Cinnamon contains a bioactive compound that can help to fight and prevent diabetes. Cinnamon is known to stimulate the insulin activity and thus regulate the blood sugar level. As excess of anything is bad, likewise cinnamon if taken in excess can increase the risk of liver damage due to a compound called coumarin present in it. The true cinnamon, not the one buy from shops (Cassia cinnamon) is safer to have.
Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.

And when I talk about reducing certain carbohydrates, I mainly mean reducing your intake of  refined carbohydrates such as pasta, rice and bread. Non starchy vegetables (such as broccoli, cabbage and cauliflower) are fine and can be eaten in abundance. Many fruits are packed with carbohydrates, so if you’re trying to reduce your carb intake, try and limit your intake to low-carb fruit, such as rhubarb, watermelon, berries, peaches and blackberries.

The physician can also make referrals to a wide variety of professionals for additional health care support. In the UK a patient training course is available for newly diagnosed diabetics (see DESMOND). In big cities, there may be diabetes centers where several specialists, such as diabetes educators and dietitians, work together as a team. In smaller towns, the health care team may come together a little differently depending on the types of practitioners in the area. By working together, doctors and patients can optimize the healthcare team to successfully manage diabetes over the long term.
Suppose your friend is diagnosed with type 2 diabetes, then works hard to lose 50 pounds. He takes himself off all his medications and his blood sugars are now normal. What would you say to him? Probably something like “Great job. You’re really taking care of yourself. Keep it up!” What you wouldn’t say is something like “You’re such a dirty, filthy liar. My doctor says this is a chronic and progressive disease so you must be lying ”. It seems perfectly obvious that diabetes reversed because your friend lost all that weight. And that’s the point. The disease is reversible.
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.

Is this okay to use against gestational diabetes? I have PCOS and am pre-diabetic. I actually followed this way of eating (before seeing the Ted talk) with my first GD pregnancy and was scolded by the nutritionist. Yet my blood sugar was kept below 98 and I lost 15 lbs and our son’s blood sugar was perfect with an apgar of 10. So I’m thinking of just going this way again despite the ADA’s recommendations.

Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..
As of now, diabetes is classified as either Type I or Type II. New research suggests there are several more types of diabetes, which all require different treatment approaches, but that’s a developing area of knowledge. On an episode of Bulletproof Radio, Dr. Steven Masley explains why doctors are starting to view Altzheimer’s disease as “type III diabetes” and picks apart the relationship between insulin and brain degeneration. Listen to it on iTunes.
Medications and insulin do nothing to slow down the progression of this organ damage, because they do not eliminate the toxic sugar load from our body. We’ve known this inconvenient fact since 2008. No less than 7 multinational, multi-centre, randomized controlled trials of tight blood glucose control with medications (ACCORD, ADVANCE, VADT, ORIGIN, TECOS, ELIXA, SAVOR) failed to demonstrate reductions in heart disease, the major killer of diabetic patients. We pretended that using medications to lower blood sugar makes people healthier. But it’s only been a lie. You can’t use drugs to cure a dietary disease.
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.
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.

However, the alternate term “reversed” often being used, may confuse people and mistake the good control of diabetes (remission) as a complete cure. Unfortunately, there is no current long term cure yet, and if one had gained back the weight they had lost or went back to old lifestyle habits, Type 2 diabetes would come back and sign and symptoms would present.

The researchers followed the participants after they had completed an eight-week low-calorie-milkshake diet and returned to normal eating. Six months later, those who had gone into remission immediately after the diet were still diabetes-free. Though most of those who reversed the disease had had it for less than four years, some had been diabetic for more than eight years.
Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
The NIDDK has played an important role in developing “artificial pancreas” technology. An artificial pancreas replaces manual blood glucose testing and the use of insulin shots or a pump. A single system monitors blood glucose levels around the clock and provides insulin or a combination of insulin and a second hormone, glucagon, automatically. The system can also be monitored remotely, for example by parents or medical staff.
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.
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