Diabetes is one of the most prevalent chronic diseases in the United States. The morbidity and mortality associated with the disease is significant and derives primarily from complications of persistent hyperglycemia. Longstanding hyperglycemia has been shown to lead to vascular complications involving large and small blood vessels, such as arteriosclerosis, glomerulosclerosis, and retinopathy. Diabetic neuropathy, characterized by pain and paresthesias, is among the most frequent complications of longstanding, poorly controlled diabetes and is often associated with a reduction in physical activity and with sleep disturbances.1,2
Several prediabetes interventions exist based on evidence from the landmark Diabetes Prevention Program (DPP) study. The DPP study reported that moderate weight loss (5-7% of body weight, or ~10-15 lbs. for someone weighing 200 lbs.), counseling, and education on healthy eating and behavior reduced the risk of developing type 2 diabetes by 58%. Data presented at the ADA 2014 conference showed that after 15 years of follow-up of the DPP study groups, the results were still encouraging: 27% of those in the original lifestyle group had a significant reduction in type 2 diabetes progression compared to the control group.
If excess energy is produced by the body, then this must be used in external physical movements or exercises. Exercise is not something that is needed or that is essential. But exercise or movements help to push the nutrients to furthermost cells in the body. If there is lack of movement, the nutrients will not be pushed to further most cells and will not generate any energy.
If the rapid changes in metabolism following bariatric surgery are a consequence of the sudden change in calorie balance, the defects in both insulin secretion and hepatic insulin sensitivity of type 2 diabetes should be correctable by change in diet alone. To test this hypothesis, a group of people with type 2 diabetes were studied before and during a 600 kcal/day diet (21). Within 7 days, liver fat decreased by 30%, becoming similar to that of the control group, and hepatic insulin sensitivity normalized (Fig. 2). The close association between liver fat content and hepatic glucose production had previously been established (20,22,23). Plasma glucose normalized by day 7 of the diet.
Acarbose (Precose) and miglitol (Glyset) are alpha-glucosidase inhibitors. These drugs help the body to lower blood glucose levels by blocking the breakdown of starches, such as bread, potatoes, and pasta in the intestine. They also slow the breakdown of some sugars, such as table sugar. Their action slows the rise in blood glucose levels after a meal. They should be taken with the first bite of a meal. These drugs may have side effects, including gas and diarrhea.
Dr Beverley Shields, at the University of Exeter Medical School, who led the research, said: "This finding is really exciting. It suggests that a person with Type 1 diabetes will keep any working beta-cells they still have seven years after diagnosis. We are not sure why this is; it may well be that there is a small group of "resilient" beta-cells resistant to immune attack and these are left after all the "susceptible" beta-cells are destroyed. Understanding what is special about these "resilient" beta-cells may open new pathways to treatment for Type 1 diabetes."
A new class of medications called DPP-4 inhibitors help improve A1C without causing hypoglycemia. They work by by preventing the breakdown of a naturally occurring compound in the body, GLP-1. GLP-1 reduces blood glucose levels in the body, but is broken down very quickly so it does not work well when injected as a drug itself. By interfering in the process that breaks down GLP-1, DPP-4 inhibitors allow it to remain active in the body longer, lowering blood glucose levels only when they are elevated. DPP-4 inhibitors do not tend to cause weight gain and tend to have a neutral or positive effect on cholesterol levels. Alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), and sitagliptin (Januvia) are the DPP-4 inhibitors currently on the market in the US.
Joseph, you should talk with your doctor or diabetes educator about this. In general, you can take metformin with most herbs, but your case might be different, and you might not need to. You might have to experiment. The same with insulin, although you have to be more careful there — in all cases you should work with your doctor or diabetes educator.
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.
When cells are resistant to insulin, they don’t use the insulin effectively to bring the glucose from the bloodstream into the cell. The pancreas needs to produce more insulin to overcome this resistance in an effort to normalize blood sugar levels. When the pancreas can’t keep up with the insulin demands in a person with insulin resistance, that person develops diabetes.
There are numerous studies of botanical medicines and herbs for diabetes that speak to the effectiveness of natural and home remedies for diabetes. I have listed the most useful herbs with the most documented benefits. A patient does not need to take one hundred bottles a day of everything out on the market, but rather it is important to focus on a few botanicals backed by the most impressive studies and the best clinical evidence. The botanicals listed below are safe and effective.
Curcumin. The compound curcumin, which is found in the spice tumeric, has been shown to both boost blood sugar control and help prevent the disease. In a nine-month study of 240 adults with pre-diabetes, those who took curcumin capsules (which are available over-the-counter) completely avoided developing diabetes while a sixth of patients in the placebo group did.
A. A couple of factors determine the optimal timing of medicine doses. Some drugs, such as rapid-acting insulin, are usually taken just before meals, and others must be taken on an empty stomach or with food. The way a drug works in the body, as well as the time it takes to start working and the duration of its action, may also determine the best time to take a medicine. Glipizide begins working in approximately 30 minutes to an hour. Since this drug increases insulin secretion, it is recommended that you take it before meals to reduce the risk of hypoglycemic episodes. If you take it only once a day, it’s best to do so prior to the largest meal of the day, or with breakfast. Saxagliptin starts working within hours and only achieves peak concentrations in the body after several hours. Saxagliptin, and other agents in the dipeptidyl peptidase-4 (DPP-4) inhibitor class, prevent the breakdown of a hormone called glucagon-like peptide (GLP) in response to the extra glucose in your blood after you eat, which increases the body’s insulin production. Although concentrations of GLP and other similar hormones are higher after eating, they are also released throughout the day under normal circumstances. So saxagliptin and other DPP-4 inhibitors can be taken without regard to meals.
Dr. May currently works as a fulltime endocrinologist and has been in private practice since 2004. He has a variety of interests, predominantly obesity and diabetes, but also sees patients with osteoporosis, thyroid disorders, men's health disorders, pituitary and adrenal disorders, polycystic ovaries, and disorders of growth. He is a leading member of several obesity and diabetes societies and runs a trial centre for new drugs.
Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
But people are curing diabetes every day. It's simple and straightforward, and when you cure diabetes, you greatly reduce your risk of heart disease, obesity and cancer at the same time. The thing is, no one will cure your diabetes for you. Sure, the drug companies want to "treat" you with diabetes drugs, but you have to keep taking those for a lifetime. They don't cure anything. The only real cure can come from YOU -- by changing what you eat and increasing your exercise.
“Diabetes type 1 is very different from your standard disease. Insulin requirements vary greatly from one day to another and there is no way patients can know what they need,” Roman Hovorka, Professor at the University of Cambridge, explained to me during an interview. His research group is working on the development of an algorithm that can accurately predict insulin requirements for a specific patient at any moment.