In addition to their usual diabetes regimen -- a careful diet, regular exercise, and in some cases, medication -- 23 type 2 diabetic patients took either 3 grams of American ginseng or a placebo each day for eight weeks, at which point they switched treatments. The diabetic patients' fasting blood sugar levels dropped about 9% more when they took ginseng compared with when they took the placebo; glycosylated hemoglobin levels between the two groups differed by 4%, with the ginseng group being lower.
Regular monitoring of clinical trial participants found that HbA1c levels of those receiving BCG had dropped by more than 10 percent at three years after treatment and by more than 18 percent at four years. That reduction was maintained over the next four years, with treated participants having an average HbA1c of 6.65, close to the 6.5 considered the threshold for diabetes diagnosis, and with no reports of severe hypoglycemia. Participants in the placebo group and in a comparison group of patients receiving no treatment experienced consistent HbA1c elevations over the same eight-year time period.
John’s naturopath, Susan DeLaney, ND, RN, from The Wellness Alliance in Carrboro, North Carolina, considers diabetes to be reversed when an individual is no longer dependent on medication to maintain blood glucose levels within a fairly normal range. Kathie Madonna Swift, MS, RD, LDN, owner of Swift Nutrition and author of The Inside Tract: Your Good Gut Guide to Great Digestive Health, describes reversal of diabetes as “restoring function and bringing the body back into glycemic balance.”
An unbalanced microbiome composition, known as dysbiosis, has been found in patients with diabetes, for whom the diversity of the gut microbiome is often reduced as compared to healthy people. Researchers from the University of Amsterdam recently showed that fecal transplants, used to transfer the microbiome of a healthy person to the gut of one with diabetes, can result in a short-term improvement of the insulin resistance found in obese patients with type 2 diabetes.
Diabetes is one of the most prevalent chronic diseases in the United States. The morbidity and mortality associated with the disease is significant and derives primarily from complications of persistent hyperglycemia. Longstanding hyperglycemia has been shown to lead to vascular complications involving large and small blood vessels, such as arteriosclerosis, glomerulosclerosis, and retinopathy. Diabetic neuropathy, characterized by pain and paresthesias, is among the most frequent complications of longstanding, poorly controlled diabetes and is often associated with a reduction in physical activity and with sleep disturbances.1,2
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.
These findings present a hopeful option not just for improved management of the condition, but a potential cure. One that doesn’t rely on expensive medications or invasive surgery, but instead, on improved diet and lifestyle — which could also be beneficial in managing and preventing a number of other chronic conditions which are affected by weight. As Taylor told The Guardian, “The weight loss goals provided by this programme [sic] are achievable for many people. The big challenge is long-term avoidance of weight re-gain.”
An unbalanced microbiome composition, known as dysbiosis, has been found in patients with diabetes, for whom the diversity of the gut microbiome is often reduced as compared to healthy people. Researchers from the University of Amsterdam recently showed that fecal transplants, used to transfer the microbiome of a healthy person to the gut of one with diabetes, can result in a short-term improvement of the insulin resistance found in obese patients with type 2 diabetes.
Both type 1 and type 2 diabetes mellitus are chronic conditions that can only be managed using insulin, anti-diabetes medications, lifestyle changes, etc., but cannot be cured. Gestational diabetes generally resolves on itself after the delivery. If not managed properly, diabetes can cause several other complications, like hypoglycemia, diabetic ketoacidosis, nonketotic hyperosmolar coma, etc. Other serious and long-term complications include cardiovascular diseases, chronic renal failure, diabetic retinopathy, etc.
Type 2 diabetes now affects more than 20 million Americans — and the diabetes epidemic shows no sign of slowing. When someone has type 2 diabetes, it needs to be controlled through controlled blood sugar levels. When diet and exercise are not enough to control blood sugar, some people with type 2 diabetes turn to medications, like metformin. However, more and more research shows that alternative medicine can also help control blood sugar. Read on for more.
This medical-grade polyester is currently used in teeth guards that kids and adults wear at night, in tiny tubes used to guide the growth of damaged nerve fibers and in surgical sutures.  Researchers are also looking at PCL’s potential as an implant to deliver medications directly to the eyes and to tumors and as a scaffold for growing human tissue.  PCL may be an ideal package for islet cells, the studies note, because it can be used to create thin, flexible membranes with pores that let in glucose and nutrients, let out insulin and exclude bigger immune-system molecules.
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.
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.
McInnes, N., Smith, A., Otto, R., Vandermey, J., Punthakee, Z., Sherifali, D., … Gerstein, H. C. (2017, March 15). Piloting a remission strategy in type 2 diabetes: Results of a randomized controlled trial. The Journal of Clinical Endocrinology and Metabolism, 2016-3373. Retrieved from https://academic.oup.com/jcem/article-abstract/doi/10.1210/jc.2016-3373/3070517/Piloting-a-Remission-Strategy-in-Type-2-Diabetes?redirectedFrom=fulltext
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.

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.
The aptly named bitter melon is thought to help cells use glucose more effectively and block sugar absorption in the intestine. When Philippine researchers had men and women take bitter melon in capsule form for three months, they had slight, but consistently, lower blood sugar than those taking a placebo. Gastrointestinal problems are possible side effects. You can reverse diabetes with these science-backed strategies.
Foods with a low glycemic load: The glycemic index of a food tells you about the blood glucose-raising potential of the food. Foods that have a high glycemic index are converted into sugar after being eaten more quickly than low glycemic foods. If you are fighting diabetes, stick to low glycemic foods like non-starchy vegetables, stone fruits and berries, nuts, seeds, avocados, coconut, organic meat, eggs, wild-caught fish, and raw pastured dairy.
Herbal prescriptions for diabetes are formulated or prescribed based on the patient’s predominant symptoms. For instance, a patient presenting primarily with excessive thirst (lung Yin deficiency) might be given a single herb, such as radix panacis quinquefolii; or a combination of herbs in a patent formulation such as yu chuan wan, which is used in general to treat diabetes of mild to moderate severity and specifically to treat excessive thirst due to Yin deficiency,12 and ba wei di huang tang (“eight-ingredient pill with rehmannia”), which was originally used to treat people exhibiting weakness, fatigue, and copious urine soon after drinking water.13
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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.
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!
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