“The cell is the original smart machine,” notes Crystal Nyitray, PhD, on the website of Encellin, the biotech start-up she founded in 2016. “All drugs, devices, and even digital health approaches are trying to restore or copy these functions. At Encellin, we believe in the human cell and creating a safe and reliable solution for patients. We are creating a technology to promote cell function and protection.” 
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."
"There have been cases where patients were treated with insulin for years until they discovered it was a rare genetic variant" of MODY, Roep told Live Science. Those people are no longer diagnosed as having type 1 diabetes, and they may be able to manage their blood sugar levels with either oral drugs or diet and exercise changes, "but that would not be the same as being cured," Roep said.  

According to the World Health Organization (WHO), global diabetes cases have increased from 108 million in 1980 to 422 million in 2014. Those numbers are expected to reach 642 million by 2040. According to data from the U.S. Centers for Disease Control and Prevention (CDC) reports, type 2 diabetes accounts for around 90 to 95 percent of cases in adults.
A: Fasting plasma glucose and weight change 2 years after randomization either to gastric banding or to intensive medical therapy for weight loss and glucose control. Data plotted with permission from Dixon et al. (13). B: Early changes in fasting plasma glucose level following pancreatoduodenal bypass surgery. A decrease into the normal range was seen within 7 days. Reproduced with permission from Taylor (98).

Diabetes is one of the most prevalent chronic diseases in the United States. The morbidity and mortality associated with the disease is significant and derives primarily from complications of persistent hyperglycemia. Longstanding hyperglycemia has been shown to lead to vascular complications involving large and small blood vessels, such as arteriosclerosis, glomerulosclerosis, and retinopathy. Diabetic neuropathy, characterized by pain and paresthesias, is among the most frequent complications of longstanding, poorly controlled diabetes and is often associated with a reduction in physical activity and with sleep disturbances.1,2


Lab studies show that Encellin’s “ultra thin-film implantable cell delivery system” keeps islet cells alive and functioning. In a 2015 study in the journal ACS Nano, Dr. Nyitray and others found that cells in the packaging survived for 90 days in lab animals. New blood vessels grew around the transplants and the cells produced insulin in response to rising glucose levels. In a 2016 study from Dr. Desai’s lab, also published in ACS Nano, human islet cells packaged in the tiny film envelopes survived for six months in mice—and the cells made and released insulin in response to rising blood glucose levels.
Dr. Nyitray established Encellin soon after she received her PhD in chemistry and chemical biology from the University of California San Francisco in 2015. Her work at UCSF, with advisor Tejal Desai, PhD, chair of the Department of Bioengineering and Therapeutic Sciences in UCSF’s schools of Pharmacy and Medicine, focused on developing a packaging system for islet cells.
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.
Trick (most important): Go for longer periods of time without eating (yes, yes, fasting). Consume water only for days or weeks at a time. Your fat will literally dissolve away, and with it your type 2 diabetes and other ailments. The definitive book here is Dr. Joel Fuhrman’s book, Fasting and Eating for Health: A Medical Doctor’s Program for Conquering Disease. I highly recommend it; if you’re skeptical, read the 200+ testimonial comments on Amazon. I and at least 20 of my friends have tried fasts lasting days to weeks. It works, and it is amazing.
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