In some kids with diabetes, repeated insulin injections can cause a thickening or lumpiness of the fatty tissue beneath the skin, called lipodystrophy (or lipohypertrophy). This is more likely if injections are given in the same area again and again rather than in different injection sites as recommended. Usually, this is only a cosmetic problem. But in some cases, insulin injected in areas of skin with lipodystrophy may not be absorbed into the bloodstream as it should. This can make the insulin dose take longer than usual to work.
Type 1 diabetes occurs when the body’s immune system mistakenly attacks itself and destroys beta cells in the pancreas. Beta cells normally produce insulin, a hormone that helps the body turn sugar from food sources into energy for cells throughout the body. But when the immune attack destroys the beta cells, insulin is no longer produced and the sugar stays in the blood where it can cause serious damage to body organs. Because of this, people with type 1 diabetes have to regularly inject insulin in order to stay alive.
It's unclear how people get the disease — genetics plays a big role, though unknown environmental factors may also trigger the disease. Either way, the disease causes the immune system to mistakenly attack and kill insulin-producing cells, called beta cells, in the pancreas. (This differs from type 2 diabetes, in which the body initially makes sufficient insulin but the cells cannot properly use it.) Without enough insulin working to remove glucose from the blood stream, and allowing glucose to enter the body's cells, blood sugar levels spike. Left untreated, this insulin deficiency leads to a deadly complication called diabetic ketoacidosis. What's more, having high blood sugar over the long term can cause life-threatening complications such as kidney damage or heart disease, according to the Mayo Clinic.
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 »
Dr Beverley Shields, at the University of Exeter Medical School, who led the research, said: "This finding is really exciting. It suggests that a person with Type 1 diabetes will keep any working beta-cells they still have seven years after diagnosis. We are not sure why this is; it may well be that there is a small group of "resilient" beta-cells resistant to immune attack and these are left after all the "susceptible" beta-cells are destroyed. Understanding what is special about these "resilient" beta-cells may open new pathways to treatment for Type 1 diabetes."
A recent study of 46 patients with painful peripheral neuropathy evaluated acupuncture analgesia to determine its short- and long-term efficacy. Using TCM acupuncture points, 34 patients (77%) experienced significant improvement in their symptoms. After a follow-up period of 18–52 weeks, 67% were able to stop or significantly reduce their pain medications. Only 8 (24%) required additional acupuncture treatment; 7 (21%) stated that their symptoms had cleared completely.11
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.

One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
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 2003, ephedrine -- also known as ma huang -- became the first herbal stimulant ever banned by the FDA. It was a popular component of over-the-counter weight loss drugs. Ephedrine had some benefits, but it could cause far more harm, especially in high doses: insomnia (difficulty falling and staying asleep), high blood pressure, glaucoma, and urinary retention. This herbal supplement has also been associated with numerous cases of stroke.
McInnes, N., Smith, A., Otto, R., Vandermey, J., Punthakee, Z., Sherifali, D., … Gerstein, H. C. (2017, March 15). Piloting a remission strategy in type 2 diabetes: Results of a randomized controlled trial. The Journal of Clinical Endocrinology and Metabolism, 2016-3373. Retrieved from https://academic.oup.com/jcem/article-abstract/doi/10.1210/jc.2016-3373/3070517/Piloting-a-Remission-Strategy-in-Type-2-Diabetes?redirectedFrom=fulltext
One easy way to increase your fat content and quit snacking is to begin your meal by eating an avocado. I and others I know have used this trick to easily quit snacking. Avocados protect you from one of the reasons some dietary research wrongly claims that high-fat diets are bad for you: the danger of gorging yourself on delicious, fatty foods. With plain avocados, there is little danger of gorging. Another danger is clogging your arteries and giving yourself heart disease. But it’s been amply shown that the blame for that falls squarely on trans fats, like margarine. If you see any product with the words “partially hydrogenated” or “hydrogenated” in the list of ingredients, put it back, it’s a trans fat. On the other hand, any fat that comes directly from an animal or plant is not a trans fat and can be safely consumed.
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