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).
There was a clinical trial conducted at Department of Biochemistry, Postgraduate Institute of Basic Medical Sciences Madras, India that studied 22 patients with type 2 diabetes. It reported that supplementing the body with 400 mg of Gymnema Sylvestre extract daily resulted in remarkable reductions in blood glucose levels, hemoglobin A1c and glycosylated plasma protein levels. What’s even more remarkable is that by the end of this 18 month study, participants were able to reduce the dosage of their prescription diabetes medication. Five were even completely off medication and attaining stable blood sugar levels with Gymnema Sylvestre supplementation alone.
The medical professionals at the Diabetes Treatment Center at Desert Springs Hospital Medical Center provide inpatient and outpatient evaluation, treatment and ongoing education for adults with Type 1 or Type 2 diabetes, as well as pre-diabetes conditions. The interdisciplinary team includes certified diabetes educators and nurses who work closely with patients' primary care physicians to work toward a common goal — to help patients lead longer, healthier lives.
As self-management of diabetes typically involves lifestyle modifications, adherence may pose a significant self-management burden on many individuals. 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. 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).
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.
Alternative: “I’m a fat-atarian,” says DeLaney, who tells her patients to avoid low-fat foods. She encourages them to eat whole-fat dairy products, egg yolks, butter, olive oil, and avocado. “Restoring healthful fats to our diets as well as eliminating trans fats and all refined oils that help deplete our fat and vitamin stores will help nourish the body and reduce the need for diabetes medication.”
Keep your immunizations up to date. High blood sugar can weaken your immune system. Get a flu shot every year, and your doctor will likely recommend the pneumonia vaccine, as well. The Centers for Disease Control and Prevention (CDC) also recommends the hepatitis B vaccination if you haven't previously received this vaccine and you're an adult age 19 to 59 with type 1 or type 2 diabetes. The CDC advises vaccination as soon as possible after diagnosis with type 1 or type 2 diabetes. If you are age 60 or older, have diabetes and haven't previously received the vaccine, talk to your doctor about whether it's right for you.
Cinnamon has long been reported as a good source for the treatment of diabetes, due to a study done in 2003 by Khan and associates. 60 people were tested in the group and one third of the group was given a placebo. The end results were very impressive and the overall health of the group was increased with glucose down 18 percent; LDL cholesterol and triglycerides also showed reduced levels. Everyone was excited and the word of using cinnamon spread.
There are many promising studies suggesting chromium supplementation may be effective, but they are far from conclusive. For example, a small study published in the journal Diabetes Care compared the diabetes medication sulfonylurea taken with 1,000 mcg of chromium to sulfonylurea taken with a placebo. After 6 months, people who did not take chromium had a significant increase in body weight, body fat, and abdominal fat, whereas people taking the chromium had significant improvements in insulin sensitivity.
Efforts to cure or stop type 1 diabetes are still in the early stages, and these approaches will also not be suitable for people that have already lost their insulin-producing cells. A solution could be the creation of an “artificial pancreas” — a fully automated system that can measure glucose levels and inject the right amount of insulin into the bloodstream, just like a healthy pancreas would.
Diabetes is a costly disease, placing a high financial burden on the patient and the healthcare system. If poorly managed or left untreated, it can cause blindness, loss of kidney function, and conditions that require the amputation of digits or limbs. The CDC reports that it’s also a major cause of heart disease and stroke and the seventh leading cause of death in the United States.
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.
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.
^ Jump up to: a b Cox DJ, Kovatchev BP, Anderson SM, Clarke WL, Gonder-Frederick LA (November 2010). "Type 1 diabetic drivers with and without a history of recurrent hypoglycemia-related driving mishaps: physiological and performance differences during euglycemia and the induction of hypoglycemia". Diabetes Care. 33 (11): 2430–35. doi:10.2337/dc09-2130. PMC 2963507. PMID 20699432.
^ Jump up to: a b Safren, S.A., Gonzalez, J.S., Wexler, D.J., Psaros, C., Delahanty, L.M., Blashill, A.J., Margolina, A.I., & Cagliero, E. (2013). "A randomized controlled trial of cognitive behavioral therapy for adherence and depression (CBT-AD) in patients with uncontrolled type 2 diabetes". Diabetes Care. 37 (3): 625–33. doi:10.2337/dc13-0816. PMC 3931377. PMID 24170758.
It’s like packing your clothes into a suitcase. At first, the clothes go without any trouble. After a certain point, though, it is just impossible to jam in those last 2 T-shirts. You can’t close the suitcase. The luggage is now ‘resistant’ to the clothes. It’s waaayyy harder to put those last 2 T-shirts than the first 2. It’s the same overflow phenomenon. The cell is filled to bursting with glucose, so trying to force more in is difficult and requires much higher doses of insulin.
Type I diabetes usually occurs in people who are below the age 20 and that is why it is also called as juvenile diabetes. In this type, the body becomes partially or completely unable to produce insulin. Type I diabetes is an autoimmune disease. In this, your immune system attacks the pancreas from where the insulin is produced, thereby making the pancreas inefficient or unable to produce insulin. Type I diabetes cannot be prevented, it can only be controlled with healthy lifestyle changes.
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.