In 2003, ephedrine -- also known as ma huang -- became the first herbal stimulant ever banned by the FDA. It was a popular component of over-the-counter weight loss drugs. Ephedrine had some benefits, but it could cause far more harm, especially in high doses: insomnia (difficulty falling and staying asleep), high blood pressure, glaucoma, and urinary retention. This herbal supplement has also been associated with numerous cases of stroke.
Cinnamonium cassia and its relative C. burmanii are the types of cinnamon that have the best effect on diabetes symptoms. There have been numerous studies on cinnamon and, overall, they have shown cinnamon can slow stomach emptying and lower postprandial glucose levels. It also reduces glucose levels in Type 2 Diabetes Mellitus patients who have had poor diabetic control. It may also be helpful in lowering insulin levels, blood pressure, and A1C, and reduce AGE formation. This is a safe herb for diabetics. A good dose is 1 to 2 g a day or 200 mg or more of a concentrated extract.
Because the drugs listed above act in different ways to lower blood glucose levels, they may be used together. For example, a biguanide and a sulfonylurea may be used together. Many combinations can be used. Though taking more than one drug can be more costly and can increase the risk of side effects, combining oral medications can improve blood glucose control when taking only a single pill does not have the desired effects. Switching from one single pill to another is not as effective as adding another type of diabetes medicine.

Diabetes is a serious disease requiring professional medical attention. The information and recipes on this site, although as accurate and timely as feasibly possible, should not be considered as medical advice, nor as a substitute for the same. All recipes and menus are provided with the implied understanding that directions for exchange sizes will be strictly adhered to, and that blood glucose levels can be affected by not following individualized dietary guidelines as directed by your physician and/or healthcare team. 

I asked a question at Quora - The first life style change a person is asked to bring in himself is - walk a lot or exercise as much as one can do. Walking or exercising is dehydration. So why dehydration is not a first line of treatment of Diabetes? He replied that walking or exercising is not dehydration. Further he said that while walking a person is suggested to keep high levels of hydration. The people are desperate to mis-lead and mis-inform.
Dr. Steven Lin is a dentist who focusses on the mouth-body connection. Through ancestral nutrition, the oral and gut microbiome, and epigenetics, his programs aim to prevent chronic dental and systemic disease. His book 'The Dental Diet', will be released on January 18'. To receive free updates on functional oral health from Dr. Lin, subscribe to his newsletter below.
In a study that looked at the anti-hyperglycemic and lipid-lowering properties of Emblica officinalis Gaertn. (Amla) fruit in normal and diabetic human volunteers, the results showed a significant decrease in fasting and 2-h post-prandial blood glucose levels on the 21st day in both normal and diabetic subjects receiving 1, 2 or 3 grams of Amla powder per day as compared with their baseline values.

Answer:  In recent years, intermittent fasting has emerged as a novel way of treating patients with type 2 diabetes. There are anecdotal reports of patients who have lost weight, their blood sugar levels have improved significantly, and they no longer need to take their diabetes medications. Their disease appears to be in remission – if not exactly cured.

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).
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
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).
When evaluating patients with a chronic illness such as diabetes, TCM practitioners take a detailed, multi-system case history and supplement this information with observations that give information about the state of the patient’s health. These observations include the shape, color, and coating of the tongue; the color and expression of the face; the odor of the breath and body; and the strength, rhythm, and quality of the pulse. Many practitioners will palpate along meridians to detect points of tenderness that may indicate a blockage in the flow of Qi at that point.6
Glycated hemoglobin (A1C) test. This blood test indicates your average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. The higher your blood sugar levels, the more hemoglobin you'll have with sugar attached. An A1C level of 6.5 percent or higher on two separate tests indicates you have diabetes. A result between 5.7 and 6.4 percent is considered prediabetes, which indicates a high risk of developing diabetes. Normal levels are below 5.7 percent.
Qi must flow in the correct quantity and quality through the meridians and organs for health to be maintained. Acupuncture, the insertion of thin, solid metal needles, is performed on 1 or more of the 361 acupuncture points distributed along the meridians in order to regulate and promote the proper flow of Qi.5 Other techniques may be used to stimulate acupuncture points, such as moxibustion, in which the herb “moxa” (Artemesia vulgaris) is used to warm the acupuncture point either above or on the skin. Applied pressure (acupressure), lasers, and magnets also may be used to stimulate acupuncture points.
Regular monitoring of clinical trial participants found that HbA1c levels of those receiving BCG had dropped by more than 10 percent at three years after treatment and by more than 18 percent at four years. That reduction was maintained over the next four years, with treated participants having an average HbA1c of 6.65, close to the 6.5 considered the threshold for diabetes diagnosis, and with no reports of severe hypoglycemia. Participants in the placebo group and in a comparison group of patients receiving no treatment experienced consistent HbA1c elevations over the same eight-year time period.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
High blood sugar (hyperglycemia). Your blood sugar level can rise for many reasons, including eating too much, being sick or not taking enough glucose-lowering medication. Check your blood sugar level often, and watch for signs and symptoms of high blood sugar — frequent urination, increased thirst, dry mouth, blurred vision, fatigue and nausea. If you have hyperglycemia, you'll need to adjust your meal plan, medications or both.

Kelly Prinkey-Krupinski, 48 and an avid dog lover, has been struggling with adult onset Type 1 diabetes for 12 years. She said the disease runs her life. “It is a constant struggle,” she said. “My mind is always aware that every bite of food that I eat, every medicine I take, every illness and emotion I experience will affect my blood sugar. There is never a vacation from the constant balancing act to stay alive. It scares me to think of a time when I can't obtain the insulin that I must take 24-7. I would pray that there will be a cure in my lifetime. I just hate to think of the kids that struggle with Type 1 diabetes. This research with dogs sounds promising. As a dog lover myself, I would love to see if our canine friends can be cured. I'm excited to see the results.”
If you have type 2 diabetes and your body mass index (BMI) is greater than 35, you may be a candidate for weight-loss surgery (bariatric surgery). Blood sugar levels return to normal in 55 to 95 percent of people with diabetes, depending on the procedure performed. Surgeries that bypass a portion of the small intestine have more of an effect on blood sugar levels than do other weight-loss surgeries.
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.
That is the goal of Imcyse, a French company running a clinical trial with an immunotherapy designed to stop type 1 diabetes. Patients that have been diagnosed within the last 6 months, who still retain some insulin-producing cells, are given a treatment designed to make the immune system destroy the specific immune cells that are attacking insulin-producing cells. Results are expected later this year and will reveal whether the treatment has the potential to become a cure.
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