The U.S. government’s study of the Diabetes Prevention Program found that in 3,000 people who had prediabetes, those who lost 5 percent to 7 percent of their body weight reduced their risk of developing Type 2 diabetes by 58 percent. The numbers were even more impressive in those over age 60. All study participants were overweight and had high blood sugar.
Can somebody at Virta help us find the actual presentation at the 2017 world polyphenol conference on lectins and polyphenols and artery flexibility? I can only find the agenda where the title of the presentation and time is made. He described what he was going to say in an interview a few weeks earlier, more rigidity of arteries with re-introduction of lectins, but I cannot find the actual presentation. He had a publication in 2013 on the reversal of endothelial dysfunction, is why I think we should take this other publication seriously:
Recent research shows that the first step in Diabetes management should be for patients to be put on a low carb diet. Patients that are put on a high carb diet find it very difficult to maintain normal blood glucose levels. Patients that are put on a low carb or restricted carbohydrate diet, manage to maintain near normal blood glucose levels and A1cs.[29][30][31][32][33][34][35][36][37]
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.
Any form of carbohydrate is eventually broken down by the body into glucose, a simple form of sugar. While the body can use glucose for fuel, levels that exceed what  is needed are toxic to the body. In the long run, that whole wheat muffin, cup of millet, or bowl of oatmeal turns into the exact same thing as a cup of soda, a donut or a handful of candy.
In the twentieth century, insulin was available only in an injectable form that required carrying syringes, needles, vials of insulin, and alcohol swabs. Clearly, patients found it difficult to take multiple shots each day; as a result, good blood sugar control was often difficult. Many pharmaceutical companies now offer discreet and convenient methods for delivering insulin.
Glycemic control is a medical term referring to the typical levels of blood sugar (glucose) in a person with diabetes mellitus. Much evidence suggests that many of the long-term complications of diabetes, especially the microvascular complications, result from many years of hyperglycemia (elevated levels of glucose in the blood). Good glycemic control, in the sense of a "target" for treatment, has become an important goal of diabetes care, although recent research suggests that the complications of diabetes may be caused by genetic factors[15] or, in type 1 diabetics, by the continuing effects of the autoimmune disease which first caused the pancreas to lose its insulin-producing ability.[16]
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.
Tooth decay and cavities are some of the first oral problems that individuals with diabetes are at risk for. Increased blood sugar levels translate into greater sugars and acids that attack the teeth and lead to gum diseases. Gingivitis can also occur as a result of increased blood sugar levels along with an inappropriate oral hygiene. Periodontitis is an oral disease caused by untreated gingivitis and which destroys the soft tissue and bone that support the teeth. This disease may cause the gums to pull away from the teeth which may eventually loosen and fall out. Diabetic people tend to experience more severe periodontitis because diabetes lowers the ability to resist infection[59] and also slows healing. At the same time, an oral infection such as periodontitis can make diabetes more difficult to control because it causes the blood sugar levels to rise.[60]
10. Molecular Hydrogen: One of the best natural remedies for diabetes, this potent antioxidant has proven successful in the treatment of several different health ailments, and is now showing promise as a treatment for diabetes. It works by triggering antioxidative activities within cells, and can promote increased metabolism as well as assist in the absorption of insulin. It’s taken topically, mixed in water, or inhaled as a gas. It has no toxicity levels, even if taken at high doses.
Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.
Before making any fiber recommendations, Dean has her patients tested for “pancreatic insufficiency.” She believes people with pancreatic insufficiency should be given digestive enzymes along with fiber, “otherwise the fiber will just bloat them up, and they’ll be quite unhappy,” she says. Dean uses a glucomannan fiber supplement for her patients with type 2 diabetes.
I agree with the group consensus. Type 2 diabetes can be reversed, or controlled, as long as the prescription sticks. Many people don’t know this and the word needs to be spread! I’ve worked with patients who have been able to reach a healthy BMI and eliminate the need for medications to treat type 2 diabetes after adopting a plant-based diet. A prescription to focus on increasing fiber intake (http://www.pcrm.org/sites/default/files/pdfs/health/dietary-fiber-checklist.pdf) instead of counting carbohydrates makes it easy to add, instead of subtract, from each meal. It’s a win-win for both patients and providers.

Treatment for diabetes requires keeping close watch over your blood sugar levels (and keeping them at a goal set by your doctor) with a combination of medications, exercise, and diet. By paying close attention to what and when you eat, you can minimize or avoid the "seesaw effect" of rapidly changing blood sugar levels, which can require quick changes in medication dosages, especially insulin.


Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.


my 7 year old neice has recently been identifed as a type 1 diabetic, she is on insulin now for 3 times short acting and 1 time long acting insulin. Changing diet of a small kid is so diffult. Besides bitter gourd what r the best solutions for a type 1. Also has anyone been CURED of this using these natural remedies. I am hoping for the best.. its un bearable the daily pricks.
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).

“I have many ways to help patients manage diabetes, but it’s very hard to reverse,” says Dr. Rita Louard, director of the Clinical Diabetes Program at Montefiore Health System in Bronx, New York. Still, some diabetes experts will use the word “reverse” when talking about this topic, Louard says, acknowledging the controversy that exists when discussing diabetes reversal.


Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.
Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.[78]

Chromium plays a vital role in binding to and activating the insulin receptor on body cells, reducing insulin resistance. Supplemental chromium has been shown to lower blood sugar levels, lipids, A1C, and insulin in diabetic patients. It can also help decrease one’s appetite, particularly for sweets. A dosage from 200 mcg to 2,000 mcg a day is safe. Higher doses are unnecessary and can cause acute kidney failure.
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. The truth was that insulin was not good for type 2 diabetes — it was only good for reducing blood glucose. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
Recently i been diagnosed with diabetes..doctor want me to take medicine i tried it for 10 days but that made me so dizzy.so i stop that medicine..i am following the fenugreek method but what i do is i soak it and i eat few of them two times a day.. i dont know how far that is working..can you anyone tell me the best way it work.and do you know if it cause any effects with eye sight????? thanks alot..
Diabetes is a chronic condition that affects an estimated 23.1 million people in the U.S., and as many as 1 in 4 people don’t know they have it.[1] Numbers have steadily climbed over the past few decades with no signs of leveling off. Diabetes symptoms include things like increased hunger, increased thirst, frequent urination, slow wound healing, and blurred vision, to name a few.

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.
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).
According to the Centers for Disease Control and Prevention (CDC), from 1980 through 2010, the number of American adults aged 18 and older with diagnosed diabetes more than tripled—soaring from 5.5 million to 20.7 million. Moreover, the diabetes epidemic shows no signs of slowing down, affecting 25.8 million people in 2011. Another 79 million adults have prediabetes, putting them at greater risk of developing type 2 diabetes down the road, according to the CDC.
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.
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