Foods with a low glycemic load: The glycemic index of a food tells you about the blood glucose-raising potential of the food. Foods that have a high glycemic index are converted into sugar after being eaten more quickly than low glycemic foods. If you are fighting diabetes, stick to low glycemic foods like non-starchy vegetables, stone fruits and berries, nuts, seeds, avocados, coconut, organic meat, eggs, wild-caught fish, and raw pastured dairy.
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.
Some medical professionals use an Oral Glucose Tolerance Test (OGTT) to test for diabetes. If you’ve ever been pregnant and had to drink the sickeningly sweet sugar cocktail and then have blood drawn, you are familiar with this one. Basically, a patient is given 50-75 grams of glucose in concentrated solution and his blood sugar response is measured. I’m not a fan of this test because no one should be ingesting that much concentrated glucose, and the test is not a completely accurate measure. (Just a side note: if you are a drinker of the “Big Gulp” drinks or large amounts of soda, you are putting your body through a similar test each day! Eventually, your body will respond, probably with something like “Fine, you want diabetes, I’ll show you diabetes!)

Curcumin is a bright yellow chemical produced by the spice turmeric, among other plants. Curcumin seems to have multiple benefits for diabetes symptoms. It has been shown to be a marked inhibitor of reactive oxygen species that promote oxidation damage in cells. Curcumin lowers inflammatory chemicals like tumor necrosis factor-alpha, and that’s good because TNF-a causes insulin resistance and irritates fatty livers. Curcumin can reduce another pro-inflammatory chemical called NF-KB. The above-mentioned actions provide a benefit in diabetes protection and reduce the risk of developing diabetes symptoms and complications. Curcumin has also been shown to enhance pancreatic beta cell functioning and reduce fatty liver deposition. It reduces high blood sugar, A1C, and insulin resistance. It was also shown to reduce the onset of Alzheimer’s disease, and that is a higher risk in diabetic patients than in nondiabetic patients. A good dose is 200 to 3,000 mg a day.


Healthy fats: Medium-chained fatty acids found in coconut and red palm oil can help balance blood sugar levels, and they serve as the preferred fuel source for your body rather than sugar. Using coconut milk, ghee and grass-fed butter can also help balance out your blood sugar levels, so include these foods into your meals and smoothies. Some research actually suggests that a high-fat, low carb diet known as the keto diet may be a novel approach to reverse diabetes naturally, although you don’t technically have to go into ketosis to achieve the benefits of healthy fats in treating diabetes. (12)


my 7 year old neice has recently been identifed as a type 1 diabetic, she is on insulin now for 3 times short acting and 1 time long acting insulin. Changing diet of a small kid is so diffult. Besides bitter gourd what r the best solutions for a type 1. Also has anyone been CURED of this using these natural remedies. I am hoping for the best.. its un bearable the daily pricks.

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.


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Enriched with phytosterols, aloe vera can have an anti-hyperglycemic effect on the people with type 2 diabetics. Nutritionists suggest that it is a safe and natural source to alleviate fasting sugar levels in your blood. Also, you can prepare a mixture of turmeric, bay leaves, and aloe vera, this herbal medicine is said to control glucose in the blood.
I bring this up because sleep apnea increases a person’s risk for developing type 2 diabetes. Also, sleep-disordered breathing is also related to proper nutrition throughout life. And perhaps most importantly, the first line of defense in catching sleep-disordered breathing in patients early, are dentists. This is another area where dentists must get involved if we want to tackle the issue of pervasive type 2 diabetes with any success.

Dr. Sarah Hallberg is a Medical Director at Virta Health. She also created the Medically Supervised Weight Loss Program at Indiana University Health Arnett and serves as its Medical Director. She is an adjunct Clinical Professor of Medicine at Indiana University School of Medicine. Dr. Hallberg is an expert in diabetes care and is board certified in Internal Medicine, Obesity Medicine, and Clinical Lipidology and also a Registered Clinical Exercise Physiologist from the ACSM.
For my diabetes control, I researched indepth true cinammon (Ceylon) and not the fake supermarket cinammon (cassia) with it's dangerous side effects. I had tried the supermarket varity for two months and noticed very little change in my blood sugar levels. After trying Ceylon cinammon in just two days my sugar readings had dropped approx 30 points. So for me...it's works. Will try it for a month and report back.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.

When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs – the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.
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).
Metformin is a biguanide drug that increases the sensitivity of the body’s cells to insulin. It also decreases the amount of glucose produced by the liver.. In 1994, the FDA approved the use of the biguanide called metformin (Glucophage) for the treatment of type 2 diabetes. Today, this is still typically the first drug prescribed for type 2 diabetes.
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