Is there any current cure for diabetes?
Yes and no.
Type 2 Diabetes is a metabolic disease in which a person’s body still produces insulin but is unable to use it effectively. Reversing Type 2 Diabetes is more a factor of improving the insulin resistance levels in the long term.
It depends on several factors whether or not is feasible to reverse the pathology, one among them is the duration of the T2D. Besides that, you can accomplish the reversal by improving your eating habits, your level of physical activity and your general lifestyle habits. There is no medicine that will reverse this pathology.
Type 2 diabetes is generally treated with metformin, which is a treatment and not a cure.
Reaching an HbA1c below 6% without hypoglycemic drugs could be considered as a reversal of the pathology.
There is no cure yet, however, there are some studies which are showing promising results.
For example, one study from 2011 demonstrated the benefits of taking β-Nicotinamide Mononucleotide (NMN) in dealing with diabetes type 2 (T2D). This a long-term metabolic disorder, is directly associated with over-use of body fat and calories. Mouse studies demonstrated that NMN enhances glucose tolerance by restoring NAD+ levels (HFD-induced T2D mice ameliorating glucose intolerance).
Another study from 2016, demonstrated the benefits of taking nicotinamide riboside (NR) by improving glucose tolerance, reduced weight gain, liver damage and while protecting against diabetic neuropathy.
Both studies suggests that increased NAD+ metabolism might address glycemic control and be neuroprotective.
Type 2 diabetes (T2D) has become epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1. Here, we show that NAMPT-mediated NAD(+) biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD(+) intermediate, ameliorates glucose intolerance by restoring NAD(+) levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD(+) and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a potential nutriceutical intervention against diet- and age-induced T2D.
Male C57BL/6J mice raised on high fat diet (HFD) become prediabetic and develop insulin resistance and sensory neuropathy. The same mice given low doses of streptozotocin are a model of type 2 diabetes (T2D), developing hyperglycemia, severe insulin resistance and diabetic peripheral neuropathy involving sensory and motor neurons. Because of suggestions that increased NAD+ metabolism might address glycemic control and be neuroprotective, we treated prediabetic and T2D mice with nicotinamide riboside (NR) added to HFD. NR improved glucose tolerance, reduced weight gain, liver damage and the development of hepatic steatosis in prediabetic mice while protecting against sensory neuropathy. In T2D mice, NR greatly reduced non-fasting and fasting blood glucose, weight gain and hepatic steatosis while protecting against diabetic neuropathy. The neuroprotective effect of NR could not be explained by glycemic control alone. Corneal confocal microscopy was the most sensitive measure of neurodegeneration. This assay allowed detection of the protective effect of NR on small nerve structures in living mice. Quantitative metabolomics established that hepatic NADP+ and NADPH levels were significantly degraded in prediabetes and T2D but were largely protected when mice were supplemented with NR. The data justify testing of NR in human models of obesity, T2D and associated neuropathies.
Article: What is nicotinamide mononucleotide?
Yes, there is a cure.
It won't be 100% effective for all diabetics to completely forgo all of their medication, but around 80% of diabetics will be able to go off all of their medication.
This is one of many articles that address this particular topic: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1325029/
In short, the cause of insulin resistance is chronic over consumption of high carbohydrate diets, and particularly high fructose diets.
This may be a little extreme a perspective for those with a more orthodox view of nutrition, but bare with me. Carbohydrates in excess is toxic to the liver and other organs, in a similar way that alcohol is. Chronic over consumption of carbohydrate, above the body's ability to process it safely, leads to long term pathology of a number of organs, the kidneys, the liver, neurons, retina, which is why diabetics often present with, kideney disease, eye issues, foot numbness, and fatty livers.
If someone got sick from over consuming alcohol (fatty liver disease) the best way to treat such a person is to reduce the alcohol consumption such that it removes the cause of the toxicity.
For diabetics, it is the same. Diabetics are no longer capable of processing any amount of sugar or carbohydrate safely on their own.
If you remove the toxin, most diabetics respond extremely well, and many even reverse much of the long term damage from being insulin resistant all those years.
Liver toxicity mediated by fructose and excess carbohydrate:
NAFLD & NASH mediated by glucose/fructose causing de novo lipogenesis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5893377/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372893/ https://openheart.bmj.com/content/4/2/e000631
The role of insulin resistance in NAFLD https://academic.oup.com/jcem/article/91/12/4753/2656230
I understand the orthodox perspective of treating insulin resistance and diabetes as chronic progressive diseases. I am not arguing about the accuracy of the orthodox contexts. I am merely suggesting that there is a host of research that suggests that diabetes is NOT a chronic and terminal illness as it is currently understood and managed, but that it is in fact, a condition that is caused by the over consumption of carbohydrate, sugar, and particularly high fructose diets.
It has also been shown, that removal of in order of impact, fructose, sucrose, glucose and starchy carbohydrates, diabetic patients respond rapidly, by showing reduced fasting insulin, glucose and HbA1c, recuced LDL and triglycerides, increased HDL, reduced inflammatory markers like GGT CRP and base white cell counts.
All of those CVD markers improve with carbohydrate restriction by reducing the need for insulin in the first place. https://peerj.com/articles/6273/