They will always have the pre-diabetes diagnosis and have the potential to develop type 2 diabetes if aggressive dietary, exercise and or medication is not followed. It is possible to achieve a normal non-diabetic HbA1c after this – virtually not having any clinical evidence of the pre-diabetes, however the disease process is still there and being held at bay.
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.
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.
For Type 1 diabetics there will always be a need for insulin injections throughout their life. However, both Type 1 and Type 2 diabetics can see dramatic effects on their blood sugars through controlling their diet, and some Type 2 diabetics can fully control the disease by dietary modification. As diabetes can lead to many other complications it is critical to maintain blood sugars as close to normal as possible and diet is the leading factor in this level of control.
In other words, we can say that diabetes is a continual metabolic disorder that prevents the body from utilizing glucose totally or partially. The disorder is characterized by raised glucose absorption in the blood. When body does not have enough insulin, it cannot use or store glucose, which raises the level of glucose in the body. Diabetes is not curable, but controllable. There are several methods and remedies which can be used to tame this dreadful disease. Such is its dreadfulness that it is one of the major causes of disability and death in USA. In most of the cases, diabetes further leads to other critical diseases, like heart failure, obesity, cardiac arrest, etc. 
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
FEED YOUR GUT BUGS, not just yourself. There are trillions of bugs that live in your gut – their health is critical in determining your health. Many studiesshow links between the state of your gut bugs (your microbiota) and type 2 diabetes. Start improving the health of your gut immediately by eating five servings of different coloured vegetables each day. The non digestible fibre in vegetables is the preferred food for your gut bacteria and when your gut bugs are happy, you will be happy. The wider the variety of colours, the more phytonutrients you will be getting.
Mango tree leaves have been found to possess medicinal values to lower down the levels of blood glucose. Soak around 30 grams of fresh and clean mango tree leaves in around half a liter of water overnight. Squeeze the leaves in water to make a concoction.Consume this mixture empty stomach in the morning. It is an effective remedy to control beginning diabetes. One can also dry some mango leaves in shade and prepare its powder to be taken twice a day with water.
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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