For our very insulin resistant patients with type 2 diabetes, after starting out at 30 grams, a few months later most of our patients find that they can increase their daily carb intake to 40 or 50 grams. Fifty grams of total carbohydrate typically allows 4-5 servings of non-starchy vegetables, 2 oz of nuts, and 3 oz of berry fruit (which includes avocado – but obviously you’d need to share it with someone unless it’s a tiny one!)”
Anti-diabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients - https://www.ncbi.nlm.nih.gov/pubmed?term=Baskaran%20K%20et%20al.%20Antidiabetic%20effect%20of%20a%20leaf%20extract%20from%20gymnema%20sylvestre%20in%20non-insulin-dependent%20diabetes%20mellitus%20patients Possible regeneration of the islets of langerhans in streptozotocin-diabetic rats given gymnema sylvestre leaf extracts - http://www.sciencedirect.com/science/article/pii/0378874190901064 Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2 - http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2362.2006.01629.x/full Effectiveness of Cinnamon for Lowering Hemoglobin A1C in Patients with Type 2 Diabetes: A Randomized, Controlled Trial - http://www.jabfm.org/content/22/5/507.short Cloves protect the heart, liver and lens of diabetic rats - http://www.sciencedirect.com/science/article/pii/S0308814610003870 Cloves improve glucose, cholesterol and triglycerides of people with type 2 diabetes mellitus - http://www.fasebj.org/content/20/5/A990.3.short Effects of rosemary on lipid profile in diabetic rats - http://www.academicjournals.org/article/article1380120780_Aljamal%20et%20al.pdf Inhibition of Advanced Glycation End-Product Formation by Origanum majorana L. In Vitro and in Streptozotocin-Induced Diabetic Rats - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3447365/ Evaluation of clonal herbs of Lamiaceae species for management of diabetes and hypertension - http://apjcn.org/update%5Cpdf%5C2006%5C1%5C107%5C107.pdf Metformin-like effect of Salvia officinalis (common sage): is it useful in diabetes prevention? - https://www.ncbi.nlm.nih.gov/pubmed/16923227 Antidiabetic effect of garlic (Allium sativum L.) in normal and streptozotocin-induced diabetic rats - http://www.sciencedirect.com/science/article/pii/S0944711305002175 Antiglycation Properties of Aged Garlic Extract: Possible Role in Prevention of Diabetic Complications - http://jn.nutrition.org/content/136/3/796S.full#fn-1 Effect of ethanolic extract of Zingiber officinale on dyslipidaemia in diabetic rats - http://www.sciencedirect.com/science/article/pii/S0378874104005732 Effect of Ginger Extract Consumption on levels of blood Glucose, Lipid Profile and Kidney Functions in Alloxan Induced-Diabetic Rats - http://s3.amazonaws.com/academia.edu.documents/35273868/17.pdf?AWSAccessKeyId=AKIAJ56TQJRTWSMTNPEA&Expires=1484639718&Signature=Zb4rY42u7WJrbngfV6pCQzu61e0%3D&response-content-disposition=inline%3B%20filename%3DEffect_of_Ginger_Extract_Consumption_on.pdf Efficacy of turmeric on blood sugar and polyol pathway in diabetic albino rats - http://link.springer.com/article/10.1023/A:1013106527829 Hypolipidemic action of curcumin, the active principle of turmeric (Curcuma longa) in streptozotocin induced diabetic rats - http://link.springer.com/article/10.1023/A:1006819605211 A REVIEW ON ROLE OF MURRAYA KOENIGII (CURRY LEAF) IN (DIABETES MELLITUS – TYPE II) PRAMEHA - http://www.journalijdr.com/sites/default/files/4740.pdf Capsaicin and glucose absorption and utilization in healthy human subjects - https://www.ncbi.nlm.nih.gov/pubmed/16612838 Inhibition of Advanced Glycation End-Product Formation by Origanum majorana L. In Vitro and in Streptozotocin-Induced Diabetic Rats - https://www.ncbi.nlm.nih.gov/pubmed/23008741 Use of Fenuqreek seed powder in the management of non-insulin dependent diabetes mellitus - http://www.sciencedirect.com/science/article/pii/0271531796001418 Ginseng and Diabetes: The Evidences from In Vitro, Animal and Human Studies - http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.797.4558&rep=rep1&type=pdf
Many studies show that lifestyle changes, such as losing weight, eating healthy and increasing physical activity, can dramatically reduce the progression of Type 2 diabetes and may control Type 1 diabetes. These lifestyle changes can also help minimize other risk factors such as high blood pressure and blood cholesterol, which can have a negative impact on people with diabetes.
Every single part of the body just starts to rot. This is precisely why type 2 diabetes, unlike virtually any other disease, affects every part of our body. Every organ suffers the long term effects of the excessive sugar load. Your eyes rot — and you go blind. Your kidneys rot — and you need dialysis. You heart rots — and you get heart attacks and heart failure. Your brain rots — and you get Alzheimers disease. Your liver rots — and you get fatty liver disease. Your legs rot — and you get diabetic foot ulcers. Your nerves rot — and you get diabetic neuropathy. No part of your body is spared.
Conventional: A dietary pattern that includes carbohydrates from fruits, vegetables, whole grains, legumes, and low-fat milk is encouraged for good health. Carbohydrate intake should be monitored using carbohydrate counting or experienced-based estimation. The Recommended Dietary Allowance for digestible carbohydrates is 130 g/day, which will provide a sufficient amount of glucose needed to fuel the central nervous system without reliance on glucose production from protein or fat. Using foods with a low glycemic index that are rich in fiber and other important nutrients is encouraged.
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.
Diabetes has grown to “epidemic” proportions, and the latest statistics revealed by the U.S. Centers for Disease Control and Prevention state that 30.3 million Americans have diabetes, including the 7.2 million people who weren’t even aware of it. Diabetes is affecting people of all ages, including 132,000 children and adolescents younger than 18 years old. (2)
The prevalence of prediabetes is also on the rise, as it’s estimated that almost 34 million U.S. adults were prediabetic in 2015. People with prediabetes have blood glucose levels that are above normal but below the defined threshold of diabetes. Without proper intervention, people with prediabetes are very likely to become type 2 diabetics within a decade.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Together with evidence of normalization of insulin secretion after bariatric surgery (84), insights into the behavior of the liver and pancreas during hypocaloric dieting lead to a hypothesis of the etiology and pathogenesis of type 2 diabetes (Fig. 6): The accumulation of fat in liver and secondarily in the pancreas will lead to self-reinforcing cycles that interact to bring about type 2 diabetes. Fatty liver leads to impaired fasting glucose metabolism and increases export of VLDL triacylglycerol (85), which increases fat delivery to all tissues, including the islets. The liver and pancreas cycles drive onward after diagnosis with steadily decreasing β-cell function. However, of note, observations of the reversal of type 2 diabetes confirm that if the primary influence of positive calorie balance is removed, then the processes are reversible (21).