Magnesium deficiency is not uncommon in people with diabetes, and it can worsen high blood sugar and insulin resistance. Some studies suggest that supplementing with magnesium may improve insulin function and lower blood sugar levels, but other studies have shown no benefit. Have your doctor check you for deficiency before supplementing with magnesium. These are signs that you’re not getting enough magnesium.
The diabetes market is expected to reach a massively big €86Bn by 2025 combining both type 1 (€32Bn) and type 2 (€54Bn) treatments, and we can expect all sort of revolutionary technologies to come forward and claim their market share. Researchers are already speculating about microchips that can diagnose diabetes type 1 before the symptoms appear or nanorobots traveling in the bloodstream while they measure glucose and deliver insulin.

Thank you Dr. Hallberg!! I am a Family Nurse Practitioner who did tele-medicine for 5 years before retiring. At 66 years of age my doctor diagnosed me with Type II Diabetes. I refused to take the medication and instead opted for a 6 month trial to lose enough weight to make the difference. After 4 months I’d lost 8 pounds and still had high blood sugars. Then my husband’s PCP recommended watching your TedTalk. That was the beginning and we both jumped into LCHF/Keto with both feet using Diet Doctor and you as our main resources. My husband has lost 38 pounds and I have lost 42 pounds since November 2017. More importantly my lab results today were a HgbA1c of 5.3 with average blood glucose of 105. I have about 50 more pounds to go to be at a healthier weight BUT I owe you a big thank you!! Now I’m working to encourage others of my friends, family and coaching clients to give LCHF/Keto a try! Thanks!!!!


Cyrus Khambatta earned a PhD in Nutritional Biochemistry from UC Berkeley after being diagnosed with type 1 diabetes in his senior year of college at Stanford University in 2002. He is an internationally recognized nutrition and fitness coach for people living with type 1, type 1.5, prediabetes and type 2 diabetes, and has helped hundreds of people around the world achieve exceptional insulin sensitivity by adopting low-fat, plant-based whole foods nutrition.
If a drug treatment’s efficacy is questionable, the adverse event and safety profile is even more important. As a popular food additive, cinnamon seems safe when consumed at doses of a few grams per day. (1 teaspoon of the powder is about 4.75 grams).  While the trials have been small and short in duration, no significant adverse events have been reported. It is Generally Recognised as Safe (GRAS), as a seasoning and flavoring. However, reversible liver damage has been reported with therapeutic use, due to coumarin, a chemical also present in Cassia cinnamon. Those with liver impairment or dysfunction may be at greater risk of harm. There are no published long-term studies with cinnamon that inform us whether chronic consumption of high doses is safe.
Magnesium deficiency is common in diabetic patients, as magnesium can be lost in the urine with hyperglycemia. A study in Diabetes Care reported that low magnesium status is common in Type 2 Diabetes Mellitus (T2DM) and showed that when low-magnesium Type 2 Diabetes Mellitus patients were given an oral dose of magnesium daily for sixteen weeks, the mineral reduced insulin resistance, fasting glucose, and A1C levels.

Conventional treatment for Type 1 Diabetes generally involves insulin supplementation in the form of injections. Because Type 1 is an autoimmune disorder, it can affect both children and adults, and it’s not uncommon for diabetics to be dependent on lifelong insulin treatments. Type 2, on the other hand, is largely a product of poor lifestyle choices or little access to healthy foods, and is more likely to occur later in life. However, in recent years, there has been an alarming rise in Type 2 Diabetes cases among children and adolescents, which largely stems from an overwhelming obesity issue.
Gymnema Sylvestre is a vine native to Central & South India. Used in traditional Indian medicine since the 6th century BC, the leaves of this plant contain ‘gymnemic acids’ that have the amazing ability to slow down the transport of glucose from the intestines to the bloodstream. Some scientists even believe that Gymnema Sylvestre extract can help repair and regenerate pancreatic beta cells that produce insulin!
Diabetes type 1 is caused by the destruction of enough beta cells to produce symptoms; these cells, which are found in the Islets of Langerhans in the pancreas, produce and secrete insulin, the single hormone responsible for allowing glucose to enter from the blood into cells (in addition to the hormone amylin, another hormone required for glucose homeostasis). Hence, the phrase "curing diabetes type 1" means "causing a maintenance or restoration of the endogenous ability of the body to produce insulin in response to the level of blood glucose" and cooperative operation with counterregulatory hormones.
Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore, by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin-producing intestinal cells die off, they are boosted by additional oral medications.[76]
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
Evidence linking hepatic insulin sensitivity to intraorgan triglyceride content has been steadily accumulating. In insulin-treated type 2 diabetes, insulin dose correlates with the extent of fatty liver (35), and in turn, this is associated with insulin sensitivity to suppression of hepatic glucose production (36). Decreasing the fat content of liver is associated with improvement in insulin suppression of glucose production and, thereby, with improvement in fasting plasma glucose (20,23).
If the rapid changes in metabolism following bariatric surgery are a consequence of the sudden change in calorie balance, the defects in both insulin secretion and hepatic insulin sensitivity of type 2 diabetes should be correctable by change in diet alone. To test this hypothesis, a group of people with type 2 diabetes were studied before and during a 600 kcal/day diet (21). Within 7 days, liver fat decreased by 30%, becoming similar to that of the control group, and hepatic insulin sensitivity normalized (Fig. 2). The close association between liver fat content and hepatic glucose production had previously been established (20,22,23). Plasma glucose normalized by day 7 of the diet.
“I have many ways to help patients manage diabetes, but it’s very hard to reverse,” says Dr. Rita Louard, director of the Clinical Diabetes Program at Montefiore Health System in Bronx, New York. Still, some diabetes experts will use the word “reverse” when talking about this topic, Louard says, acknowledging the controversy that exists when discussing diabetes reversal.
Low blood sugar, or hypoglycemia, is a syndrome in which a person's blood sugar is dangerously low. People with type 1 and type 2 diabetes are at risk for this condition. There are other diseases that can cause a person's blood sugar levels to go too low, for example, pancreatitis, Cushing's syndrome, and pancreatic cancer. Symptoms and signs that your blood sugar levels are too low include:
A patient diagnosed with type 2 diabetes (HbA1c of 6.5% or above) will always have type 2 diabetes. Interventions such as medication (including insulin), staying active and making good diet choices must be maintained to prevent the disease from progressing further. However, even if the patient undergoes strict medication, diet and exercise adherence and manages to lower the HbA1c they will still have type 2 diabetes.
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 problem is, glucose is actually toxic if it is just floating around in your bloodstream, so that body has a defense mechanism. Any glucose that is not immediately used is stored as glycogen in the liver and the muscles. This would be all well and good except that your body has a limited number of glycogen receptors. When these are full, as they almost always are in inactive people, the body only has one option left: to store all the excess glucose as saturated fat within the body.
The chart above gives averages. Follow your doctor’s advice on when and how to take your insulin. Your doctor might also recommend premixed insulin, which is a mix of two types of insulin. Some types of insulin cost more than others, so talk with your doctor about your options if you're concerned about cost. Read about financial help for diabetes care.

Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.[48] This new method autologous nonmyeloablative hematopoietic stem cell transplantation was developed by a research team composed by Brazilian and American scientists (Dr. Julio Voltarelli, Dr. Carlos Eduardo Couri, Dr Richard Burt, and colleagues) and it was the first study to use stem cell therapy in human diabetes mellitus This was initially tested in mice and in 2007 there was the first publication of stem cell therapy to treat this form of diabetes.[73] Until 2009, there was 23 patients included and followed for a mean period of 29.8 months (ranging from 7 to 58 months). In the trial, severe immunosuppression with high doses of cyclophosphamide and anti-thymocyte globulin is used with the aim of "turning off" the immunologic system", and then autologous hematopoietic stem cells are reinfused to regenerate a new one. In summary it is a kind of "immunologic reset" that blocks the autoimmune attack against residual pancreatic insulin-producing cells. Until December 2009, 12 patients remained continuously insulin-free for periods ranging from 14 to 52 months and 8 patients became transiently insulin-free for periods ranging from 6 to 47 months. Of these last 8 patients, 2 became insulin-free again after the use of sitagliptin, a DPP-4 inhibitor approved only to treat type 2 diabetic patients and this is also the first study to document the use and complete insulin-independendce in humans with type 1 diabetes with this medication. In parallel with insulin suspension, indirect measures of endogenous insulin secretion revealed that it significantly increased in the whole group of patients, regardless the need of daily exogenous insulin use.[74]
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.
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