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.”
By checking your own blood sugar levels, you can track your body's changing needs for insulin and work with your doctor to figure out the best insulin dosage. People with diabetes check their blood sugar up to several times a day with an instrument called a glucometer. The glucometer measures glucose levels in a sample of your blood dabbed on a strip of treated paper. Also, there are now devices, called continuous glucose monitoring systems (CGMS), that can be attached to your body to measure your blood sugars every few minutes for up to a week at a time. But these machines check glucose levels from skin rather than blood, and they are less accurate than a traditional glucometer.
Mr. Tutty said he jumped at the chance, becoming one of 30 men and women ages 25 to 80 to sign up. Mr. Tutty was one of 13 participants whose fasting plasma glucose dropped, and during the six-month follow-up remained below the seven millimole per liter (or 126 milligrams per deciliter) that defines diabetes. Although Mr. Tutty completed the study nearly three years ago, his fasting blood sugars continue to range from 5.2 to 5.6 mmol/L, he said.
Some studies suggest that low magnesium levels may worsen blood glucose control in type 2 diabetes. There is also some evidence that magnesium supplementation may help with insulin resistance. For example, a study examined the effect of magnesium or placebo in 63 people with type 2 diabetes and low magnesium levels who were taking the medication glibenclamide. After 16 weeks, people who took magnesium had improved insulin sensitivity and lower fasting glucose levels.
These seeds, used in Indian cooking, have been found to lower blood sugar, increase insulin sensitivity, and reduce high cholesterol, according to several animal and human studies. The effect may be partly due to the seeds’ high fiber content. The seeds also contain an amino acid that appears to boost the release of insulin. In one of the largest studies on fenugreek, 60 people who took 25 grams daily showed significant improvements in blood sugar control and post-meal spikes.
I do not believe it can be an actual reversal, more of a remission. If no longer needing medication to control blood sugar looks like reversal it is only possible if the person maintains regular exercise and a healthy weight. The length of time one has diabetes plays a role as does one’s genes. There are some thin people who have type 2 diabetes due to heredity.
Peripheral neuropathy is a problem with the functioning of the nerves outside of the spinal cord. Symptoms may include numbness, weakness, burning pain (especially at night), and loss of reflexes. Possible causes may include carpel tunnel syndrome, shingles, vitamin or nutritional deficiencies, and illnesses like diabetes, syphilis, AIDS, and kidney failure. Peripheral neuropathy is diagnosed with exams and tests. Treatment for the condition depends on the cause. Usually, the prognosis for peripheral neuropathy is good if the cause can be successfully treated or prevented.
Second, hypoglycemia can affect a person’s thinking process, coordination, and state of consciousness.[45][46] This disruption in brain functioning is called neuroglycopenia. Studies have demonstrated that the effects of neuroglycopenia impair driving ability.[45][47] A study involving people with type 1 diabetes found that individuals reporting two or more hypoglycemia-related driving mishaps differ physiologically and behaviorally from their counterparts who report no such mishaps.[48] For example, during hypoglycemia, drivers who had two or more mishaps reported fewer warning symptoms, their driving was more impaired, and their body released less epinephrine (a hormone that helps raise BG). Additionally, individuals with a history of hypoglycemia-related driving mishaps appear to use sugar at a faster rate[49] and are relatively slower at processing information.[50] These findings indicate that although anyone with type 1 diabetes may be at some risk of experiencing disruptive hypoglycemia while driving, there is a subgroup of type 1 drivers who are more vulnerable to such events.
” 200 consecutive pts, aged 51-86, M:F ratio 3/2, with known vascular risk factors of HTN, DM, Hypercholesterolemia, hx of MI, Stent, CABG, were enrolled in a dietary program, which emphasizes large amts of leafy green vegetables, olive oil, radical reduction of grain, legumes, nightshades, and fruits; and generous amts of grassfed animal proteins, emphasizing Shellfish and avoiding commercial poultry (Diet Evolution). All pts were instructed to take 2-4,000 mg of high DHA fish oil, 200mg of Grape Seed Extract, and 50 mg of Pycnogenol per day. All pts had Endothelial Reactivity (ER) using PAT before and after a 5-minute arm occlusion using the EndoPAT 2000 (Itamar, Israel) at baseline and at 6 months.

When the weight loss lessens the liver and pancreas fat, the insulin-producing beta cells in the pancreas come to life again. "Almost everyone will return to normal if they lose a substantial amount of weight," Taylor says. "This is a simple disease." What's yet to be figured out, he says, is why the weight loss doesn't lead to a reversal in everyone.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
The men took a six-hour educational course on diabetes and intermittent fasting prior to fasting. For the experiment, one man fasted for 24 hours three days per week, and the other two alternated their fasting days throughout the week. On fast days, they ate one low-calorie meal in the evening, and drank low-cal beverages, such as water, coffee, tea, and broth. The authors encouraged participants to opt for low-carb on the eating days.
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.
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