Cyrus Khambatta earned a PhD in Nutritional Biochemistry from UC Berkeley after being diagnosed with type 1 diabetes in his senior year of college at Stanford University in 2002. He is an internationally recognized nutrition and fitness coach for people living with type 1, type 1.5, prediabetes and type 2 diabetes, and has helped hundreds of people around the world achieve exceptional insulin sensitivity by adopting low-fat, plant-based whole foods nutrition.
According to the Centers for Disease Control and Prevention (CDC), from 1980 through 2010, the number of American adults aged 18 and older with diagnosed diabetes more than tripled—soaring from 5.5 million to 20.7 million. Moreover, the diabetes epidemic shows no signs of slowing down, affecting 25.8 million people in 2011. Another 79 million adults have prediabetes, putting them at greater risk of developing type 2 diabetes down the road, according to the CDC.
Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.

Knowing your blood-sugar levels and acting accordingly are among the most important ways to treat T1D. Monitoring lets a person know when insulin may be needed to correct high blood sugar or when carbohydrates may be needed to correct low blood sugar. Monitoring blood sugar can be done using traditional blood-sugar meters or continuous glucose monitors (CGMs).
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.

Known as gurmar, or “sugar destroyer,” in Aryuvedic medicine, Gymnema has consistently shown benefits in patients with diabetes. The most active part of Gymnema seems to be gymnemic acids, and many products list the percentage each capsule contains. Analyses of the herb for diabetes have shown it may be helpful in lowering high blood sugar levels. It can delay glucose absorption from the intestine. It was shown to regenerate pancreatic tissues, allowing more insulin to be produced, and help regulate insulin secretion. It also increases the utilization of glucose by the cell, reducing insulin resistance and decreasing appetite, especially for sweets. I usually use it in capsules, or in liquid form in some patients. Due to Gymnema having a very similar shape to glucose, it can fit into the taste bud receptors for sugar; it thus has unbelievable power to actually prevent the taste of sweets in the mouth for up to 1.5 hours. When I have a patient who is still struggling to not eat cake and cookies and so forth at parties or celebrations (or just in general), I will give her a tincture of Gymnema sylvestre. This is one of my favorite herbs for diabetes. In capsule form doses of 400 to 2,400 mg a day are recommended.
This article is great, it combines all of the info I have found, not only putting it into a well written article but adds info I had not found yet. I have struggled with type 2 and losing weight, starting an aggressive weight cardio plan in 2016 with an A1C level of 9.7%. Even after three months of an hour or more of weight lifting and 30-50 mins of hard hilly terrain bike riding, my bets A1C was 7.7% with lowering my carb count to the recommended range. After an injury caused me to have to stop many of the exercises for a bit my A1C went up to the 9% range. July this year my A1C was 9.9% and my Dr was talking about insulin shots, which I hate needles. One last ditch effort to find a solution and avoid the shots, I found an article about the benefits of intermittent fasting. I did a lot of research on the matter before creating my own version of a Keto diet, and went on a strict diet of 5-8 servings of green leafy vegetables a day, around 45g of carbs a day, 3oz of lean or healthy fat protein a meal and fasting for 18 hours between Dinner till lunch the next day for two and a half months. My A1C was 6.5, I lost 20lbs, and have tons of energy and no cravings. I have altered my diet to fit my new exercise plan, still 5-8 servings of vegetables a day, but have added occasional breakfasts of two eggs and 1/2 cup salsa, no more than 100g of carbs a day except my once a week cheat day that might go slightly higher if my blood sugar is in a good range, 6oz lean healthy fat protein, and a hard boiled egg in between meals.
It is great to read these columns of Diabetes. I have tried feenugreek but it raises my blood pressure. Since, I am a patient of High Blood pressure, this does not help me. I am 65, control my diet, walk daily for 6-7 km too and take my medication regularly but still blood sugar is out of control. Fasting is usually 150. Any suggestions from friends. Thanks and Cheers for all.
Primary Care Provider: Your primary care provider is the provider you see for general checkups or when you get sick. Your primary care provider may also be the one who refers you to specialists or other team members. Other health care providers who provide primary care include nurse practitioners and physician assistants, who typically work with a physician.

In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).
The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.
Poor glycemic control refers to persistently elevated blood glucose and glycosylated hemoglobin levels, which may range from 200–500 mg/dl (11–28 mmol/L) and 9–15% or higher over months and years before severe complications occur. Meta-analysis of large studies done on the effects of tight vs. conventional, or more relaxed, glycemic control in type 2 diabetics have failed to demonstrate a difference in all-cause cardiovascular death, non-fatal stroke, or limb amputation, but decreased the risk of nonfatal heart attack by 15%. Additionally, tight glucose control decreased the risk of progression of retinopathy and nephropathy, and decreased the incidence peripheral neuropathy, but increased the risk of hypoglycemia 2.4 times.[21]
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.
Recent advances and research in management of Diabetes with traditionally used natural therapies have resulted in development of products from that facilitate production and proper utilization of insulin in the body. These preparations (Biogetica) are natural and work in conjugation with conventional therapies as supportive treatment protocols, they are absolutely safe and the patients are never at risk of developing hypoglycemic attacks due to the therapies.
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?
Depending on the severity of diabetes, an individual can keep control on his/her disease using diet alone, diet & oral hypoglycemic drugs, and diet & insulin. While a mild diabetic can practice disease control with diet alone, a severe diabetic might need to practice diet control along with insulin administration. Whatever the method of controlling diabetes, routine and reliability should be strictly pursued. A person suffering from diabetes should have limited amount of carbohydrates and fats along with moderate amount of protein in the diet. High-fiber diet like vegetables, whole wheat products, oats, whole legumes prove to be more beneficial. Let us have a look at what all should be had and what all should be avoided.

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.

Because blood sugar levels fluctuate throughout the day and glucose records are imperfect indicators of these changes, the percentage of hemoglobin which is glycosylated is used as a proxy measure of long-term glycemic control in research trials and clinical care of people with diabetes. This test, the hemoglobin A1c or glycosylated hemoglobin reflects average glucoses over the preceding 2–3 months. In nondiabetic persons with normal glucose metabolism the glycosylated hemoglobin is usually 4–6% by the most common methods (normal ranges may vary by method).
When stress occurs, whatever the source, the hypothalamus signals the adrenals to release cortisol (and adrenaline). These hormones are life-saving in true “fight or flight” situations like running away from a charging animal or hoisting a car off a small child, but they cause big problems when they are regularly produced in excess. Excess cortisol can contribute to hormone imbalance in the body since the body uses hormones like progesterone to manufacture cortisol. Excess cortisol absent of a charging animal can also interfere with the body’s ability to regulate blood sugar, reduce fat burning ability, raise insulin, suppress thyroid function and cause gain in belly fat.
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.