Thank you so much for providing this expert panel. The varying views helped me understand which areas are somewhat vague and which areas overlap. As a Type2 pre-diabetic of 7 years, I have been informed that I need to take a cholesterol drug, even though my cholesterol has always been low. I was told it’s to help remove calcification in my arteries. I have been considered obese for over 20 years and recently lost 50 lbs (I now weight 197) and am continuing to lose weight. I was told that I would always be a diabetic and would have to take medication. I was so proud of my progress (A1c now 5.6), but this news depressed me. I refused to take the cholesterol drug until I could do some research. This expert panel helped me to realize that it is possible to get off the medication if I continue to eat a healthy diet (low saturated fats) and exercise at least 150 minutes a week. Thank you!
If you have type 2 diabetes and your body mass index (BMI) is greater than 35, you may be a candidate for weight-loss surgery (bariatric surgery). Blood sugar levels return to normal in 55 to 95 percent of people with diabetes, depending on the procedure performed. Surgeries that bypass a portion of the small intestine have more of an effect on blood sugar levels than do other weight-loss surgeries.
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:
In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).
Insulin therapy is taken by diabetics who have type 1 diabetes mellitus, or IDDM, i.e., insulin-dependent diabetes mellitus. In this condition, body is not able to produce any insulin, therefore, it has to be administered externally. Patients with type 2 diabetes mellitus are either resistant to insulin or have relatively low insulin production, or both.
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.