Poor glycemic control refers to persistently elevated blood glucose and glycosylated hemoglobin levels, which may range from 200–500 mg/dl (11–28 mmol/L) and 9–15% or higher over months and years before severe complications occur. Meta-analysis of large studies done on the effects of tight vs. conventional, or more relaxed, glycemic control in type 2 diabetics have failed to demonstrate a difference in all-cause cardiovascular death, non-fatal stroke, or limb amputation, but decreased the risk of nonfatal heart attack by 15%. Additionally, tight glucose control decreased the risk of progression of retinopathy and nephropathy, and decreased the incidence peripheral neuropathy, but increased the risk of hypoglycemia 2.4 times.[21]
Baseline Endothelial Reactivity was 1.88+/-0.7 (range 1.0-3.3), with 145/200 pts (72%)having endothelial dysfunction (less than 1.60). At 6 months, ER increased to 2.25+/-0.5 (range 1.2-3.6) (p<0.01). Only 40/200 (20%) remained with ED, but all had increased ER numbers. Ten pts stopped the polyphenols after a normal PAT; all developed ED on repeat PAT "
The problem with the medication-based approach is that you’ll most likely have to be on these medications for the rest of your life. They are expensive and many come with a host of side effects. The medication approach focuses on management of diabetes, not reversal. Taking medications for type 2 diabetes combats the end result, which is rising blood sugar, but does not address the root causes—insulin resistance and carbohydrate intolerance.
Jump up ^ Farmer, A; Wade, A; French, DP; Goyder, E; Kinmonth, AL; Neil, A (2005). "The DiGEM trial protocol – a randomised controlled trial to determine the effect on glycaemic control of different strategies of blood glucose self-monitoring in people with type 2 diabetes ISRCTN47464659". BMC Family Practice. 6 (1): 25. doi:10.1186/1471-2296-6-25. PMC 1185530. PMID 15960852.
Magnesium deficiency is common in diabetic patients, as magnesium can be lost in the urine with hyperglycemia. A study in Diabetes Care reported that low magnesium status is common in Type 2 Diabetes Mellitus (T2DM) and showed that when low-magnesium Type 2 Diabetes Mellitus patients were given an oral dose of magnesium daily for sixteen weeks, the mineral reduced insulin resistance, fasting glucose, and A1C levels.
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).
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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