Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
The food pyramid recommended 6-11 servings of carbs per day, and very little fat — a low-fat, high-carb diet. As we outlined in our last video, type 2 diabetes is a disease of carbohydrate intolerance. Someone with type 2 diabetes or prediabetes has a low carbohydrate tolerance, so eating carbs will lead to exaggerated blood sugar spikes. While those with a high carb tolerance may be able to eat a carb-heavy diet and remain healthy, someone with a low carb tolerance will experience chronic high blood sugar and likely even weight gain if they eat a high-carb diet.
There is no prescribed diet plan for diabetes and no single “diabetes diet”. Eating plans are tailored to fit each individual's needs, schedules, and eating habits. Each diabetes diet plan must be balanced with the intake of insulin and other diabetes medications. In general, the principles of a healthy diabetes diet are the same for everyone. Consumption of various foods in a healthy diet includes whole grains, fruits, non-fat dairy products, beans, lean meats, vegetarian substitutes, poultry, or fish.
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.

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.

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.


Could restricting your diet for a couple of days a week put type 2 diabetes in remission? That’s the controversial claim scientists of a small new study are making as they fan the fire around a diet fad known as intermittent fasting. But many health professionals, including those at the American Diabetes Association, argue that the approach can be dangerous for people with diabetes, whose bodies cannot control their blood sugar without careful diet, medication, and sometimes insulin management.
My Mother is suffering from type 1 diabetes since last 20yrs..she is using alopathy medicines but.. we are not able to control the sugar levels to normal. today only i gone thru this site..and got very usefull information on diabetes treatment natural way. its really a great effort ..i wish that every one get very usefull tips for their health problems..

Over a period of years, you went from pre-diabetes, to diabetes, to taking one medication, then two then three and then finally large doses of insulin. Here’s the thing. If you are taking more and more medications to keep your blood sugars at the same level, your diabetes is getting worse! Even if your blood sugars get better, your diabetes is getting worse. This is unfortunately what happens to virtually every patient. The body is already overflowing with sugar. The medications only hide the blood sugar by cramming it into the engorged body.
The new research ties in with recent thinking among experts about what happens when type 2 diabetes develops, says Domenico Accili, MD, chief of endocrinology at Columbia University Vagelos College of Physicians and Surgeons. "We have been talking for some time, that in diabetes, primarily type 2, the insulin-producing [beta] cell is not dead but simply inactive," he says. "If you put patients with diabetes on a diet, you can do marvels with their beta cells."
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).
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.
NOTE: Do not eat or drink anything else during the three hours of testing. You may be able to get an accurate baseline of your insulin response after only a few days, but a week provides more data. If you are already diabetic, you probably have close ideas on these numbers, but take readings at the suggested times anyway to figure out your baseline.
Diabetes can be very complicated, and the physician needs to have as much information as possible to help the patient establish an effective management plan. Physicians may often experience data overload resulting from hundreds of blood-glucose readings, insulin dosages and other health factors occurring between regular office visits which must be deciphered during a relatively brief visit with the patient to determine patterns and establish or modify a treatment plan.[5]

Gestational diabetes develops during pregnancy because hormones interfere with how the body uses insulin. When the pancreas can’t keep up with the insulin demand and blood glucose levels get too high, the result is gestational diabetes. About 2-7 percent of expectant mothers develop gestational diabetes during their pregnancy. Learn more about diabetes and pregnancy.
Also called weight-loss surgery or metabolic surgery, bariatric surgery may help some people with obesity and type 2 diabetes lose a large amount of weight and regain normal blood glucose levels. Some people with diabetes may no longer need their diabetes medicine after bariatric surgery. Whether and for how long blood glucose levels improve seems to vary by the patient, type of weight-loss surgery, and amount of weight the person loses. Other factors include how long someone has had diabetes and whether or not the person uses insulin.1
The medications only hide the blood sugar by cramming it into the engorged body. The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.
Diabetes is an illness related to elevated blood sugar levels. When you stop releasing and responding to normal amounts of insulin after eating foods with carbohydrates, sugar and fats, you have diabetes. Insulin, a hormone that’s broken down and transported to cells to be used as energy, is released by the pancreas to help with the storage of sugar and fats. But people with diabetes don’t respond to insulin properly, which causes high blood sugar levels and diabetes symptoms.
Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.
According to studies, cinnamon may have a positive effect on the glycemic control and the lipid profile in patients with diabetes mellitus type 2. This is because it contains 18% polyphenol content in dry weight. This popular Indian spice can improve insulin sensitivity and blood glucose control. According to a study published in Journal Of The American Board Of Family Medicine, “cinnamon lowered HbA1C by 0.83% compared with standard medication alone lowering HbA1C  0.37%. Taking cinnamon could be useful for lowering serum HbA1C in type 2 diabetics with HbA1C >7.0 in addition to usual care.”
And when I talk about reducing certain carbohydrates, I mainly mean reducing your intake of  refined carbohydrates such as pasta, rice and bread. Non starchy vegetables (such as broccoli, cabbage and cauliflower) are fine and can be eaten in abundance. Many fruits are packed with carbohydrates, so if you’re trying to reduce your carb intake, try and limit your intake to low-carb fruit, such as rhubarb, watermelon, berries, peaches and blackberries.
Insulin is a naturally occurring hormone in your pancreas that helps your body use blood sugar and keeps blood sugar within a healthy range. But in the case of type 2 diabetes, a person’s body doesn’t use insulin properly, leading to insulin resistance. When your pancreas simply can't make enough insulin or use it well enough to control blood sugar, your doctor is likely to prescribe insulin injections.
Late in the 19th century, sugar in the urine (glycosuria) was associated with diabetes. Various doctors studied the connection. Frederick Madison Allen studied diabetes in 1909–12, then published a large volume, Studies Concerning Glycosuria and Diabetes, (Boston, 1913). He invented a fasting treatment for diabetes called the Allen treatment for diabetes. His diet was an early attempt at managing diabetes.
When a patient is ready to make a big commitment to get their blood sugar under control, Simos works with them to help tease apart what may be causing their blood sugar to spiral. Sometimes it’s what they're eating, sometimes it’s stress at home and at work and sometimes it’s a day full of sitting versus moving. Often, it’s a mix of these things. Other factors may contribute to diabetes risk, including a family history of the disease.
As self-management of diabetes typically involves lifestyle modifications, adherence may pose a significant self-management burden on many individuals.[65] 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.[65] 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).[66]
Conventional: A dietary pattern that includes carbohydrates from fruits, vegetables, whole grains, legumes, and low-fat milk is encouraged for good health. Carbohydrate intake should be monitored using carbohydrate counting or experienced-based estimation. The Recommended Dietary Allowance for digestible carbohydrates is 130 g/day, which will provide a sufficient amount of glucose needed to fuel the central nervous system without reliance on glucose production from protein or fat. Using foods with a low glycemic index that are rich in fiber and other important nutrients is encouraged.
An injection port has a short tube that you insert into the tissue beneath your skin. On the skin’s surface, an adhesive patch or dressing holds the port in place. You inject insulin through the port with a needle and syringe or an insulin pen. The port stays in place for a few days, and then you replace the port. With an injection port, you no longer puncture your skin for each shot—only when you apply a new port.
In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).

Curcumin is a bright yellow chemical produced by the spice turmeric, among other plants. Curcumin seems to have multiple benefits for diabetes symptoms. It has been shown to be a marked inhibitor of reactive oxygen species that promote oxidation damage in cells. Curcumin lowers inflammatory chemicals like tumor necrosis factor-alpha, and that’s good because TNF-a causes insulin resistance and irritates fatty livers. Curcumin can reduce another pro-inflammatory chemical called NF-KB. The above-mentioned actions provide a benefit in diabetes protection and reduce the risk of developing diabetes symptoms and complications. Curcumin has also been shown to enhance pancreatic beta cell functioning and reduce fatty liver deposition. It reduces high blood sugar, A1C, and insulin resistance. It was also shown to reduce the onset of Alzheimer’s disease, and that is a higher risk in diabetic patients than in nondiabetic patients. A good dose is 200 to 3,000 mg a day.


When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs — the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.
An insulin pump is composed of a reservoir similar to that of an insulin cartridge, a battery-operated pump, and a computer chip that allows the user to control the exact amount of insulin being delivered. The pump is attached to a thin plastic tube (an infusion set) that has a cannula (like a needle but soft) at the end through which insulin passes. This cannula is inserted under the skin, usually on the abdomen.. The pump continuously delivers insulin, 24 hours a day. The amount of insulin is programmed and is administered at a constant rate (basal rate). Often, the amount of insulin needed over the course of 24 hours varies, depending on factors like exercise, activity level, and sleep. The insulin pump allows the user to program many different basal rates to allow for variations in lifestyle. The user can also program the pump to deliver additional insulin during meals, covering the excess demands for insulin caused by eating carbohydrates.
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