and fasting for 18 hours between Dinner till lunch the next day for two and a half months. My A1C was 6.5, I lost 20lbs, and have tons of energy and no cravings. I have altered my diet to fit my new exercise plan, still 5-8 servings of vegetables a day, but have added occasional breakfasts of two eggs and 1/2 cup salsa, no more than 100g of carbs a day except my once a week cheat day that might go slightly higher if my blood sugar is in a good range, 6oz lean healthy fat protein, and a hard boiled egg in between meals.
Yet Gabbay says preliminary human studies with positive results, like this week’s in BMJ Case Reports, suggest the diet is worthy of further study in a larger population over a longer period of time. For now, he cautions people with diabetes, especially those on insulin and sulfonylureas to lower their blood sugar, against trying intermittent fasting before speaking with their healthcare provider.
Bitter in taste, neem is beneficial in treating diabetes. Studies have proved that incorporating Indian lilac can maintain blood sugar levels stimulating insulin activity without hindrance. Although natural sources do not contain adverse effects, it is still suggested to consult with your endocrinologist in case constant high glucose content in the bloodstream.
10. Molecular Hydrogen: One of the best natural remedies for diabetes, this potent antioxidant has proven successful in the treatment of several different health ailments, and is now showing promise as a treatment for diabetes. It works by triggering antioxidative activities within cells, and can promote increased metabolism as well as assist in the absorption of insulin. It’s taken topically, mixed in water, or inhaled as a gas. It has no toxicity levels, even if taken at high doses.
According to studies, cinnamon may have a positive effect on the glycemic control and the lipid profile in patients with diabetes mellitus type 2. This is because it contains 18% polyphenol content in dry weight. This popular Indian spice can improve insulin sensitivity and blood glucose control. According to a study published in Journal Of The American Board Of Family Medicine, “cinnamon lowered HbA1C by 0.83% compared with standard medication alone lowering HbA1C 0.37%. Taking cinnamon could be useful for lowering serum HbA1C in type 2 diabetics with HbA1C >7.0 in addition to usual care.”
There has been a good amount of attention and time spent on discussing the “reversal” of diabetes, but there’s not been a lot of good facts to explain what this means. First, type 1 diabetes (an autoimmune disease) cannot be reversed, cured or avoided – period. It can be managed with insulin and made easier with good lifestyle choices like staying active and eating a healthy diet.
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
This essentially means that the type 2 diabetes is being managed at a level that seems as if the diabetes isn’t there at all. Choosing a healthy diet, exercising regularly and maintaining a healthy weight is the key. Eventually, what will likely happen is that blood glucose levels will increase again at a later time, as the person gets older, or if the person returns to an inactive and unhealthy lifestyle and regains weight because the beta cells of the pancreas have already been stressed.
Chromium plays a vital role in binding to and activating the insulin receptor on body cells, reducing insulin resistance. Supplemental chromium has been shown to lower blood sugar levels, lipids, A1C, and insulin in diabetic patients. It can also help decrease one’s appetite, particularly for sweets. A dosage from 200 mcg to 2,000 mcg a day is safe. Higher doses are unnecessary and can cause acute kidney failure.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.