Both type 1 and type 2 diabetes mellitus are chronic conditions that can only be managed using insulin, anti-diabetes medications, lifestyle changes, etc., but cannot be cured. Gestational diabetes generally resolves on itself after the delivery. If not managed properly, diabetes can cause several other complications, like hypoglycemia, diabetic ketoacidosis, nonketotic hyperosmolar coma, etc. Other serious and long-term complications include cardiovascular diseases, chronic renal failure, diabetic retinopathy, etc.
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.
If I could only prescribe one supplement for a diabetes patient, I would prescribe R-alpha-lipoic acid. Alpha-lipoic acid has numerous benefits to the diabetic patient. It is a water- and fat-soluble antioxidant and has been shown to protect patients with fatty liver from liver disease progression. It can help reduce insulin resistance and has been shown to protect people with diabetes from developing complications in their nerves, eyes, and kidneys. R-ALA can prevent glycosylation of proteins, which reduces the A1C level. It is safe, although very rarely it can cause stomach upset. Alpha-lipoic acid is listed either as ALA or R-ALA. When listed as ALA, this means it contains two forms—the S isomer form and the R isomer form, in a 50:50 ratio. The key is to find a product that says it contains “R-ALA” instead of just “ALA.” A good daily working dose of R-ALA is 300 to 1,200 mg a day, which is the equivalent of 600 to 2,400 mg a day of regular ALA, if you buy a regular ALA listed product.
7. Choose a real food diet: Sugary, processed foods are mainly simple carbohydrates and when ingested cause spikes in blood sugar levels and are all-around unhealthy for the body. Make sure you steer clear of candy, soda, snacks like potato chips and cookies, starches like white rice and potatoes, and processed “quick meals.” Though natural sugars such as honey and maple syrup are better, you still need to limit them because they can cause sugar spikes. Fruit should be eaten in moderation as well and kept to the lower sugar varieties. Additionally, gluten, cow’s milk, alcohol, refined oils like canola oil, and GMO’s should be avoided. Stick with whole foods from healthy sources instead.
To help you avoid or limit fast food, Chong recommends planning ahead by packing healthy meals or snacks. Diabetes-friendly snack ideas include a piece of fruit, a handful of nuts, and yogurt. Also, if you absolutely must stop at a fast-food restaurant, steer clear of anything that’s deep-fried — such as french fries, chicken nuggets, and breaded fish or chicken, Chong says.
If however, type 2 diabetes is a result of insulin resistance and being overweight, there is excellent evidence that exercise, decreasing added sugars and saturated fats in the diet, choosing low glycaemic index foods and losing weight – particularly around the abdominal region, can improve blood glucose levels to the extent that it seems like diabetes has been reversed.
Lunch. Salads are always a good option for lunch – load it up with meat or tofu, cheese, avocado, veggies and a full-fat dressing like olive oil or ranch. In a rush? Grab a lettuce-wrapped burger or bread-less sandwich from any fast food outlet. Like to cook? Try steak and brussels sprouts smothered in butter, salmon and asparagus with hollandaise sauce or a Thai curry made with tofu, coconut milk and green beans.
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).
In a person with carbohydrate intolerance, type 2 diabetes or prediabetes, this system breaks down. The body loses its insulin sensitivity and more and more insulin is required to remove the excess blood sugar. As a result, blood sugar levels remain high and insulin levels are high as well, and these high insulin levels can make your body even less sensitive to insulin.
Some people with diabetes use a computerized pump -- called an insulin pump -- that gives insulin on a set basis. You and your doctor program the pump to deliver a certain amount of insulin throughout the day (the basal dose). Plus, you program the pump to deliver a certain amount of insulin based on your blood sugar level before you eat (bolus dose).
Recently[when?] it has been suggested that a type of gastric bypass surgery may normalize blood glucose levels in 80–100% of severely obese patients with diabetes. The precise causal mechanisms are being intensively researched; its results may not simply be attributable to weight loss, as the improvement in blood sugars seems to precede any change in body mass. This approach may become a treatment for some people with type 2 diabetes, but has not yet been studied in prospective clinical trials. This surgery may have the additional benefit of reducing the death rate from all causes by up to 40% in severely obese people. A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.
Testosterone replacement therapy may improve glucose tolerance and insulin sensitivity in diabetic hypogonadal men. The mechanisms by which testosterone decreases insulin resistance is under study. Moreover, testosterone may have a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Several types of plants are referred to as ginseng, but most studies have used American ginseng. They've shown some sugar-lowering effects in fasting and after-meal blood sugar levels, as well as in A1c results (average blood sugar levels over a 3-month period). But we need larger and more long-term studies. Researchers also found that the amount of sugar-lowering compound in ginseng plants varies widely.
It is a good idea to wear a MedicAlert bracelet or tag that says you have diabetes. This will make others aware of your condition in case you have a severe hypoglycemic attack and are not able to make yourself understood, or if you are in an accident and need emergency medical care. Identifying yourself as having diabetes is important because hypoglycemic attacks can be mistaken for drunkenness, and victims often aren't able to care for themselves. Without prompt treatment, hypoglycemia can result in a coma or seizures. And, because your body is under increased stress when you are ill or injured, your blood sugar levels will need to be checked by the medical personnel who give you emergency care.
There are several great exercises for diabetes, including biking, running, swimming, walking, strength training, and the like. The Centers for Disease Control and Prevention (CDC) recommends getting at least 150 minutes of moderate-intensity aerobic activity per week — that’s five 30-minute workouts — or 75 minutes of vigorous-intensity aerobic activity per week.
"Perfect glycemic control" would mean that glucose levels were always normal (70–130 mg/dl, or 3.9–7.2 mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications.
Although chromium does have an effect on insulin and on glucose metabolism, there is no evidence that taking chromium supplements can help in the treatment of diabetes. But chromium is found in many healthy foods, such as green vegetables, nuts, and grains. Studies have suggested that biotin, also called vitamin H, when used with chromium, may improve glucose metabolism in people with diabetes. But no studies have shown that biotin by itself is helpful.
the remedies you have mentioned has given me heart ,as i am having half cup of of karela juice....but i have not taken my blood test as i am fed up and my finger tips are also fed up...so i take my dose of insulin and also the juice.;-)...and hope it works. or is working . i do my daily morning and evening walk of half hour.eat nothing sweet.or starchy 15th july 08
Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..