So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.
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.
"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.
11. Get regular eye exams: Diabetic retinopathy is caused by elevated levels of blood sugar, which can happen when diabetes goes out of control. The disease can damage the blood vessels around the eye and retina, leading to blurred vision and blindness. Diabetic retinopathy cannot be cured, and often has no early symptoms, which makes it difficult to catch. Diabetics should make sure they get regular eye exams, for early detection and treatment.
Before making any fiber recommendations, Dean has her patients tested for “pancreatic insufficiency.” She believes people with pancreatic insufficiency should be given digestive enzymes along with fiber, “otherwise the fiber will just bloat them up, and they’ll be quite unhappy,” she says. Dean uses a glucomannan fiber supplement for her patients with type 2 diabetes.
“High glycemic index foods are going to be primarily processed foods,” says Lori Chong, RD, CDE, at The Ohio State University Wexner Medical Center in Columbus. Those processed foods tend to have more white sugar and flour in them, which are higher on the GI, she says. Foods lower on the GI include vegetables, especially non-starchy vegetables, like broccoli, cauliflower, and leafy greens and whole-grain products, such as brown rice (as opposed to white rice), Chong says. She notes that even many fruits are low on the GI, with pineapple and dried fruit being some of the highest (Berries, apples, and pears tend to be fairly low.)
“People need to understand the continuum of diabetes,” she says. “If they’re on an upward trajectory of insulin resistance and a downward trajectory of insulin production weight loss, healthful eating and physical activity will slow down the insulin-loss trajectory and improve insulin sensitivity.” But, she says, “If they gain weight back, the diabetes comes back.”
Well, I don’t know much about VCRs, but I do know about type 2 diabetes. I could write an entire book about obesity (oh, wait, I did that already), or fasting (oh, wait, done too) or type 2 diabetes (next up for 2018). But many of you will not want to go through the entire instruction manual. So this is your quick start guide for reversing your type 2 diabetes.
Tooth decay and cavities are some of the first oral problems that individuals with diabetes are at risk for. Increased blood sugar levels translate into greater sugars and acids that attack the teeth and lead to gum diseases. Gingivitis can also occur as a result of increased blood sugar levels along with an inappropriate oral hygiene. Periodontitis is an oral disease caused by untreated gingivitis and which destroys the soft tissue and bone that support the teeth. This disease may cause the gums to pull away from the teeth which may eventually loosen and fall out. Diabetic people tend to experience more severe periodontitis because diabetes lowers the ability to resist infection and also slows healing. At the same time, an oral infection such as periodontitis can make diabetes more difficult to control because it causes the blood sugar levels to rise.
Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Type 2 diabetes is a chronic disease (meaning there isn’t a “cure”) and tends to be progressive. The longer that someone has been living with Type 2 diabetes the less insulin their beta cells may be producing. This doesn’t mean that lifestyle modification is irrelevant–but does mean that individuals should work on accepting their Type 2 diabetes diagnosis so they can focus on managing their diabetes in the best way possible.
Cutting out the refined, processed starches and sugars, BG rebound into a normal range very quickly. My experience is when people begin to be more conscious of their food intake and physical activity, which happens immediately after being diagnosed with pre diabetes or diabetes, they begin to make better food choices and cut out the foods they know are not healthy.
Jump up ^ Inzucchi, SE; Bergenstal, RM; Buse, JB; Diamant, M; Ferrannini, E; Nauck, M; Peters, AL; Tsapas, A; Wender, R; Matthews, DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.
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.
Levels which are significantly above or below this range are problematic and can in some cases be dangerous. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycemic attack (low blood sugar). Most diabetics know when they are going to "go hypo" and usually are able to eat some food or drink something sweet to raise levels. A patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic, under certain conditions (e.g. not eating regularly, or after strenuous exercise, followed by fatigue). Intensive efforts to achieve blood sugar levels close to normal have been shown to triple the risk of the most severe form of hypoglycemia, in which the patient requires assistance from by-standers in order to treat the episode. In the United States, there were annually 48,500 hospitalizations for diabetic hypoglycemia and 13,100 for diabetic hypoglycemia resulting in coma in the period 1989 to 1991, before intensive blood sugar control was as widely recommended as today. One study found that hospital admissions for diabetic hypoglycemia increased by 50% from 1990–1993 to 1997–2000, as strict blood sugar control efforts became more common. Among intensively controlled type 1 diabetics, 55% of episodes of severe hypoglycemia occur during sleep, and 6% of all deaths in diabetics under the age of 40 are from nocturnal hypoglycemia in the so-called 'dead-in-bed syndrome,' while National Institute of Health statistics show that 2% to 4% of all deaths in diabetics are from hypoglycemia. In children and adolescents following intensive blood sugar control, 21% of hypoglycemic episodes occurred without explanation. In addition to the deaths caused by diabetic hypoglycemia, periods of severe low blood sugar can also cause permanent brain damage. Although diabetic nerve disease is usually associated with hyperglycemia, hypoglycemia as well can initiate or worsen neuropathy in diabetics intensively struggling to reduce their hyperglycemia.
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.
Obesity is a disease, not something created by lack of character. It is a hormonal disease. There are many hormones involved, and one of the main ones is a hormone called insulin. The vast majority of obese individuals are resistant to insulin and that causes a lot of trouble. So, what does being insulin-resistant mean? Insulin resistance is essentially ‘pre-pre-type 2 diabetes.’ Insulin’s job is to drive glucose or blood sugar into cells where it can be used. In a nutshell, when someone has insulin resistance, they are having trouble getting glucose where it needs to go, into the cells. It can’t all hang out in the blood after we eat, or we would all have a diabetic crisis after every meal. When there is resistance to insulin, our bodies will just make more of it. The insulin levels rise and rise and for a while, years usually, this will keep up and blood sugar will stay normal. However, eventually it can’t keep up, and even elevate insulin levels are not enough to keep blood sugar normal, and blood sugar rises. And that is diabetes.
“Whether it be the patient saying for the fifth time ‘I will start watching my diet and start exercising,’ or a physician saying ‘the A1c is close to goal and I don’t really want to add yet another medication and copay, we will wait and see what happens in another 3 months,’ the end result is lack of intensification and A1c goal attainment,” Pantalone said.
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.