I was diagnosed with Type 2 diabetes and started with a nutritionist two years ago. I was losing weight (20 lbs) and doing well on her prescribes diet. She reviewed my food log and comment that I was cutting down too low on my carbs. She said that it would damage my kidneys. I was concerned and slightly increased my carbs — which led to cravings and weight gain. Why was that the advice given? It failed.
Big pharma are in the early stages of developing their own cell therapy approaches for diabetes. Novo Nordisk, one of the largest providers of diabetes treatments, is bidding for stem cells and an encapsulation device, stating that the first clinical trial could take place in the “next few years.” Sanofi, also a big name in diabetes, is working with the German Evotec in a beta cell replacement therapy for diabetics.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
Chinese medicine has been using cinnamon for medicinal purposes for hundreds of years. It has been the subject of numerous studies to determine its effect on blood glucose levels. A 2011 study has shown that cinnamon, in whole form or extract, helps lower fasting blood glucose levels. More studies are being done, but cinnamon is showing promise for helping to treat diabetes.
So, can you “reverse” diabetes? No – but you can manage it very well with the help of a Certified Diabetes Educator (CDE) and a knowledgeable primary care physician or endocrinologist. There are even prescription apps available to bridge the care that your clinicians can give you between visits and apps that offer virtual CDE’s for greater assistance.
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 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.
“Diabetes type 1 is very different from your standard disease. Insulin requirements vary greatly from one day to another and there is no way patients can know what they need,” Roman Hovorka, Professor at the University of Cambridge, explained to me during an interview. His research group is working on the development of an algorithm that can accurately predict insulin requirements for a specific patient at any moment.
Implementing integrative and functional medical nutrition therapy, I helped the patient understand that she could reverse the trajectory she was on by making lifestyle changes—and that’s what she did. We engaged in shared decision making in our ongoing nutrition consultations. Over the course of one year, her physiology and health status changed for the better. Her A1c dropped from 7.2% to 5.6%, and she no longer required medications. She continues to adhere to her new lifestyle program and is confident she’ll remain free of a diabetes diagnosis.
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The study wasn’t a controlled experiment designed to prove whether or how treatment intensification might directly improve blood sugar. Researchers also lacked data to explain why doctors or patients might have decided against a change in therapy. And the study didn’t show whether failure to switch treatment regimens resulted in diabetes complications.
As of 2015 the guidelines called for an HbA1c of around 7% or a fasting glucose of less than 7.2 mmol/L (130 mg/dL); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy. Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms and long-term benefits, many people – for example people with a life expectancy of less than nine years – who will not benefit are over-treated and do not experience clinically meaningful benefits.
Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars better, but not the diabetes. We can pretend the disease is better, but that doesn’t make it true.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Because the initial symptoms (fatigue, weakness, frequent urination) are usually mild, about 30 percent of all people with diabetes do not realize that they have the disease. And that can have tragic consequences, because with early diagnosis and treatment, the chances of living a long and productive life are higher than if the disease creeps along until irreversible damage occurs.
I have been suffering with diabetes since 2008. In the beginning of my being diagnosed I was in control of it. but now it seems that nothing works. I have lost 36 lbs. and still nothing. I can drink one soda one eat a cookie and my sugar will sky rocket. Please tell me what I can do the get this under control. There is a lot of good info here. I will be starting with the gooseberry juice tomorrow
Cinnamon contains a bioactive compound that can help to fight and prevent diabetes. Cinnamon is known to stimulate the insulin activity and thus regulate the blood sugar level. As excess of anything is bad, likewise cinnamon if taken in excess can increase the risk of liver damage due to a compound called coumarin present in it. The true cinnamon, not the one buy from shops (Cassia cinnamon) is safer to have.
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.
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.
Dr. Steven Lin is a dentist who focusses on the mouth-body connection. Through ancestral nutrition, the oral and gut microbiome, and epigenetics, his programs aim to prevent chronic dental and systemic disease. His book 'The Dental Diet', will be released on January 18'. To receive free updates on functional oral health from Dr. Lin, subscribe to his newsletter below.
Data from the Swedish randomized study of gastric banding showed that a loss of 20% body weight was associated with long-term remission in 73% of a bariatric surgery group, with weight change itself being the principal determinant of glucose control (13). Dietary weight loss of 15 kg allowed for reversal of diabetes in a small group of individuals recently receiving a diagnosis (21). In individuals strongly motivated to regain normal health, substantial weight loss is entirely possible by decreasing food consumption (88). This information should be made available to all people with type 2 diabetes, even though with present methods of changing eating habits, it is unlikely that weight loss can be achieved in those not strongly motivated to escape from diabetes. Some genetic predictors, especially the Ala12 allele at PPARG, of successful long-term weight loss have been identified (89), and use of such markers could guide future therapy. It must be noted that involuntary food shortage, such as a result of war, results in a sharp fall in type 2 diabetes prevalence (90,91).
Focus on low glycemic index foods: While reducing fat and increasing fiber can significantly improve insulin sensitivity, low glycemic index (GI) foods reduce after-meal blood glucose levels. Low GI foods include pumpernickel or rye bread, oats, beans, bran cereals, most fruit, and sweet potatoes, compared to higher GI foods such as white potatoes, processed foods, and cold cereals.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.