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.
Genetic factors do play a role in any disease, but I put this factor last for a reason. Genetic predisposition to a given disease will increase the chances of getting the disease, but not in a vacuum. People with a strong predisposition to liver disease manage to avoid it, and some with a family history of heart disease remain heart-attack free. Even studies among identical twins show that in most cases, twins will get the same diseases, even in different environments, but sometimes they don’t. This means there are other factors involved (see above).
A healthy balance of carbohydrates, proteins, and fats in your diet will help keep your blood glucose on target. How much of each will depend on many factors, including your weight and your personal preferences. Watching your carbohydrates -- knowing how much you need and how many you are eating -- is key to blood sugar control. If you are overweight, either a low-carbohydrate, low-fat/low calorie, or Mediterranean diet may help you get your weight to goal. No more than 7% of your diet should come from saturated fat, and you should try to avoid trans fats altogether.
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
Even if you aim to lose 5% of your body weight, if overweight, you are likely to see a fall in your blood glucose levels back into the normal range but even then we can’t say diabetes has been reversed or gone away. These actions build-up the body’s ability to respond to rising levels but if you get sick, eat more carbohydrate or gain some weight, more than likely your blood glucose levels will be on the rise again into the diabetes range.
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.
Most doctors, dietitians and diabetes specialists claim that type 2 diabetes is a chronic and progressive disease. The American Diabetes Association, for example, almost proudly proclaims this on its website. Once you get the diagnosis, it’s a life sentence. But, it’s actually a great big lie. Type 2 diabetes is almost always reversible and this is almost ridiculously easy to prove. This is great news for the more than 50% of American adults who have been diagnosed with pre-diabetes or diabetes. Recognizing this truth is the crucial first step in reversing your diabetes or pre-diabetes. Actually, it something that most people already instinctively recognized to be true.
Carbs and fats provide energy for the body. When carbs are limited in the diet, fat becomes the preferred and efficient fuel source. When you reduce your intake of one macronutrient, you have to increase your intake of at least one other macronutrient—otherwise you’ll feel hungry and not have enough energy. The low-fat craze started with flawed science that incorrectly stated that fat was dangerous. In a low carb, high-fat diet, fat provides you with the energy your body needs, and also helps knock out hunger and cravings.
Given the above research findings, it is recommended that drivers with type 1 diabetes with a history of driving mishaps should never drive when their BG is less than 70 mg/dl (3.9 mmol/l). Instead, these drivers are advised to treat hypoglycemia and delay driving until their BG is above 90 mg/dl (5 mmol/l). Such drivers should also learn as much as possible about what causes their hypoglycemia, and use this information to avoid future hypoglycemia while driving.
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
Although the relationship between magnesiumand diabetes has been studied for decades, we still don't fully understand it. Low magnesium may worsen blood sugar control in type 2 diabetes. Scientists say that it interrupts insulin secretion in the pancreas and builds insulin resistance in the body's tissues. And evidence suggests that a magnesium deficiency may contribute to some diabetes complications. People who get more magnesium in their diet (by eating whole grains, nuts, and green leafy vegetables) have a lower risk of type 2 diabetes.
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.
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.
O-3 oils, with both EPA and DHA, can help patients by lowering lipid panels (reduce triglycerides and cholesterol); reducing insulin resistance; reducing pain and inflammation so exercise and sleep are easier; reducing the risk of cardiovascular disease by lowering blood pressure; reducing the risk of dementia and Alzheimer’s disease; preventing and treating anxiety and depression; and promoting antioxidant actions in the body and brain to help reduce developing diabetic complications.
These substances are not considered to be medications by the US FDA and are therefore not regulated as such. This means that there are no standards in place to ensure that a given product contains the substance or dose as described on the label. There are also no requirements to perform studies showing that the products are safe or effective. Side effects of supplements are typically not well understood, and some supplements can interfere with the action of medications.