With a background in science and software technology, Adams is the original founder of the email newsletter technology company known as Arial Software. Using his technical experience combined with his love for natural health, Adams developed and deployed the content management system currently driving NaturalNews.com. He also engineered the high-level statistical algorithms that power SCIENCE.naturalnews.com, a massive research resource featuring over 10 million scientific studies.
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.
Diabetes has grown to “epidemic” proportions, and the latest statistics revealed by the U.S. Centers for Disease Control and Prevention state that 30.3 million Americans have diabetes, including the 7.2 million people who weren’t even aware of it. Diabetes is affecting people of all ages, including 132,000 children and adolescents younger than 18 years old. (2)

The fact these improvements can happen independently of weight loss should also signify a shift in how we conceptualize both obesity and diabetes, according to Peter Billings, the Seattle bariatric surgeon who operated on Benari. Billings, a nearly 20-year veteran in the field, has started to perform surgery on other lower-BMI patients similar to Benari, though they often pay out of pocket.
“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.” 

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"We plan to account for differences from mouse to human by helping dogs first. This way, the dogs can inform us on how well the treatment might work in humans," said Clarissa Hernandez Stephens, first author on the research and a graduate researcher in Purdue’s Weldon School of Biomedical Engineering. Findings appear in early view for a forthcoming issue of the American Journal of Physiology – Endocrinology and Metabolism.
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.
After two months under the care of the naturopath, John returned to his primary care doctor to discover that his hemoglobin A1c had dropped from 8.9% to 4.9%—a nondiabetic range. For eight months and counting, he’s been off all his diabetes medication. His last A1c reading was 5.1%. With the help of his naturopath, John seems to have reversed his diabetes.
Other research conducted at the same institute studied possible regeneration of the islets of langerhans in rats that were made diabetic for the study and then given gymnema sylvestre leaf extracts. The diabetic rats were able to double the number of their islets and beta cell numbers. Researchers felt that the herbal therapy was able to bring blood sugar stability by repairing the pancreas and increasing insulin secretion.
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
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).
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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.
“I am extremely pleased to see that technology developed in Tejal Desai’s group is getting to the point that we can explore this for therapeutic purposes,” Matthias Hebrok, PhD, the director of the Diabetes Center at UCSF and a member of Encellin’s scientific advisory board, noted on the UCSF website. “Encapsulation and protection of islet cells remain a critical hurdle that needs to be overcome before cell therapy becomes a reality in type 1 diabetes.”
Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
In the mean time, by eating lots of non starchy veggies, and not much else, especially not snacking, no sugar at all, I personally lost some weight too, together with exercising more (50–60 minutes of moderate exercises a day instead of 30) to lower my insulin resistance for the time being have but my type 2 diabetes in remission, fasting blood sugar now 5.2 mmol/~L ≈ 94 mg/dL.
The above two rules are the only dietary rules you need to maintain ideal weight for the rest of your life, assuming you apply common sense and avoid extremes. The diet works by building in regular periods of insulin relief, keeping your body from becoming resistant to insulin. Following these two rules, you will maintain your weight and health by never entering the vicious cycle of increasing insulin resistance.
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