Tooth decay and cavities are some of the first oral problems that individuals with diabetes are at risk for. Increased blood sugar levels translate into greater sugars and acids that attack the teeth and lead to gum diseases. Gingivitis can also occur as a result of increased blood sugar levels along with an inappropriate oral hygiene. Periodontitis is an oral disease caused by untreated gingivitis and which destroys the soft tissue and bone that support the teeth. This disease may cause the gums to pull away from the teeth which may eventually loosen and fall out. Diabetic people tend to experience more severe periodontitis because diabetes lowers the ability to resist infection and also slows healing. At the same time, an oral infection such as periodontitis can make diabetes more difficult to control because it causes the blood sugar levels to rise.
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.
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.
When a patient is ready to make a big commitment to get their blood sugar under control, Simos works with them to help tease apart what may be causing their blood sugar to spiral. Sometimes it’s what they're eating, sometimes it’s stress at home and at work and sometimes it’s a day full of sitting versus moving. Often, it’s a mix of these things. Other factors may contribute to diabetes risk, including a family history of the disease.
Carbs and fats provide energy for the body. When carbs are limited in the diet, fat becomes the preferred and efficient fuel source. When you reduce your intake of one macronutrient, you have to increase your intake of at least one other macronutrient—otherwise you’ll feel hungry and not have enough energy. The low-fat craze started with flawed science that incorrectly stated that fat was dangerous. In a low carb, high-fat diet, fat provides you with the energy your body needs, and also helps knock out hunger and cravings.
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.
Thank you Dr. Hallberg!! I am a Family Nurse Practitioner who did tele-medicine for 5 years before retiring. At 66 years of age my doctor diagnosed me with Type II Diabetes. I refused to take the medication and instead opted for a 6 month trial to lose enough weight to make the difference. After 4 months I’d lost 8 pounds and still had high blood sugars. Then my husband’s PCP recommended watching your TedTalk. That was the beginning and we both jumped into LCHF/Keto with both feet using Diet Doctor and you as our main resources. My husband has lost 38 pounds and I have lost 42 pounds since November 2017. More importantly my lab results today were a HgbA1c of 5.3 with average blood glucose of 105. I have about 50 more pounds to go to be at a healthier weight BUT I owe you a big thank you!! Now I’m working to encourage others of my friends, family and coaching clients to give LCHF/Keto a try! Thanks!!!!
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).
This information is solely for informational purposes. IT IS NOT INTENDED TO PROVIDE MEDICAL ADVICE. Neither the Editors of Consumer Guide (R), Publications International, Ltd., the author nor publisher take responsibility for any possible consequences from any treatment, procedure, exercise, dietary modification, action or application of medication which results from reading or following the information contained in this information. The publication of this information does not constitute the practice of medicine, and this information does not replace the advice of your physician or other health care provider. Before undertaking any course of treatment, the reader must seek the advice of their physician or other health care provider.
A OGTT glucose of less than 140 ml/dl is considered normal, with 141-199 being pre-diabetic and levels above 200 mg/dL considered full-blown diabetes. From my research, I believe that OGTT blood sugar levels above 140 mg/dL , especially regularly, can increase risk of vision problems, cancer, stroke and cardiovascular disease, even without an official diabetes diagnosis.
Taylor and his colleagues observed that people who were unable to restart normal insulin production had lived with diabetes for a longer time. Individuals who had lived with diabetes for an average of 3.8 years could not correct their condition through weight loss, while those who had it for an average of 2.7 years were able to regain normal blood sugar control.
Recently i been diagnosed with diabetes..doctor want me to take medicine i tried it for 10 days but that made me so dizzy.so i stop that medicine..i am following the fenugreek method but what i do is i soak it and i eat few of them two times a day.. i dont know how far that is working..can you anyone tell me the best way it work.and do you know if it cause any effects with eye sight????? thanks alot..
The problem with the medication-based approach is that you’ll most likely have to be on these medications for the rest of your life. They are expensive and many come with a host of side effects. The medication approach focuses on management of diabetes, not reversal. Taking medications for type 2 diabetes combats the end result, which is rising blood sugar, but does not address the root causes—insulin resistance and carbohydrate intolerance.
Get Your Fats in Good Balance– Overabundance of Omega-6 fats in the diet is a contributing factor in diabetes. Pay attention to your intake of Omega-3 and Omega-6 fats and try to get them closer to a 1:1 ratio. For many people, supplementing with a good quality Omega-3 oil can help while dietary adjustments are being made. Avoid Omega-6 seed oils and their sources (these are used at almost every restaurant). Eat fatty fish like salmon and sardines for the Omega-3s.
“Whether it be the patient saying for the fifth time ‘I will start watching my diet and start exercising,’ or a physician saying ‘the A1c is close to goal and I don’t really want to add yet another medication and copay, we will wait and see what happens in another 3 months,’ the end result is lack of intensification and A1c goal attainment,” Pantalone said.