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?

Good research and fascinating, but so far does not look to be a “cure”. It may prevent the development of type 1 diabetes and other autoimmune diseases but an A1C of 6.5 is not a cure. It would interesting to see how much insulin each group is using and by what means. Making diabetes easier to manage is certainly a noble goal as well. If someone can keep an A1C of 6.5 without much effort, that is great progress. But with the new 670g and other “bionic pancreas” projects, people may have an easy time keeping A1C in the 6-7… Read more »
It is important to note that these herbs and spices are intended to support blood sugar maintenance and are not meant to replace diabetes/hyperglycemic medications. Research does show benefits to incorporating these herbs and spices, so enjoy incorporating them daily into your favorite recipes for a boost of flavor and blood sugar-lowering benefit.
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).

Qigong (pronounced “chi gong”) is literally translated as “function of Qi.” It emphasizes the connection between the mind and body. It is a meditative method that consists of breathing techniques that can be combined with body movements in order to regulate, harness, and enhance Qi. Qigong is used as a means of promoting health, healing, spiritual growth, and overall well-being. While Qigong is not typically used as a major treatment modality for diabetes, it has been found to be a valuable adjunctive therapy for this condition. There are specific Qigong exercises for diabetes.15


But people are curing diabetes every day. It's simple and straightforward, and when you cure diabetes, you greatly reduce your risk of heart disease, obesity and cancer at the same time. The thing is, no one will cure your diabetes for you. Sure, the drug companies want to "treat" you with diabetes drugs, but you have to keep taking those for a lifetime. They don't cure anything. The only real cure can come from YOU -- by changing what you eat and increasing your exercise.

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).


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).
Another study published in the same journal, however, examined the effect of chromium on glycemic control in insulin-dependent people with type 2 diabetes. People were given either 500 or 1,000 mcg a day of chromium or a placebo for six months. There was no significant difference in glycosylated hemoglobin, body mass index, blood pressure, or insulin requirements across the three groups.
During digestion, pancreatic beta cells release not only insulin, but in a much smaller amount, the hormone amylin, which helps mediate sharp rises in blood glucose levels following meals. Pramlintide (Symlin) is a new, synthetic form of amylin that may help improve blood glucose control for some type 1 and type 2 diabetic people who use insulin. Pramlintide has few side effects (nausea is the main one) but it adds another set of injections to a diabetic person's daily pharmaceutical routine, as it cannot be mixed in the same syringe with insulin.
Refined sugar: Refined sugar rapidly spikes blood glucose, and soda, fruit juice and other sugary beverages are the worst culprits. These forms of sugar enter the bloodstream rapidly and can cause extreme elevations in blood glucose. (7) Even though natural sweeteners like raw honey and maple syrup are better options, they can still affect blood sugar levels, so only use these foods on occasion. Your best option is to switch to stevia, a natural sweetener that won’t have as much of an impact.

The acids and digestive juices in the stomach and intestines can break down and destroy insulin if it is swallowed, so it can't be taken as a pill. The only way to get insulin into the body now is by injection with a needle or with an insulin pump. Unless they're using an insulin pump, most kids need two or more injections every day to keep blood sugar levels under control. Usually, two different types of insulin are needed to handle blood sugar needs both after eating and between meals.
“For me it’s a personal challenge – going from being completely 100% sedentary to climbing the highest mountain in Africa. One thing I’ve learnt on this journey is that I’m capable of so much more than I ever thought possible – and this is just another way of proving that to myself. It’s also a way of showing people with diabetes that there is always greatness within you; that you have the power to change your diagnosis and your destiny one step at a time.”
This seems hard to do, but really it’s not if you know one secret: Replace snacking with something far more satisfying — fat. That’s right, the government is wrong to recommend a low fat diet. Fat is what makes you feel full until your next meal. Take away the fat, take away the full. Don’t go to an extreme, but do lean strongly toward a high-fat low-carb diet.
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