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]
Gymnema Sylvestre is a vine native to Central & South India. Used in traditional Indian medicine since the 6th century BC, the leaves of this plant contain ‘gymnemic acids’ that have the amazing ability to slow down the transport of glucose from the intestines to the bloodstream. Some scientists even believe that Gymnema Sylvestre extract can help repair and regenerate pancreatic beta cells that produce insulin!
Diabetics often find their bodies swinging wildly out of equilibrium. In Type 1 Diabetes, the body attacks insulin-producing cells in the pancreas, causing a rise in blood sugar levels. In Type 2 Diabetes there is insufficient insulin produced in the pancreas, which slows the metabolism and elevates blood sugar levels. Both conditions, if not treated correctly, can cause a host of unpleasant side effects including high blood pressure, neuropathy, kidney damage, and in extreme cases amputation and even death.
Taking a fish oil supplement can help improve markers of diabetes by reducing triglyceride levels and raising HDL cholesterol levels. Research published in the Journal of Research in Medical Sciences shows that omega-3 fatty acids found in fish oil are necessary for proper insulin function, preventing insulin intolerance and reducing inflammation. (16) To use fish oil as a natural remedy for diabetes, take 1,000 milligrams daily.
Eating a balanced diet is vital for people who have diabetes, so work with your doctor or dietitian to set up a menu plan. If you have type 1 diabetes, the timing of your insulin dosage is determined by activity and diet. When you eat and how much you eat are just as important as what you eat. Usually, doctors recommend three small meals and three to four snacks every day to maintain the proper balance between sugar and insulin in the blood.
After two months under the care of the naturopath, John returned to his primary care doctor to discover that his hemoglobin A1c had dropped from 8.9% to 4.9%—a nondiabetic range. For eight months and counting, he’s been off all his diabetes medication. His last A1c reading was 5.1%. With the help of his naturopath, John seems to have reversed his diabetes.
These substances are not considered to be medications by the US FDA and are therefore not regulated as such. This means that there are no standards in place to ensure that a given product contains the substance or dose as described on the label. There are also no requirements to perform studies showing that the products are safe or effective. Side effects of supplements are typically not well understood, and some supplements can interfere with the action of medications.
Foods high in chromium: Chromium is a nutrient that’s involved in normal carbohydrate and lipid metabolism. Foods high in chromium can improve the glucose tolerance factor in your body and naturally balance out blood glucose levels. It plays a role in insulin pathways, helping bring glucose into our cells so it can be used for bodily energy. Broccoli has the highest amounts of chromium, but you can also find it in raw cheese, green beans, brewer’s yeast and grass-fed beef. (10)

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).


Anti-diabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients - https://www.ncbi.nlm.nih.gov/pubmed?term=Baskaran%20K%20et%20al.%20Antidiabetic%20effect%20of%20a%20leaf%20extract%20from%20gymnema%20sylvestre%20in%20non-insulin-dependent%20diabetes%20mellitus%20patients Possible regeneration of the islets of langerhans in streptozotocin-diabetic rats given gymnema sylvestre leaf extracts - http://www.sciencedirect.com/science/article/pii/0378874190901064 Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2 - http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2362.2006.01629.x/full Effectiveness of Cinnamon for Lowering Hemoglobin A1C in Patients with Type 2 Diabetes: A Randomized, Controlled Trial - http://www.jabfm.org/content/22/5/507.short Cloves protect the heart, liver and lens of diabetic rats - http://www.sciencedirect.com/science/article/pii/S0308814610003870 Cloves improve glucose, cholesterol and triglycerides of people with type 2 diabetes mellitus - http://www.fasebj.org/content/20/5/A990.3.short Effects of rosemary on lipid profile in diabetic rats - http://www.academicjournals.org/article/article1380120780_Aljamal%20et%20al.pdf Inhibition of Advanced Glycation End-Product Formation by Origanum majorana L. In Vitro and in Streptozotocin-Induced Diabetic Rats - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3447365/ Evaluation of clonal herbs of Lamiaceae species for management of diabetes and hypertension - http://apjcn.org/update%5Cpdf%5C2006%5C1%5C107%5C107.pdf Metformin-like effect of Salvia officinalis (common sage): is it useful in diabetes prevention? - https://www.ncbi.nlm.nih.gov/pubmed/16923227 Antidiabetic effect of garlic (Allium sativum L.) in normal and streptozotocin-induced diabetic rats - http://www.sciencedirect.com/science/article/pii/S0944711305002175 Antiglycation Properties of Aged Garlic Extract: Possible Role in Prevention of Diabetic Complications - http://jn.nutrition.org/content/136/3/796S.full#fn-1 Effect of ethanolic extract of Zingiber officinale on dyslipidaemia in diabetic rats - http://www.sciencedirect.com/science/article/pii/S0378874104005732 Effect of Ginger Extract Consumption on levels of blood Glucose, Lipid Profile and Kidney Functions in Alloxan Induced-Diabetic Rats - http://s3.amazonaws.com/academia.edu.documents/35273868/17.pdf?AWSAccessKeyId=AKIAJ56TQJRTWSMTNPEA&Expires=1484639718&Signature=Zb4rY42u7WJrbngfV6pCQzu61e0%3D&response-content-disposition=inline%3B%20filename%3DEffect_of_Ginger_Extract_Consumption_on.pdf Efficacy of turmeric on blood sugar and polyol pathway in diabetic albino rats - http://link.springer.com/article/10.1023/A:1013106527829 Hypolipidemic action of curcumin, the active principle of turmeric (Curcuma longa) in streptozotocin induced diabetic rats - http://link.springer.com/article/10.1023/A:1006819605211 A REVIEW ON ROLE OF MURRAYA KOENIGII (CURRY LEAF) IN (DIABETES MELLITUS – TYPE II) PRAMEHA - http://www.journalijdr.com/sites/default/files/4740.pdf Capsaicin and glucose absorption and utilization in healthy human subjects - https://www.ncbi.nlm.nih.gov/pubmed/16612838 Inhibition of Advanced Glycation End-Product Formation by Origanum majorana L. In Vitro and in Streptozotocin-Induced Diabetic Rats - https://www.ncbi.nlm.nih.gov/pubmed/23008741 Use of Fenuqreek seed powder in the management of non-insulin dependent diabetes mellitus - http://www.sciencedirect.com/science/article/pii/0271531796001418 Ginseng and Diabetes: The Evidences from In Vitro, Animal and Human Studies - http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.797.4558&rep=rep1&type=pdf  
Yes and no. If you learn to live a healthier lifestyle and stay with it for your remaining years, then yes it can be reversed. This assumes you realized your diagnosis early and you are able to get your A1c below 6%. If you realized your diabetes too late or your A1c is not coming down without insulin then probably not. This is easier to reverse when you are overweight or obese but not so if your BMI is below 25.
As the fats decreased inside the liver and the pancreas, some individuals also experienced improved functioning of their pancreatic beta cells, which store and release insulin, a hormone that helps control blood sugar levels. The likelihood of regaining normal glucose control depends on the ability of the beta cells to recover, the study authors say.
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!)
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).
In discussing self management with the person with diabetes I focus on how healthy lifestyle behaviors can change the treatment plan. Introducing healthy lifestyle behaviors by providing consistent and predictable meals, daily activity, healthy coping and consistent medication management can improve overall glucose control and may change the overall treatment plan for managing diabetes.

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.


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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