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Conventional treatment for Type 1 Diabetes generally involves insulin supplementation in the form of injections. Because Type 1 is an autoimmune disorder, it can affect both children and adults, and it’s not uncommon for diabetics to be dependent on lifelong insulin treatments. Type 2, on the other hand, is largely a product of poor lifestyle choices or little access to healthy foods, and is more likely to occur later in life. However, in recent years, there has been an alarming rise in Type 2 Diabetes cases among children and adolescents, which largely stems from an overwhelming obesity issue.
If your carb consumption is on the high side (once you add sugar into the mix, you’re most certainly on the high side), it’s stored as fat and you end up with insulin resistance or non-alcoholic fatty liver disease.[14] The reason behind it is that carbs metabolize into glucose, and limiting carbs helps your body control blood sugar more efficiently.[15][16] It improves overall blood sugar profiles, insulin sensitivity, and hemoglobin A1c, which is a diabetes marker.[17] Going low-carb is especially effective if you’re in the early stages when you do not yet need to administer insulin.[18]
Diabetes is a well-established problem and a multi-billion dollar industry. It is medically characterized by Fasting Blood Glucose higher than 126 mg/dL , which ranges between 100-125 mg/dL are considered pre-diabetic and ranges below 99 mg/dL are considered normal. Studies are finding that a fasting blood glucose below 83 mg/dL is actually a better benchmark, as risk of heart disease begins to increase at anything above that.
In Type 2 diabetes, the insulin that is produced does not work effectively. This is referred to as “insulin resistance.” Previously referred to as “adult-onset diabetes,” Type 2 diabetes is the most common form and occurs most frequently in inactive, overweight adults. With rising rates of childhood obesity, we are now seeing Type 2 diabetes diagnosed in more children and teens. Type 2 diabetes is usually treated with a diet that promotes weight loss, exercise and oral medications. Over time, most with Type 2 diabetes produce less insulin. Because of this,insulin may also be required to treat Type 2 diabetes. 
Gestational diabetes develops during pregnancy because hormones interfere with how the body uses insulin. When the pancreas can’t keep up with the insulin demand and blood glucose levels get too high, the result is gestational diabetes. About 2-7 percent of expectant mothers develop gestational diabetes during their pregnancy. Learn more about diabetes and pregnancy.

Imagine that you hide your kitchen garbage under the rug instead throwing it outside in the trash. You can’t see it, so you can pretend your house is clean. When there’s no more room underneath the rug, you throw the garbage into your bedroom, and bathroom, too. Anywhere where you don’t have to see it. Eventually, it begins to smell. Really, really bad.
Magnesium is a mineral found naturally in foods such as green leafy vegetables, nuts, seeds, and whole grains and in nutritional supplements. Magnesium is needed for more than 300 biochemical reactions. It helps regulate blood sugar levels and is needed for normal muscle and nerve function, heart rhythm, immune function, blood pressure, and for bone health.
Gestational diabetes develops during pregnancy because hormones interfere with how the body uses insulin. When the pancreas can’t keep up with the insulin demand and blood glucose levels get too high, the result is gestational diabetes. About 2-7 percent of expectant mothers develop gestational diabetes during their pregnancy. Learn more about diabetes and pregnancy.
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.
Taylor and his colleagues observed that people who were unable to restart normal insulin production had lived with diabetes for a longer time. Individuals who had lived with diabetes for an average of 3.8 years could not correct their condition through weight loss, while those who had it for an average of 2.7 years were able to regain normal blood sugar control.
Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore, by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin-producing intestinal cells die off, they are boosted by additional oral medications.[76]
“I have many ways to help patients manage diabetes, but it’s very hard to reverse,” says Dr. Rita Louard, director of the Clinical Diabetes Program at Montefiore Health System in Bronx, New York. Still, some diabetes experts will use the word “reverse” when talking about this topic, Louard says, acknowledging the controversy that exists when discussing diabetes reversal.
Cinnamon has long been reported as a good source for the treatment of diabetes, due to a study done in 2003 by Khan and associates. 60 people were tested in the group and one third of the group was given a placebo. The end results were very impressive and the overall health of the group was increased with glucose down 18 percent; LDL cholesterol and triglycerides also showed reduced levels. Everyone was excited and the word of using cinnamon spread.
A popular spice used in Indian cooking, and the main ingredient of ‘curry’ that has taken the world by storm, turmeric has antibacterial, anti-inflammatory and antioxidant properties that all come together to help diabetics manage more stable blood sugar levels. It helps boost immunity and prevent infections that diabetics are often vulnerable to. Studies conducted on rats prove that curcumin, the active ingredient in turmeric, is effective in reducing plasma glucose level and HbA1C as well as improving the lipid profile. Many diabetics also suffer from arthritis, since the sugar laden blood and inflammatory processes typical to diabetes often damage joints. Turmeric, with its anti-inflammatory abilities, also helps with these joint pains.
Diabetic persons are advised to make morning appointments to the dental care provider as during this time of the day the blood sugar levels tend to be better kept under control. Not least, individuals who suffer from diabetes must make sure both their physician and dental care provider are informed and aware of their condition, medical history and periodontal status.
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).

The medical professionals at the Diabetes Treatment Center at Desert Springs Hospital Medical Center provide inpatient and outpatient evaluation, treatment and ongoing education for adults with Type 1 or Type 2 diabetes, as well as pre-diabetes conditions. The interdisciplinary team includes certified diabetes educators and nurses who work closely with patients' primary care physicians to work toward a common goal — to help patients lead longer, healthier lives.
11. Get regular eye exams: Diabetic retinopathy is caused by elevated levels of blood sugar, which can happen when diabetes goes out of control. The disease can damage the blood vessels around the eye and retina, leading to blurred vision and blindness. Diabetic retinopathy cannot be cured, and often has no early symptoms, which makes it difficult to catch. Diabetics should make sure they get regular eye exams, for early detection and treatment.
An unbalanced microbiome composition, known as dysbiosis, has been found in patients with diabetes, for whom the diversity of the gut microbiome is often reduced as compared to healthy people. Researchers from the University of Amsterdam recently showed that fecal transplants, used to transfer the microbiome of a healthy person to the gut of one with diabetes, can result in a short-term improvement of the insulin resistance found in obese patients with type 2 diabetes.
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.
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.

But is John “free of diabetes”? This is where the lines become blurred. Medically speaking, the term “cure” is usually associated with acute disease—a temporary medical condition, such as bacterial pneumonia, that can be cured with antibiotics. For diabetes, which is a chronic disease, it may be more accurate to use the term “remission” rather than cure. Particularly when considering the pathology associated with diabetes and the individual’s genetic predisposition, relapse is always possible. In a consensus statement issued by the ADA, the term remission is defined based on the following definitions:2
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.
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