Obesity is a disease, not something created by lack of character. It is a hormonal disease. There are many hormones involved, and one of the main ones is a hormone called insulin. The vast majority of obese individuals are resistant to insulin and that causes a lot of trouble. So, what does being insulin-resistant mean? Insulin resistance is essentially ‘pre-pre-type 2 diabetes.’ Insulin’s job is to drive glucose or blood sugar into cells where it can be used. In a nutshell, when someone has insulin resistance, they are having trouble getting glucose where it needs to go, into the cells. It can’t all hang out in the blood after we eat, or we would all have a diabetic crisis after every meal. When there is resistance to insulin, our bodies will just make more of it. The insulin levels rise and rise and for a while, years usually, this will keep up and blood sugar will stay normal. However, eventually it can’t keep up, and even elevate insulin levels are not enough to keep blood sugar normal, and blood sugar rises. And that is diabetes.
In general, “remission” in diabetes means a person’s blood sugar levels remain normal. While some refer to this as a “cure,” diabetes is not a “one and done,” disease. That is, it could always return if the patient regains the weight or returns to unhealthy habits. In 2009, a group of diabetes experts wrote that “remission” is a term used when a person has normal blood sugar levels for one year without therapy or surgery.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.

John’s naturopath, Susan DeLaney, ND, RN, from The Wellness Alliance in Carrboro, North Carolina, considers diabetes to be reversed when an individual is no longer dependent on medication to maintain blood glucose levels within a fairly normal range. Kathie Madonna Swift, MS, RD, LDN, owner of Swift Nutrition and author of The Inside Tract: Your Good Gut Guide to Great Digestive Health, describes reversal of diabetes as “restoring function and bringing the body back into glycemic balance.”


Chinese medicine teaches us that we do not treat a patient based solely on a Western medical diagnosis, but, rather, based on the symptoms that present, and the health of the body as a whole system. There are several beneficial herbal formulas that have been developed to treat some of the general symptoms, but it is important to remember that not everyone will present symptoms in the same way, and treatment should be individualized to suit the specific needs of the patient.
Your care team may recommend that you use a continuous glucose monitor (CGM). A CGM is a wearable device that can measure blood sugar every few minutes around the clock. It's measured by a thread-like sensor inserted under the skin and secured in place. The more frequent CGM blood sugar readings can help you and the care team do an even better job of troubleshooting and adjusting your insulin doses and diabetes management plan to improve blood sugar control.

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The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
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?
Also called weight-loss surgery or metabolic surgery, bariatric surgery may help some people with obesity and type 2 diabetes lose a large amount of weight and regain normal blood glucose levels. Some people with diabetes may no longer need their diabetes medicine after bariatric surgery. Whether and for how long blood glucose levels improve seems to vary by the patient, type of weight-loss surgery, and amount of weight the person loses. Other factors include how long someone has had diabetes and whether or not the person uses insulin.1
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).
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. It was not good. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
For seven days take 6 teaspoons of the oil. Take the oil three different times of the day. Then take 2 teaspoons in the morning and 2 in the evening for 4 days. Follow by taking 2 teaspoons of the oil for two days. Take plenty of water in the morning and rub the oil all over the body for 10 days. You must mix the oil with fruit juice. Repeat this treatment if you do not see any improvement.
Low blood sugar, or hypoglycemia, is a syndrome in which a person's blood sugar is dangerously low. People with type 1 and type 2 diabetes are at risk for this condition. There are other diseases that can cause a person's blood sugar levels to go too low, for example, pancreatitis, Cushing's syndrome, and pancreatic cancer. Symptoms and signs that your blood sugar levels are too low include:

One of my patients, aged 58, had an initial hemoglobin A1c of 7.2%. She was taking oral hypoglycemic agents, statins, and proton pump inhibitors—the basic treatment for every diabetes diagnosis. The patient was 28 lbs overweight and worked long hours. She didn’t exercise, mostly ate a processed food diet, and was sleep deprived. The patient had a family history of diabetes, and ultimately her lifestyle expressed her genetic tendencies.
Patients with type 1 diabetes mellitus require direct injection of insulin as their bodies cannot produce enough (or even any) insulin. As of 2010, there is no other clinically available form of insulin administration other than injection for patients with type 1: injection can be done by insulin pump, by jet injector, or any of several forms of hypodermic needle. Non-injective methods of insulin administration have been unattainable as the insulin protein breaks down in the digestive tract. There are several insulin application mechanisms under experimental development as of 2004, including a capsule that passes to the liver and delivers insulin into the bloodstream.[39] There have also been proposed vaccines for type I using glutamic acid decarboxylase (GAD), but these are currently not being tested by the pharmaceutical companies that have sublicensed the patents to them.
Type 2 diabetes is a condition that is characterised by chronically elevated blood sugar levels. However, the main cause as well as the driver for this condition is something called Insulin Resistance. When you eat certain foods, particularly refined carbohydrates, that food is converted to sugar inside your body. Your body’s way of dealing with this sugar is to produce a hormone called insulin. Insulin moves the sugar inside your cells so that it can be used for energy. Sounds great, right?
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
Even if making small gradual changes over time doesn’t cure you, you’ll feel so much better when you give your body what it needs and when you don’t burden it with what it doesn’t need. Whether you’re reducing your risk of developing diabetes or eliminating your need for medication, it’s worth incorporating worthwhile changes so you can be the best version of yourself.
Omega 6 oils are also a relatively new addition to the diet, making their appearance in the early 1900s. Oils in this category include vegetable, canola, cottonseed, soybean, corn, safflower, sunflower, etc. Consumption of these oils increased in the 1950s when they were promoted as a “healthy” alternative to saturated fats (they weren’t). Research is now showing that consumption of these oils increases risk for obesity and can damage thyroid function. They contribute to insulin resistance and inflammation, further aggravating the poor pancreas.
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Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).


Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.
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