As a result of his research and his success stories, Taylor encourages other doctors to stop turning to diabetes medicines right away and more strongly encourage weight loss as the first step for their patients newly diagnosed with type 2 diabetes. And the sooner, the better, he says. While Maher reversed his diabetes decades later, that's not typical, Taylor says. The ideal management, he says, is to start serious weight loss efforts right away.
Medications and insulin do nothing to slow down the progression of this organ damage, because they do not eliminate the toxic sugar load from our body. We’ve known this inconvenient fact since 2008. No less than 7 multinational, multi-centre, randomized controlled trials of tight blood glucose control with medications (ACCORD, ADVANCE, VADT, ORIGIN, TECOS, ELIXA, SAVOR) failed to demonstrate reductions in heart disease, the major killer of diabetic patients. We pretended that using medications to lower blood sugar makes people healthier. But it’s only been a lie. You can’t use drugs to cure a dietary disease.
Replacing humans with computers could make patients better control their sugar levels and suffer less complications in the long term. The French company Cellnovo has already shown that just a partially automated system, where blood sugar levels can be monitored wirelessly but patients still select insulin amounts, can reduce the chances of reaching life-threatening low sugar levels up to 39%. The company is now working towards developing a fully automated artificial pancreas in collaboration with Imperial College, the Diabeloop consortium and the Horizon2020 program.
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:
12. Consult a naturopathic, homeopathic, and/or Chinese medical doctor: Alternative practitioners are trained to treat the patient as a whole, organic being — not just their disease. This may help you develop a well-rounded treatment approach, as well as provide you with new information and perspectives on the disease and form of natural remedies for diabetes.

Reduce Stress–  Stress raises cortisol and can lead to hormone imbalance, insulin issues and increases risk for certain types of disease. Work to reduce your sources of stress from lack of sleep, exposure to toxins, mental and emotional sources and poor diet. Getting quality sleep every night can help reduce stress hormone levels and is great for blood sugar.


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.
Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..

Normally, the process goes like this: The carbohydrates from your food are converted into a form of sugar called glucose. Glucose is the preferred fuel for your body's cells, and it's the only food your brain can use. The glucose floats along in the bloodstream until the pancreas, a large gland located behind the stomach, goes into action. The pancreas produces insulin, a hormone that signals body cells to take in the glucose. Once inside the cell, the glucose is either used as fuel to produce heat or energy or is stored as fat.
The problem, of course, has not been solved – the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take metformin to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of metformin cannot force any more sugar into the body.
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).
Milk thistle is an herb that has been used since ancient times for many different ailments and is considered a tonic for the liver. The most studied extract from milk thistle is called silymarin, which is a compound that has antioxidant and anti-inflammatory properties. It is these properties that may make milk thistle a great herb for people with diabetes.
Reduce Stress–  Stress raises cortisol and can lead to hormone imbalance, insulin issues and increases risk for certain types of disease. Work to reduce your sources of stress from lack of sleep, exposure to toxins, mental and emotional sources and poor diet. Getting quality sleep every night can help reduce stress hormone levels and is great for blood sugar.

The only way to effectively reverse type 2 diabetes (or even pre-diabetes) is to deal with the underlying cause – Insulin Resistance. Trying to address the blood sugar levels (with medication) without addressing the insulin levels is treating the symptoms, not treating the root cause. It is similar to using a bucket to remove water from an overflowing sink rather than actually turning off the tap!

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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