Momordica Charantia goes under a variety of names and is native to some areas of Asia, India, Africa and South America. Marketed as charantia, it is also known as karela or karolla and bitter melon. The herb may be prepared in a variety of different ways, and may be able to help diabetics with insulin secretion, glucose oxidation and other processes.
Once you have diabetes, it is there for life. I help people to get their blood glucose levels back to or as near as possible the normal range. Firstly this will help you to feel better in the short term but it also helps to protect your blood vessels which can become very irritated and damaged by high glucose levels. Focussing on healthy eating, limiting unprocessed foods and getting a wide variety of fruits and vegetables in the diet helps.
Insulin therapy requires close monitoring and a great deal of patient education, as improper administration is quite dangerous. For example, when food intake is reduced, less insulin is required. A previously satisfactory dosing may be too much if less food is consumed causing a hypoglycemic reaction if not intelligently adjusted. Exercise decreases insulin requirements as exercise increases glucose uptake by body cells whose glucose uptake is controlled by insulin, and vice versa. In addition, there are several types of insulin with varying times of onset and duration of action.
Given the prevalence of diabetes and the chronic nature of the disease, it’s no surprise that CAM is a popular treatment option. I don’t see a lot of CAM use in Type 1 diabetics. Insulin is the primary treatment, it works well, and patients can objectively measure their own blood sugar. Type 1 diabetics don’t seem to experiment with supplements that might alter their blood sugars. Those patients end up hospitalized or dead.
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).
Consider a form of regular fasting (more to come in a later blog), such as intermittent fasting or time-restricted feeding (TRF). TRF means eating your calories during a specific window of the day, and choosing not to eat food for the rest. It’s a great way to reduce insulin levels in your body and help undo the effects of chronically elevated levels.
The primary issue requiring management is that of the glucose cycle. In this, glucose in the bloodstream is made available to cells in the body; a process dependent upon the twin cycles of glucose entering the bloodstream, and insulin allowing appropriate uptake into the body cells. Both aspects can require management. Another issue that ties along with the glucose cycle is getting a balanced amount of the glucose to the major organs so they are not affected negatively.
I was diagnosed with Type 2 diabetes and started with a nutritionist two years ago. I was losing weight (20 lbs) and doing well on her prescribes diet. She reviewed my food log and comment that I was cutting down too low on my carbs. She said that it would damage my kidneys. I was concerned and slightly increased my carbs — which led to cravings and weight gain. Why was that the advice given? It failed.
If your cells aren’t responding to insulin, your pancreas produces more to turn up the volume on the signal that glucose is available and the cells should absorb it. When your pancreas can keep up, blood glucose stays within healthy ranges, and all is well. When your pancreas starts to poop out, you end up with insulin deficiency, which leads to blood sugar fluctuations and weight gain.
Genetic predisposition to liver problems or certain autoimmune diseases often correlate to higher rates of diabetes. This is likely because proper insulin response is handled by the pancreas and liver, so problems here could affect the body’s normal response. Studies have linked certain autoimmune disease and leaky gut syndrome with higher instances of diabetes also, so this correlation is logical as well.
Metformin is a biguanide drug that increases the sensitivity of the body’s cells to insulin. It also decreases the amount of glucose produced by the liver.. In 1994, the FDA approved the use of the biguanide called metformin (Glucophage) for the treatment of type 2 diabetes. Today, this is still typically the first drug prescribed for type 2 diabetes.