Yet Gabbay says preliminary human studies with positive results, like this week’s in BMJ Case Reports, suggest the diet is worthy of further study in a larger population over a longer period of time. For now, he cautions people with diabetes, especially those on insulin and sulfonylureas to lower their blood sugar, against trying intermittent fasting before speaking with their healthcare provider.
Is this okay to use against gestational diabetes? I have PCOS and am pre-diabetic. I actually followed this way of eating (before seeing the Ted talk) with my first GD pregnancy and was scolded by the nutritionist. Yet my blood sugar was kept below 98 and I lost 15 lbs and our son’s blood sugar was perfect with an apgar of 10. So I’m thinking of just going this way again despite the ADA’s recommendations.
When this happens for a period of time, the cells start to become resistant to the presence of insulin, causing a vicious cycle. The body then releases even more insulin, trying desperately to get the cells to uptake the toxic glucose. The presence of excess insulin in the bloodstream is also toxic and further damages the receptors on these cells. Eventually, the insulin allows the glucose access to your fat cells to get it out of the bloodstream. In other words- Fat isn’t stored as fat in the body- Sugar (from carbohydrates) is stored as fat!
It isn’t just keeping blood sugar levels down through insulin control that helps diabetes, but fixing the actual problem causing the diabetes. Addressing just one aspect of the problem (blood sugar or insulin) ignores all the other factors like poor diet, toxins, stress, gut problems, immune issues etc. Instead, this single focuses approach can contribute to the problem, making insulin resistance worse and eventually leading to insulin dependent diabetes when the pancreas shuts down completely. Many doctors and nutrition experts recommend the typical 6-11 servings of complex carbs from whole grain sources daily, suggesting that the fiber helps mitigate insulin response. As I have shown before, 6-11 servings of carbohydrates a day is bad for anyone, but is gasoline on a fire to anyone with an impaired insulin response.
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.

Keep your immunizations up to date. High blood sugar can weaken your immune system. Get a flu shot every year, and your doctor will likely recommend the pneumonia vaccine, as well. The Centers for Disease Control and Prevention (CDC) also recommends the hepatitis B vaccination if you haven't previously received this vaccine and you're an adult age 19 to 59 with type 1 or type 2 diabetes. The CDC advises vaccination as soon as possible after diagnosis with type 1 or type 2 diabetes. If you are age 60 or older, have diabetes and haven't previously received the vaccine, talk to your doctor about whether it's right for you.
At the start of the study, all of the patients had been taking two oral diabetes drugs for at least six months. But they still had poorly controlled diabetes based on blood tests showing so-called hemoglobin A1c levels, which reflect average blood sugar levels over about three months. Readings above 6.5 signal diabetes, and everyone in the study had readings of at least 7.
Pramlintide (Symlin) was the first in a class of injectable, anti-hyperglycemic medications for use in addition to insulin for type 1 diabetes or type 2 diabetes. Pramlintide is a synthetic analog of human amylin, a naturally occurring hormone made by the pancreas to help control glucose after meals. Similar to insulin, amylin is absent or deficient in person with diabetes.

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.
First, avoid the One-A-Day brand. All of the well-known One-A-Day products contain poor-quality products at low doses, and are full of unhealthy excipients, fillers, and preservatives. A high-quality multiple will require you to take three to six capsules a day, but will cover all the nutrients your body needs. For children, there are good liquid or powder multiples.

When this happens for a period of time, the cells start to become resistant to the presence of insulin, causing a vicious cycle. The body then releases even more insulin, trying desperately to get the cells to uptake the toxic glucose. The presence of excess insulin in the bloodstream is also toxic and further damages the receptors on these cells. Eventually, the insulin allows the glucose access to your fat cells to get it out of the bloodstream. In other words- Fat isn’t stored as fat in the body- Sugar (from carbohydrates) is stored as fat!
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.
The American Diabetes Association publishes treatment guidelines for physicians based on all available scientific evidence. In the 2018 guidelines document, Standard of Medical Care in Diabetes, the ADA states that there is not sufficient evidence to support the use of any of the proposed alternative treatments for diabetes. These guidelines state that:
Cinnamon contains a bioactive compound that can help to fight and prevent diabetes. Cinnamon is known to stimulate the insulin activity and thus regulate the blood sugar level. As excess of anything is bad, likewise cinnamon if taken in excess can increase the risk of liver damage due to a compound called coumarin present in it. The true cinnamon, not the one buy from shops (Cassia cinnamon) is safer to have.
The medications only hide the blood sugar by cramming it into the engorged body. The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.
Consider a form of regular fasting (more to come in a later blog), such as intermittent fasting or time-restricted feeding (TRF). TRF means eating your calories during a specific window of the day, and choosing not to eat food for the rest. It’s a great way to reduce insulin levels in your body and help undo the effects of chronically elevated levels.
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.
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.

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:

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.


Vanadium is a compound found in tiny amounts in plants and animals. Early studies showed that vanadium normalized blood sugar levels in animals with type 1 and type 2 diabetes. When people with diabetes were given vanadium, they had a modest increase in insulin sensitivity and were able to lower their need for insulin. Researchers want to understand how vanadium works in the body, find potential side effects, and set safe dosages.


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.
Imagine our bodies to be a sugar bowl. A bowl of sugar. When we are young, our sugar bowl is empty. Over decades, we eat too much of the wrong things – sugary cereals, desserts and white bread. The sugar bowl gradually fills up with sugar until completely full. The next time you eat, sugar comes into the body, but the bowl is full, so it spills out into the blood.
Drugs of this class decrease the absorption of carbohydrates from the intestine. Before being absorbed into the bloodstream, enzymes in the small intestine must break down carbohydrates into smaller sugar particles, such as glucose. One of the enzymes involved in breaking down carbohydrates is called alpha-glucosidase. By inhibiting this enzyme, carbohydrates are not broken down as efficiently, and glucose absorption is delayed.
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