It isn’t just keeping blood sugar levels down through insulin control that helps diabetes, but fixing the actual problem causing the diabetes. Addressing just one aspect of the problem (blood sugar or insulin) ignores all the other factors like poor diet, toxins, stress, gut problems, immune issues etc. Instead, this single focuses approach can contribute to the problem, making insulin resistance worse and eventually leading to insulin dependent diabetes when the pancreas shuts down completely. Many doctors and nutrition experts recommend the typical 6-11 servings of complex carbs from whole grain sources daily, suggesting that the fiber helps mitigate insulin response. As I have shown before, 6-11 servings of carbohydrates a day is bad for anyone, but is gasoline on a fire to anyone with an impaired insulin response.

Bitter in taste, neem is beneficial in treating diabetes. Studies have proved that incorporating Indian lilac can maintain blood sugar levels stimulating insulin activity without hindrance. Although natural sources do not contain adverse effects, it is still suggested to consult with your endocrinologist in case constant high glucose content in the bloodstream.


FEED YOUR GUT BUGS, not just yourself. There are trillions of bugs that live in your gut – their health is critical in determining your health. Many studiesshow links between the state of your gut bugs (your microbiota) and type 2 diabetes. Start improving the health of your gut immediately by eating five servings of different coloured vegetables each day. The non digestible fibre in vegetables is the preferred food for your gut bacteria and when your gut bugs are happy, you will be happy. The wider the variety of colours, the more phytonutrients you will be getting.
Although the promises are big, these technologies are still far from the market. First, clinical trials will have to show they do work. Then, the price could be steep, as cell therapy precedents for other applications, such as oncology, come with price tags that reach the six figures and are finding difficulties to get reimbursed. Considering that compared to cancer, diabetes is not an immediately life-threatening disease, health insurers in some countries might be reluctant to cover the treatment.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.

“Diabetes type 1 is very different from your standard disease. Insulin requirements vary greatly from one day to another and there is no way patients can know what they need,” Roman Hovorka, Professor at the University of Cambridge, explained to me during an interview. His research group is working on the development of an algorithm that can accurately predict insulin requirements for a specific patient at any moment.
Diabetes is the major cause of blindness, kidney failure, heart attack and stroke. The number of people affected by all types of diabetic disorders is now over four times higher than just 40 years ago. This has led the World Health Organization (WHO) to consider diabetes an epidemic, predicting it will soon be the seventh biggest cause of death worldwide.
However, the alternate term “reversed” often being used, may confuse people and mistake the good control of diabetes (remission) as a complete cure. Unfortunately, there is no current long term cure yet, and if one had gained back the weight they had lost or went back to old lifestyle habits, Type 2 diabetes would come back and sign and symptoms would present.
Conventional cow’s milk: Conventional cow’s milk and dairy products should be eliminated, especially for people with type 1 diabetes. Dairy can be a fantastic food for balancing blood sugar if it comes from goat’s, sheep or A2 cows. But stay away from all other forms of dairy because the A1 casein produced by conventional cows will harm the body and trigger an immune response similar to gluten. When buying dairy, only purchase raw and organic products from pasture-raised animals.

 This powerful herb promotes glucose utilization in the cells thus lowering blood glucose. It also prevents the liver from releasing more glucose into the blood stream, lowers cholesterol and triglycerides. Some people feel Gymnema Sylvestre is one of the most powerful herbs for treating high blood glucose – both type 1 and 2 diabetics. Also Gymnema Sylvestre may help rejuvenate beta cells in the pancreas thus helping heal the condition.
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.
Chromium plays a vital role in binding to and activating the insulin receptor on body cells, reducing insulin resistance. Supplemental chromium has been shown to lower blood sugar levels, lipids, A1C, and insulin in diabetic patients. It can also help decrease one’s appetite, particularly for sweets. A dosage from 200 mcg to 2,000 mcg a day is safe. Higher doses are unnecessary and can cause acute kidney failure.

A: Fasting plasma glucose and weight change 2 years after randomization either to gastric banding or to intensive medical therapy for weight loss and glucose control. Data plotted with permission from Dixon et al. (13). B: Early changes in fasting plasma glucose level following pancreatoduodenal bypass surgery. A decrease into the normal range was seen within 7 days. Reproduced with permission from Taylor (98).
Taking 200 micrograms of chromium picolinate three times daily with meals can help improve insulin sensitivity. A review published in Diabetes Technology and Therapeutics evaluated 13 studies that reported significant improvement in glycemic control and substantial reductions in hyperglycemia and hyperinsulinemia after patients used chromium picolinate supplementation. Other positive outcomes from supplementing with chromium picolinate included reduced cholesterol and triglyceride levels and reduced requirements for hypoglycemic medication. (14)
It’s not just easy, but also tasty to add spices and herbs that lower blood sugar to your diet. Most of these can be used in everyday recipes. If you are looking for inspiration on how to start cooking with these, try out these recipes from our recipe section – Mushroom-stuffed Turkey, Stuffed Peppers, Apple Cinnamon Breakfast Pizza, Courgette Carrot & Tomato Frittata, Moussaka, Vegetable Stir Fry, and Roasted Butternut Squash

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).


The medications only hide the blood sugar by cramming it into the engorged body. The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.
Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.
Big pharma are in the early stages of developing their own cell therapy approaches for diabetes. Novo Nordisk, one of the largest providers of diabetes treatments, is bidding for stem cells and an encapsulation device, stating that the first clinical trial could take place in the “next few years.” Sanofi, also a big name in diabetes, is working with the German Evotec in a beta cell replacement therapy for diabetics.
Over a period of years, you went from pre-diabetes, to diabetes, to taking one medication, then two then three and then finally large doses of insulin. Here’s the thing. If you are taking more and more medications to keep your blood sugars at the same level, your diabetes is getting worse! Even if your blood sugars get better, your diabetes is getting worse. This is unfortunately what happens to virtually every patient. The body is already overflowing with sugar.
As time goes on, however, blood sugar levels can begin to rise again. Diabetes is a progressive disease which means that what is done today to care for it, may not work as well a year or two from now. A key to keeping blood sugar levels under control is to be active, watch portions of all foods, include all food groups and visit your doctor to make sure the blood sugar levels are staying at a safe level.
“Diabetes type 1 is very different from your standard disease. Insulin requirements vary greatly from one day to another and there is no way patients can know what they need,” Roman Hovorka, Professor at the University of Cambridge, explained to me during an interview. His research group is working on the development of an algorithm that can accurately predict insulin requirements for a specific patient at any moment.

Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.
For type 2 diabetics, diabetic management consists of a combination of diet, exercise, and weight loss, in any achievable combination depending on the patient. Obesity is very common in type 2 diabetes and contributes greatly to insulin resistance. Weight reduction and exercise improve tissue sensitivity to insulin and allow its proper use by target tissues.[40] Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. A study conducted in 2008 found that increasingly complex and costly diabetes treatments are being applied to an increasing population with type 2 diabetes. Data from 1994 to 2007 was analyzed and it was found that the mean number of diabetes medications per treated patient increased from 1.14 in 1994 to 1.63 in 2007.[41]
Fasting is the simplest and fastest method to force your body to burn sugar for energy. Glucose in the blood is the most easily accessible source of energy for the body. Fasting is merely the flip side of eating — if you are not eating you are fasting. When you eat, your body stores food energy. When you fast, your body burns food energy. If you simply lengthen out your periods of fasting, you can burn off the stored sugar.
The problem, of course, has not been solved – the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take metformin to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of metformin cannot force any more sugar into the body.
Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.

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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