The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
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.
The essential feature of type 2 diabetes and pre-diabetes is that our bodies are completely filled with sugar. It’s not just too much sugar in the blood. That’s only part of the problem. There’s too much sugar in our entire body. Imagine our bodies to be a sugar bowl. A bowl of sugar. When we are young, our sugar bowl is empty. Over decades, we eat too much of the wrong things — sugary cereals, desserts and white bread. The sugar bowl gradually fills up with sugar until completely full. The next time you eat, sugar comes into the body, but the bowl is full, so it spills out into the blood.
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).
“This is a radical change in our understanding of Type 2 diabetes,” said Dr. Roy Taylor, a professor at Newcastle University in England and the study’s senior author. “If we can get across the message that ‘yes, this is a reversible disease — that you will have no more diabetes medications, no more sitting in doctors’ rooms, no more excess health charges’ — that is enormously motivating.”
As a bonus, stress relief may help you sleep better, which is important because studies show that not getting enough sleep can worsen type 2 diabetes. Sleeping less than six hours a night has also been found to contribute to impaired glucose tolerance, a condition that often precedes type 2 diabetes. In fact, a review published in 2015 in Diabetes Care analyzed 10 studies that involved more than 18,000 participants combined and found the lowest risk of type 2 diabetes in the group of participants that slept seven to eight hours per day. That’s the minimum recommended amount of sleep for most adults, according to the National Sleep Foundation.
Fix your Gut– Not the beer gut, your intestines. Grains and toxins cause damage to the intestinal lining and facilitate leaky gut syndrome. Depleted beneficial bacteria in the gut caused by poor diet, antibiotic use or being bottle fed as a baby can make the problem worse. Remove the grains, avoid toxins whenever possible and take a high quality probiotic to help the intestines heal. As a note: some people will have continued damage to the gut with exposure to grains, especially gluten, as little as only every 10 days or even every 6 months.
I made a mistake in an earlier comment that I need to correct. I thought the VLDL represented the very small particles, and that is totally wrong. Here are the actual test results of the very small particles from a Quest Diagnostics after about 18 months on a ketogenic diet, with abundant use of MCT oil as caprylic acid. If the administrator deletes that comment, to avoid confusion, that would be fine with me. I can also provide much more data, as that test is pretty comprehensive.
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.
Recently i been diagnosed with diabetes..doctor want me to take medicine i tried it for 10 days but that made me so dizzy.so i stop that medicine..i am following the fenugreek method but what i do is i soak it and i eat few of them two times a day.. i dont know how far that is working..can you anyone tell me the best way it work.and do you know if it cause any effects with eye sight????? thanks alot..
This information is solely for informational purposes. IT IS NOT INTENDED TO PROVIDE MEDICAL ADVICE. Neither the Editors of Consumer Guide (R), Publications International, Ltd., the author nor publisher take responsibility for any possible consequences from any treatment, procedure, exercise, dietary modification, action or application of medication which results from reading or following the information contained in this information. The publication of this information does not constitute the practice of medicine, and this information does not replace the advice of your physician or other health care provider. Before undertaking any course of treatment, the reader must seek the advice of their physician or other health care provider.
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.
As self-management of diabetes typically involves lifestyle modifications, adherence may pose a significant self-management burden on many individuals. For example, individuals with diabetes may find themselves faced with the need to self-monitor their blood glucose levels, adhere to healthier diets and maintain exercise regimens regularly in order to maintain metabolic control and reduce the risk of developing cardiovascular problems. Barriers to adherence have been associated with key psychological mechanisms: knowledge of self-management, beliefs about the efficacy of treatment and self-efficacy/perceived control. Such mechanisms are inter-related, as one's thoughts (e.g. one's perception of diabetes, or one's appraisal of how helpful self-management is) is likely to relate to one's emotions (e.g. motivation to change), which in turn, affects one's self-efficacy (one's confidence in their ability to engage in a behaviour to achieve a desired outcome).
People with type 1 diabetes (T1D) can live long, happy lives with proper care and disease management. Advancements in medication types and delivery methods give people the freedom to choose which treatment options work best with their particular circumstance. T1D prognoses can be greatly improved with a combination of treatments and lifestyle choices.
With diabetes, however, either the pancreas doesn’t produce the correct amount of insulin (Type 1) or the body’s cells are unable to process and utilize the insulin (Type 2). In both cases, this causes a buildup of glucose in the blood, which results in inadequate energy supply for the body and can cause dehydration, kidney and nerve damage, blindness, an increased risk for heart attack and stroke, and more.
The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.