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 "
In the twentieth century, insulin was available only in an injectable form that required carrying syringes, needles, vials of insulin, and alcohol swabs. Clearly, patients found it difficult to take multiple shots each day; as a result, good blood sugar control was often difficult. Many pharmaceutical companies now offer discreet and convenient methods for delivering insulin.
(NewsTarget) Kirt Tyson, former type I diabetic was interviewed by Mike Adams. In the interview Kirt Tyson revealed that his diet was completely raw with no fruits. He ate only vegetables, seeds and nuts. He cured his diabetes on this simple 30 day raw diet. The once debilitating disease can now be treated with going on a raw diet and making some life changing decisions. Not only can you go raw, but you can also use these eight natural herbs and remedies to survive diabetes.
Curcumin is a bright yellow chemical produced by the spice turmeric, among other plants. Curcumin seems to have multiple benefits for diabetes symptoms. It has been shown to be a marked inhibitor of reactive oxygen species that promote oxidation damage in cells. Curcumin lowers inflammatory chemicals like tumor necrosis factor-alpha, and that’s good because TNF-a causes insulin resistance and irritates fatty livers. Curcumin can reduce another pro-inflammatory chemical called NF-KB. The above-mentioned actions provide a benefit in diabetes protection and reduce the risk of developing diabetes symptoms and complications. Curcumin has also been shown to enhance pancreatic beta cell functioning and reduce fatty liver deposition. It reduces high blood sugar, A1C, and insulin resistance. It was also shown to reduce the onset of Alzheimer’s disease, and that is a higher risk in diabetic patients than in nondiabetic patients. A good dose is 200 to 3,000 mg a day.
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).
If your cells aren’t responding to insulin, your pancreas produces more to turn up the volume on the signal that glucose is available and the cells should absorb it. When your pancreas can keep up, blood glucose stays within healthy ranges, and all is well. When your pancreas starts to poop out, you end up with insulin deficiency, which leads to blood sugar fluctuations and weight gain.
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. The truth was that insulin was not good for type 2 diabetes — it was only good for reducing blood glucose. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
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).
Since the body functions as a whole, it is logical that when one hormone or part of the endocrine system is suffering, the other would be affected as well. This is the reason behind the recent research linking high stress levels to diabetes and other health problems. Most people think of stress only in the mental context (as in, “I’ve got a million things to do, I’m running late and I don’t have time to get anything done… I’m so stressed”) but stress can be physical, psychological, emotional, or mental and can be triggered by many factors including:

Peripheral artery disease (PAD), which commonly affects the legs, is the hardening and narrowing of the arteries that can result from a build-up of plaque or fatty deposits in blood vessels outside the heart or brain. Because diabetics sometimes have reduced feeling in their feet and legs, they often do not feel symptoms of PAD and it goes undiagnosed and untreated. The Diabetes Treatment Center at Desert Springs Hospital take a proactive approach to PAD and provides free Ankle Brachial Index screenings for patients.

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.

A further danger of insulin treatment is that while diabetic microangiopathy is usually explained as the result of hyperglycemia, studies in rats indicate that the higher than normal level of insulin diabetics inject to control their hyperglycemia may itself promote small blood vessel disease.[14] While there is no clear evidence that controlling hyperglycemia reduces diabetic macrovascular and cardiovascular disease, there are indications that intensive efforts to normalize blood glucose levels may worsen cardiovascular and cause diabetic mortality.[42]
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs – the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.

Green tea contains the bioflavinoid epigallocatechin gallate (EGCG), which has been shown to be a safe and effective antioxidant. In a study in Japan, green tea was shown to reduce the risk for Type 2 Diabetes Mellitus onset. It has been shown to improve glucose tolerance in patients, and decrease blood sugar production and over-secretion in Type 2 Diabetes Mellitus  patients. Green tea has also been shown to have an effective anti-angiogenesis factor, that is, it reduces problematic overgrowth of blood vessels, which may have a significant effect on preventing diabetic retinopathy. It has also been shown to promote fat oxidation and thermogenesis. Last, green tea can provide antioxidant protection for the pancreas and the fatty liver. A good dose is 200 to 400 mg a day. It’s also beneficial to drink organic green tea.

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.
If your cells aren’t responding to insulin, your pancreas produces more to turn up the volume on the signal that glucose is available and the cells should absorb it. When your pancreas can keep up, blood glucose stays within healthy ranges, and all is well. When your pancreas starts to poop out, you end up with insulin deficiency, which leads to blood sugar fluctuations and weight gain.

And when I talk about reducing certain carbohydrates, I mainly mean reducing your intake of  refined carbohydrates such as pasta, rice and bread. Non starchy vegetables (such as broccoli, cabbage and cauliflower) are fine and can be eaten in abundance. Many fruits are packed with carbohydrates, so if you’re trying to reduce your carb intake, try and limit your intake to low-carb fruit, such as rhubarb, watermelon, berries, peaches and blackberries.

Dr. Mona Morstein is a naturopathic physician with a medical practice focused in integrative diabetes treatment. Her clinic, Arizona Integrative Medical Solutions, is located in Tempe, Arizona, where she sees patients of all ages and genders for acute and chronic conditions. An expert on prediabetes and diabetes, she is a frequent lecturer at conferences and webinars, and is the founder and executive director of The Low Carb Diabetes Association. Dr. Morstein is also a member of the Arizona Diabetes Coalition. Visit her website
Efforts to cure or stop type 1 diabetes are still in the early stages, and these approaches will also not be suitable for people that have already lost their insulin-producing cells. A solution could be the creation of an “artificial pancreas” — a fully automated system that can measure glucose levels and inject the right amount of insulin into the bloodstream, just like a healthy pancreas would.

There has been a slew of studies done on the topic of alternative and naturopathic treatments and natural remedies for diabetes, and many of them exhibit long-lasting, beneficial results. While conventional medicine tends to treat only the symptoms of disease, alternative medicine focuses on both the underlying causes of the ailment, as well as the symptoms, evaluating the body as an interconnected whole.
Known for its immune-boosting and disease-fighting benefits, this Chinese herb has several positive diabetes studies behind it. Re­searchers have found that ginseng slows carbohydrate absorption; increases cells’ ability to use glucose; and increases insulin secretion from the pancreas. A team from the University of Toronto has repeatedly demonstrated that ginseng capsules lower blood glucose 15 to 20 percent compared to placebo pills. These are the best superfoods for people with diabetes.
Grape seed extract has been proven to improve the conditions associated with this disease. Grape seed performed greatly in studies conducted in 2006 in Toyama Japan, in 2009 in Romania and also in Portsmouth UK. Grape seed was successful in protecting the liver cells and setting up defense mechanisms against reactive oxygen species produced by hyperglycemic conditions.

Note that these medications used to treat type 2 diabetes are typically not used in pregnant or breastfeeding women. At present the only recommended way of controlling diabetes in women who are pregnant or breastfeeding is by diet, exercise, and insulin therapy. You should speak with your health-care professional if you are taking these medications, are considering becoming pregnant, or if you have become pregnant while taking these medications.