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).

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:
Testosterone replacement therapy may improve glucose tolerance and insulin sensitivity in diabetic hypogonadal men. The mechanisms by which testosterone decreases insulin resistance is under study.[81] Moreover, testosterone may have a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines.[82]
A 2012 review of ginseng in animals and human beings found that not only does ginseng reduce insulin resistance, it also lowers HbA1C levels. It’s been used in traditional Chinese medicine for centuries as one of the most potent herbs for blood sugar control. Indian ginseng, also called Ashwagandha, offers fantastic all round benefits. Scientists are also researching the connection between diabetes and Alzhiemer’s. Panax Ginseng is a type of ginseng that is able to help with both diabetes and Alzheimer’s.

All carbohydrates – to some degree at least – will raise your blood insulin levels. That is why I consider type 2 diabetes a form of “carbohydrate intolerance”. Protein can also raise levels but to a much lesser degree. The only macronutrient that keeps your insulin levels and, therefore, your blood sugar stable is FAT! Therefore, if you are trying to reduce insulin levels, you need to reduce your amount of certain carbohydrates and replace them instead with healthy, natural fats.

As diabetes management is affected by an individual's emotional and cognitive state, there has been evidence suggesting the self-management of diabetes is negatively affected by diabetes-related distress and depression.[67] There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population.[68][69] Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms.[70] This suggests that it may be important to target mood in treatment.

All of the above contributing factors don’t usually happen by themselves. Since the body functions as a whole, a problem in one area will usually correlate to problems in others. A combination of the factors above can be the catalyst for a full blown case of diabetes (or a lot of other diseases). While researchers often look at a single variable when trying to discover a cure for a disease, often the best approach is one that addresses the body as a whole. As with all diseases, the best cure is good prevention, but certain measures can help reverse disease once it has occurred.
Another study published in the same journal, however, examined the effect of chromium on glycemic control in insulin-dependent people with type 2 diabetes. People were given either 500 or 1,000 mcg a day of chromium or a placebo for six months. There was no significant difference in glycosylated hemoglobin, body mass index, blood pressure, or insulin requirements across the three groups.

Schedule a yearly physical exam and regular eye exams. Your regular diabetes checkups aren't meant to replace regular physicals or routine eye exams. During the physical, your doctor will look for any diabetes-related complications, as well as screen for other medical problems. Your eye care specialist will check for signs of retinal damage, cataracts and glaucoma.
So, can you “reverse” diabetes? No – but you can manage it very well with the help of a Certified Diabetes Educator (CDE) and a knowledgeable primary care physician or endocrinologist. There are even prescription apps available to bridge the care that your clinicians can give you between visits and apps that offer virtual CDE’s for greater assistance.
Isobel Murray, 65 from North Ayrshire, was one of those who took part. Over two years she lost three and a half stone (22kg) and no longer needs medication. “It has transformed my life,” she said. “I had type 2 diabetes for two to three years before the study. I was on various medications which were constantly increasing and I was becoming more and more ill every day.
When a patient is ready to make a big commitment to get their blood sugar under control, Simos works with them to help tease apart what may be causing their blood sugar to spiral. Sometimes it’s what they're eating, sometimes it’s stress at home and at work and sometimes it’s a day full of sitting versus moving. Often, it’s a mix of these things. Other factors may contribute to diabetes risk, including a family history of the disease.

This article is great, it combines all of the info I have found, not only putting it into a well written article but adds info I had not found yet. I have struggled with type 2 and losing weight, starting an aggressive weight cardio plan in 2016 with an A1C level of 9.7%. Even after three months of an hour or more of weight lifting and 30-50 mins of hard hilly terrain bike riding, my bets A1C was 7.7% with lowering my carb count to the recommended range. After an injury caused me to have to stop many of the exercises for a bit my A1C went up to the 9% range. July this year my A1C was 9.9% and my Dr was talking about insulin shots, which I hate needles. One last ditch effort to find a solution and avoid the shots, I found an article about the benefits of intermittent fasting. I did a lot of research on the matter before creating my own version of a Keto diet, and went on a strict diet of 5-8 servings of green leafy vegetables a day, around 45g of carbs a day, 3oz of lean or healthy fat protein a meal and fasting for 18 hours between Dinner till lunch the next day for two and a half months. My A1C was 6.5, I lost 20lbs, and have tons of energy and no cravings. I have altered my diet to fit my new exercise plan, still 5-8 servings of vegetables a day, but have added occasional breakfasts of two eggs and 1/2 cup salsa, no more than 100g of carbs a day except my once a week cheat day that might go slightly higher if my blood sugar is in a good range, 6oz lean healthy fat protein, and a hard boiled egg in between meals.
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).

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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