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Glycemic control is a medical term referring to the typical levels of blood sugar (glucose) in a person with diabetes mellitus. Much evidence suggests that many of the long-term complications of diabetes, especially the microvascular complications, result from many years of hyperglycemia (elevated levels of glucose in the blood). Good glycemic control, in the sense of a "target" for treatment, has become an important goal of diabetes care, although recent research suggests that the complications of diabetes may be caused by genetic factors[15] or, in type 1 diabetics, by the continuing effects of the autoimmune disease which first caused the pancreas to lose its insulin-producing ability.[16]
When islet cells have been transplanted via the Edmonton protocol, insulin production (and glycemic control) was restored, but at the expense of continued immunosuppression drugs. Encapsulation of the islet cells in a protective coating has been developed to block the immune response to transplanted cells, which relieves the burden of immunosuppression and benefits the longevity of the transplant.[72]
Recently, a small clinical trial in England studied the effects of a strict liquid diet on 30 people who had lived with Type 2 diabetes for up to 23 years. Nearly half of those studied had a remission that lasted six months after the diet was over. While the study was small, the finding offers hope to millions who have been told they must live with the intractable disease.

Most doctors, dietitians and diabetes specialists claim that type 2 diabetes is a chronic and progressive disease. The American Diabetes Association, for example, almost proudly proclaims this on its website. Once you get the diagnosis, it’s a life sentence. But, it’s actually a great big lie. Type 2 diabetes is almost always reversible and this is almost ridiculously easy to prove. This is great news for the more than 50% of American adults who have been diagnosed with pre-diabetes or diabetes. Recognizing this truth is the crucial first step in reversing your diabetes or pre-diabetes. Actually, it something that most people already instinctively recognized to be true.
The bottom line is that diabetes can be bad news—but this doesn’t have to be the case. Interventions can prevent or delay the disease in people with prediabetes. The Diabetes Prevention Program (DPP), a large study of people at high risk of diabetes, has established a prevention plan that’s both feasible and cost-effective. The DPP showed that weight loss and increased physical activity reduced the development of type 2 diabetes by 58% during a three-year period.
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Yuri Elkaim is one of the world’s most trusted health and fitness experts. A former pro soccer player turned NYT bestselling author of The All-Day Energy Diet and The All-Day Fat Burning Diet, his clear, science-backed advice has transformed the lives of more than 500,000 men and women and he’s on a mission to help 100 million people by 2040. Read his inspiring story, “From Soccer to Bed to No Hair on My Head” that started it all.

“The degree of carbohydrate restriction that we recommend to establish and then maintain nutritional ketosis depends upon individual factors such degree of insulin resistance (metabolic syndrome or type 2 diabetes?) and physical activity. These starting levels of carb restriction typically vary between 30 and 60 grams per day of total carbs. The best way to determine one’s carbohydrate tolerance is to directly measure blood ketones with a finger-stick glucometer that also accommodates ketone testing.
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.

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).


Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.[78]
“High glycemic index foods are going to be primarily processed foods,” says Lori Chong, RD, CDE, at The Ohio State University Wexner Medical Center in Columbus. Those processed foods tend to have more white sugar and flour in them, which are higher on the GI, she says. Foods lower on the GI include vegetables, especially non-starchy vegetables, like broccoli, cauliflower, and leafy greens and whole-grain products, such as brown rice (as opposed to white rice), Chong says. She notes that even many fruits are low on the GI, with pineapple and dried fruit being some of the highest (Berries, apples, and pears tend to be fairly low.)
A spice that is popular for soothing your stomach and aiding digestion, Ginger also has the ability to normalize blood sugar levels. Multiple studies conducted on rats show that ginger extract can have a significant anti-hyperglycemic effect. It lowers serum total cholesterol, triglycerides and increases the HDL-cholesterol levels. Diabetes is a digestive disorder. Diabetics often face issues with acid reflux. Ginger soothes the entire digestive tract, giving diabetics another reason to add ginger to their supplement regimen.
A good multiple vitamin and mineral product (or “multiple,” for short) is a great way to start supporting nutrient intake in all diabetic patients. This ensures every day that the body receives all the key nutrients it needs so that all its biochemical, hormonal, nutritional, detoxifying, healing, rebuilding, protecting, and strengthening processes can be performed easily and smoothly. The body runs on enzymes, as enzymes speed up reactions to make the body function more efficiently; all enzymes require nutrient cofactors to enable them to effectively engage the action they are designed to do. A good multiple vitamin supplement for diabetes ensures all those cofactors are available every minute, every day.
In a person with carbohydrate intolerance, type 2 diabetes or prediabetes, this system breaks down. The body loses its insulin sensitivity and more and more insulin is required to remove the excess blood sugar. As a result, blood sugar levels remain high and insulin levels are high as well, and these high insulin levels can make your body even less sensitive to insulin.
Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.[78]
The good news though is that this can be delayed, and we can do something about preventing and managing the early stages of diabetes through simple lifestyle modifications, and the body will remember these efforts if they can be maintained early in the diagnosis and for as long as possible. This in turn will delay the progression of diabetes and development of diabetes complications.
First, the health of your gut is critical to your overall health. This is because your gut is home of trillions of microbes called the gut microbiome. These microbes work in symbiotic and antagonistic relationships within your body. A 2017 study using multiple therapies to manipulate the gut microbiome composition, found they could impact the individual’s health more rapidly. This study also found manipulating the gut microbiome as an effective way to avoid insulin resistance and therefore prevent diabetes.
Indian gooseberry is one of the richest sources of vitamin C. When mixed with bitter gourd juice, its efficacy manifolds, and it can prove to be a highly effective concoction against diabetes. The mixture arouses the islets of Langerhans, that is, the isolated group of cells that secrete the hormone insulin in the pancreas. Just consume one tablespoon of Indian gooseberry juice mixed with one cup of bitter gourd juice daily for 8 to 12 weeks. It is recommended to take it first thing in the morning, if possible. The mixture has also been found to trigger insulin production. All in all, a great herbal remedy for diabetes.
Dr. Sarah Hallberg is a Medical Director at Virta Health. She also created the Medically Supervised Weight Loss Program at Indiana University Health Arnett and serves as its Medical Director. She is an adjunct Clinical Professor of Medicine at Indiana University School of Medicine. Dr. Hallberg is an expert in diabetes care and is board certified in Internal Medicine, Obesity Medicine, and Clinical Lipidology and also a Registered Clinical Exercise Physiologist from the ACSM.

Practitioners agree that nutrition is the cornerstone of diabetes management, and that a range of nutrition intervention strategies can be used to meet the metabolic goals and individual preferences of the person with diabetes. However, there are significant differences in the approach and methodologies used by alternative and conventional practitioners to manage the disease. One difference is in terminology. When is remission really remission?


The new research ties in with recent thinking among experts about what happens when type 2 diabetes develops, says Domenico Accili, MD, chief of endocrinology at Columbia University Vagelos College of Physicians and Surgeons. "We have been talking for some time, that in diabetes, primarily type 2, the insulin-producing [beta] cell is not dead but simply inactive," he says. "If you put patients with diabetes on a diet, you can do marvels with their beta cells."
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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.
Type 2 diabetes is usually first treated by increasing physical activity, and eliminating saturated fat and reducing sugar and carbohydrate intake with a goal of losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. Diets that are very low in saturated fats have been claimed to reverse insulin resistance.[79][80]
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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