Because blood sugar levels fluctuate throughout the day and glucose records are imperfect indicators of these changes, the percentage of hemoglobin which is glycosylated is used as a proxy measure of long-term glycemic control in research trials and clinical care of people with diabetes. This test, the hemoglobin A1c or glycosylated hemoglobin reflects average glucoses over the preceding 2–3 months. In nondiabetic persons with normal glucose metabolism the glycosylated hemoglobin is usually 4–6% by the most common methods (normal ranges may vary by method).
In addition to weight loss through traditional methods, some patients with diabetes can have bariatric surgery and then find that their diabetes goes away. Yet not everyone qualifies with this. The person usually needs to have a body mass index of 40 or higher and uncontrolled diabetes, Louard says. “If you regain the weight, the diabetes comes back,” Louard cautions.
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.
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.
It’s the patients with type 2 diabetes that lean towards supplements. While lifestyle modifications (exercise, weight loss, and smoking cessation) are the foundation for managing diabetes, drug treatment is usually also required. There are an array of prescription drugs like metformin and glyburide with a long history of use and demonstrated efficacy. Some drugs even decrease mortality – the primary outcome we’re after. But proper treatment has also been shown to the reduce the risk of an array of other consequences: Diabetes is the biggest cause of blindness, kidney failure and non-traumatic amputation. Diabetes is associated with an elevated risk of cardiovascular disease, too. Yet despite the irreversible consequences of diabetes, and the availability of effective medications, type 2 diabetes remains poorly-controlled in many, often because of poor self-management.
Recently, a small clinical trial in England studied the effects of a strict liquid diet on 30 people who had lived with Type 2 diabetes for up to 23 years. Nearly half of those studied had a remission that lasted six months after the diet was over. While the study was small, the finding offers hope to millions who have been told they must live with the intractable disease.

For type 2 diabetics, diabetic management consists of a combination of diet, exercise, and weight loss, in any achievable combination depending on the patient. Obesity is very common in type 2 diabetes and contributes greatly to insulin resistance. Weight reduction and exercise improve tissue sensitivity to insulin and allow its proper use by target tissues.[40] Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. A study conducted in 2008 found that increasingly complex and costly diabetes treatments are being applied to an increasing population with type 2 diabetes. Data from 1994 to 2007 was analyzed and it was found that the mean number of diabetes medications per treated patient increased from 1.14 in 1994 to 1.63 in 2007.[41]
A popular spice used in Indian cooking, and the main ingredient of ‘curry’ that has taken the world by storm, turmeric has antibacterial, anti-inflammatory and antioxidant properties that all come together to help diabetics manage more stable blood sugar levels. It helps boost immunity and prevent infections that diabetics are often vulnerable to. Studies conducted on rats prove that curcumin, the active ingredient in turmeric, is effective in reducing plasma glucose level and HbA1C as well as improving the lipid profile. Many diabetics also suffer from arthritis, since the sugar laden blood and inflammatory processes typical to diabetes often damage joints. Turmeric, with its anti-inflammatory abilities, also helps with these joint pains.
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).
7. Choose a real food diet: Sugary, processed foods are mainly simple carbohydrates and when ingested cause spikes in blood sugar levels and are all-around unhealthy for the body. Make sure you steer clear of candy, soda, snacks like potato chips and cookies, starches like white rice and potatoes, and processed “quick meals.” Though natural sugars such as honey and maple syrup are better, you still need to limit them because they can cause sugar spikes. Fruit should be eaten in moderation as well and kept to the lower sugar varieties. Additionally, gluten, cow’s milk, alcohol, refined oils like canola oil, and GMO’s should be avoided. Stick with whole foods from healthy sources instead.
I would love to hear what you have to say about a person that is 5’5″ and 110 lbs. My blood sugar was was in the 90s to 112 when fasting. My A1C was 5.7. So I started to eat less carbs but my A1C stayed elevated. I was then diagnosed with Glucose intolerance and prescribed Tradjenta 5mg. I also read several books on the subject and came across your TEDTalk video. I then adjusted my low carb eating and on the meds since 2017. I still need the meds to maintain my A1C at 5.2.
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.
Following these five principles can significantly influence blood glucose levels. However, not everyone responds the same. Some people with have immediate low blood glucose levels. Others may experience a slow and steady improvement of glucose control. Some may have temporary high glucose levels. Our experience is that this is transient and most people will improve.

Lose Excess Weight– Obesity and Diabetes often go hand in hand, and while the debate still rages on if one causes the other, studies show that losing weight can help mitigate diabetes, and also lowers your risk of getting it to begin with. Certain dietary and lifestyle improvements can help you lose weight and are beneficial for diabetes reversal as well.
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.

Diabetic persons are advised to make morning appointments to the dental care provider as during this time of the day the blood sugar levels tend to be better kept under control. Not least, individuals who suffer from diabetes must make sure both their physician and dental care provider are informed and aware of their condition, medical history and periodontal status.
“The degree of carbohydrate restriction that we recommend to establish and then maintain nutritional ketosis depends upon individual factors such degree of insulin resistance (metabolic syndrome or type 2 diabetes?) and physical activity. These starting levels of carb restriction typically vary between 30 and 60 grams per day of total carbs. The best way to determine one’s carbohydrate tolerance is to directly measure blood ketones with a finger-stick glucometer that also accommodates ketone testing.

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.