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
Adams is the founder and publisher of the open source science journal Natural Science Journal, the author of numerous peer-reviewed science papers published by the journal, and the author of the world's first book that published ICP-MS heavy metals analysis results for foods, dietary supplements, pet food, spices and fast food. The book is entitled Food Forensics and is published by BenBella Books.
Good research and fascinating, but so far does not look to be a “cure”. It may prevent the development of type 1 diabetes and other autoimmune diseases but an A1C of 6.5 is not a cure. It would interesting to see how much insulin each group is using and by what means. Making diabetes easier to manage is certainly a noble goal as well. If someone can keep an A1C of 6.5 without much effort, that is great progress. But with the new 670g and other “bionic pancreas” projects, people may have an easy time keeping A1C in the 6-7… Read more »
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.
Hi, it’s midnight where I am and my family and I have been awake for an hour post intense leg cramps that I got from my obsessive eating disorder making my blood sugar reach extreme levels (rant!). To anyone who is unfamiliar with diabeties: The experience is hell. It is waking up at ungoldy hours from pain in your legs, bladder, sanity. You’re not the same person with erradic blood sugars. It’s sleeping 16 hours a day-unwillingly falling behind in everything. Keeping GALLONS of water near you to drink, and yet still being thirsty. It’s almost been two years for… Read more »
Secret #5) Avoid all processed foods. Avoid eating refined anything. That includes white breads, processed meat (which strongly promotes diabetes) and dairy products. Switch from cow's milk to almond milk (Blue Diamond brand is good, but I suggest you avoid the Silk brand). Reduce or eliminate cheese from your diet. If you eat meat, eat only fresh unprocessed meat, never eat processed packaged meat because it contains sodium nitrite, a chemical that destroys pancreas function. This means no pepperoni pizza, no ham and potato soup, no deli meat sandwiches and so on.
“Type 1 diabetes affects about one in every 100 companion animals in the U.S., including dogs and cats, and approximately 1.25 million American children and adults,” Purdue University reports. “Because diabetes in dogs happens similarly in humans, treatment has so far been largely the same: Both need their glucose to be monitored throughout the day and insulin to be administered after meals.”
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.
Low glycemic index foods also may be helpful. The glycemic index is a measure of how quickly a food causes a rise in your blood sugar. Foods with a high glycemic index raise your blood sugar quickly. Low glycemic index foods may help you achieve a more stable blood sugar. Foods with a low glycemic index typically are foods that are higher in fiber.
Another non-insulin injection for people with diabetes is exenatide (Byetta). This medication, originally derived from a compound found in the saliva of the Gila monster, triggers insulin release from the pancreas when blood glucose levels rise. Exenatide is meant to be used along with oral diabetes drugs. It is dosed twice daily and should be injected within an hour of the morning and evening meals. Recently, the FDA warned that exenatide may increase the risk of severe even fatal pancreatitis (inflammation of the pancreas) and that the drug should be discontinued and not restarted if signs and symptoms of pancreatitis develop (severe abdominal pain, for example). It is not for use in people with type 1 diabetes.
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
Evidence linking hepatic insulin sensitivity to intraorgan triglyceride content has been steadily accumulating. In insulin-treated type 2 diabetes, insulin dose correlates with the extent of fatty liver (35), and in turn, this is associated with insulin sensitivity to suppression of hepatic glucose production (36). Decreasing the fat content of liver is associated with improvement in insulin suppression of glucose production and, thereby, with improvement in fasting plasma glucose (20,23).
Who is at risk of developing prediabetes? A well-known paper published in the Lancet in 2010 recommends screening for type 2 diabetes (which would also screen for prediabetes) every 3-5 years in all adults over the age of 45, regardless of other risk factors. Overweight and obese adults (a BMI >25 kg/m2) are also at significantly greater risk for developing prediabetes, as well as people with a family history of type 2 diabetes.
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Signs and symptoms of this life-threatening condition include a blood sugar reading higher than 600 mg/dL (33.3 mmol/L), dry mouth, extreme thirst, fever greater than 101 F (38 C), drowsiness, confusion, vision loss, hallucinations and dark urine. Your blood sugar monitor may not be able to give you an exact reading at such high levels and may instead just read "high."
Beware of claims that seem too good to be true. Look for scientific-based sources of information. The National Diabetes Information Clearinghouse collects resource information for the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Reference Collection, a service of the National Institutes of Health. To learn more about alternative therapies for diabetes treatment, contact the National Center for Complementary and Alternative Medicine Clearinghouse.
The immune system of a person with diabetes kills off useful “beta” cells, but the UT researchers say they have found a way to make other cells in the pancreas perform the necessary work. Their approach, announced earlier this month in the academic journal Current Pharmaceutical Biotechnology, not only would have implications for Type 1, formerly called juvenile diabetes, but also could help treat the far more common Type 2 variety, also known as adult-onset diabetes.
The ripe fruit of this cactus has been shown in some small studies to lower blood sugar levels. You may be able to find the fruit in your grocery store, but if not, look for it as a juice or powder at health food stores. Researchers speculate that the fruit may possibly lower blood sugar because it contains components that work similarly to insulin. The fruit is also high in fiber. Try these foods for the best diabetic diet.
The only reason to continue to give this bad advice is the lingering fear of natural fat. If you’re going to avoid fat you need to eat more carbohydrates in order to get satiated. But in recent years the old theory about fat being dangerous has been proven incorrect and is today on its way out. Low-fat products are simply unnecessary. So this reason doesn’t hold up either.
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).
Darkes said several medical professionals worked with him when he was in St. Louis, but he could name only his senior consultant, Dr. Michael Berk. Berk is an endocrinologist who runs his own practice in St. Louis and is also a clinical associate at Washington University. Because Darkes declined a request to submit a medical release form to Berk's office, Live Science could not confirm key elements of his story, or whether or not he was even a patient of Dr. Berk.