Controlling Diabetes is Easier Than You Think
The number of children and adults diagnosed with diabetes in the United States has become staggering: Approximately 40 million, or almost 15% of the American population, have diabetes, and it is pretty evenly distributed between women and men.
While an estimated 32 million have been diagnosed with diabetes, an additional 8 million people (or nearly 1 in every 4) are unaware that they have the disease.
One of the keys to maintaining optimal health and wellbeing is keeping blood glucose levels as close to normal as possible.
Good control can prevent or slow the progress of many complications of diabetes, giving a person extra years of healthy, active life.
Good control means getting as close to a normal (non-diabetic) blood glucose level as can be done safely. Ideally, this means levels between 65 and 120 mg/dL before meals, and less than 180 two hours after starting a meal, with an A1C level between 6.5 and 7%.
The target number for A1C will vary depending on the type of test the doctor’s laboratory uses. In real life, people should set goals with their doctor. Keeping a normal level all the time is impractical, and it isn’t needed to get results. Every bit the blood glucose level is lowered helps to prevent complications.
To get good control, more attention must be paid to diet and exercise. Blood glucose levels must be measured more often. So a person being told by the doctor that he or she has diabetes does not have to be frightening.
Following the physiology of the body in conjunction with proper nutrition and exercise can help to control diabetes. Controlling diabetes will depend on many variables, but the most profound one will be blood glucose regulation (BGR) and its effect on insulin levels in the blood.
Blood Glucose Regulation
Blood glucose regulation (BGR) is one of the centerpieces of any diabetes program. If an person wishes to control pre-diabetes and diabetes, it is essential to know how to control the body’s BGR.
Blood glucose regulation and its effect on diabetes is based on the scientific findings that a rise in blood sugar creates excess insulin in the blood, puts the pancreas—which in the first place is not functioning to its optimum level—into overdrive, and therefore increases the possibility for pre-diabetes and/or diabetes.
Moreover, excess insulin also diminishes the body’s ability to effectively use fat for energy, thereby greatly reducing its ability to burn fat and lose weight. Being overweight was found to have a huge correlation with pre- diabetes and diabetes conditions
An increase in blood sugar increases pancreatic production of insulin blood levels, which sends an overworked pancreas into overtime, which slows down (fatigues) the functioning ability of the pancreas, which increases pre-diabetes and diabetes incidents.?
An increase in blood sugar increases insulin blood levels, thereby decreasing fat burning, which means either no weight loss or increased weight gain. So what causes blood sugar to rise, triggering an increase of blood insulin levels, an overworked pancreas, weight gain, and an increase in pre- diabetes and diabetes incidents?
The 5 mechanisms that raise blood-glucose levels
Missed meals or prolonged periods between meals
Increase in simple sugars
Large food quantities per meal
Double carbohydrate intake in one serving
Lack of exercise
Missed meals or prolonged periods between meals
Not eating for three or more hours will cause blood sugar levels to drop below normal.
As a response, the body compensates for this hypoglycemic status by creating a sharp rise in blood sugar the next time food is provided. This in turn creates an increase in insulin production and secretion into the blood.
Solution: One must eat 6–8 times per day, every two to two-and-a-half hours, to regulate blood glucose and eliminate insulin production.
Increase in Simple Sugars
An increase in simple sugar intake (more than 10 grams per serving) will increase blood sugar level sharply, resulting in excess insulin production and secretion into the blood, and it will demolish the capacity of the body to burn fat, lose weight, and control diabetes.
Solution: Keep sugar intake per serving under 10 grams, don’t eat desserts more than 2–3 times per week, and make sure those desserts are consumed on non-consecutive days.
Large Food Quantities Per Meal
Food that is consumed is broken down by the liver into three major macronutrients: carbohydrates to glycogen, protein to amino acids, and fats to fats.
When excessive quantities of foods are eaten at one serving, the liver is unable to break down the food into glycogen, amino acids, and fats only. At the same time, the liver increases its production of triglycerides (fats in the blood) and glucose (sugars in the blood).
When this happens, blood sugar elevates, as does the body’s blood insulin level, thereby preventing the body from using fat for energy or weight loss, and puts the pancreas on overdrive, increasing the probability for pre- diabetes and diabetes.
Solution: Consume only one serving, one plate, and avoid a second serving at any given time.
Double Carbohydrate Sitting in One Serving
The liver breaks down carbohydrates into glycogen. However, when two or more starchy carbohydrates enter the liver at or near the same time, the liver breaks them down into glycogen, triglycerides, and glucose, thereby raising blood sugar and insulin levels. This prevents the body from utilizing fats and losing weight, and in that way increases pre-diabetes/diabetes incidents.
Solution: Don’t eat double carbs (for example, pasta and bread, or potato and bread) at the same meal.
Lack of Exercise
Activities, movement, and exercise require constant muscle contractions. To power these contractions, the body uses glucose as one of its energy sources.
While activity is good, a lack of activity decreases sugar use and causes a slow rise in blood sugar and a slow release of insulin, thus fatiguing the pancreas, increasing pre-diabetes and diabetes incidents, and greatly reducing the body’s capability to burn fat for weight loss.
Solution: A cardiovascular and strength program must be an integral part of a prevention and treatment plan if an athlete is pre-diabetic or diabetic.
REFERENCES
Bhupathiraju, Shilpa N. “Caffeinated and Caffeine-Free Beverages and Risk of Type 2 Diabetes.” Am J Clin Nutr, 97(January 2013): 155–166.
Bijlani, R. L., R. P. Vempati, R. K. Yadav, R. B. Ray, V. Gupta, R. Sharma, N. Mehta, and S. C. Mahapatra. “A Brief but Comprehensive Lifestyle Education Program Based on Yoga Reduces Risk Factors for Cardiovascular Disease and Diabetes Mellitus.” Journal of Alternative and Complementary Medicine, 11 (April 2005), 267–274.
Cullmann, M. “Alcohol Consumption and Risk of Pre-Diabetes and Type 2 Diabetes Development in a Swedish Population.” Diabetic Medicine, 29 (April 2012): 441–452.
DeNoon, Daniel J. “Caffeine Risks May Rattle Diabetic People.” WebMD (January 28, 2008). Retrieved from http://diabetes.webmd.com/news/20080128/caffeine- risks-may-rattle-diabetics.
Egede, L. E., X. Ye, D. Zheng, and M. D. Silverstein. “The Prevalence and Pattern of Complementary and Alternative Medicine Use in Individuals with Diabetes.” Diabetes Care, 25 (February 2002): 324–329.
Elder, C. “Ayurveda for Diabetes Mellitus: A Review of the Biomedical Literature.” Alternative Therapies in Health and Medicine, 10 (January–February 2004), 44–50.
Eriksson, J., S. Taimela, K. Eriksson, S. Parviainen, J. Peltonen, and U. Kujala. “Resistance Training in the Treatment of Non-Insulin Dependent Diabetes Mellitus.” International Journal of Sports Medicine, 18 (1997): 242–246.
Hattersley, A. T., R. C. Turner, P. Patel, et al. “Linkage of Type 2 Diabetes to the Glucokinase Gene.” The Lancet, 339 (May 30, 1992): 1307–1310. Retrieved from http://www.sciencedirect.com/science/article/pii/014067369291958B.
Hegde, Shreelaxmi V., Prabha Adhikari, Shashidhar Kotian, Veena J. Pinto, Sydney D’Souza, and Vivian D’Souza. “Effect of 3-Month Yoga on Oxidative Stress in Type 2 Diabetes With or Without Complications.” Diabetes Care (August 11, 2011). Retrieved from http://care.diabetesjournals.org/content/ early/2011/08/05/dc10-2430.abstract.
Horikawa, Y., N. Oda, N. J. Cox, et al. “Genetic Variation in the Gene Encoding Calpain-10 Is Associated with Type 2 Diabetes Mellitus.” Nature Genetics, 26 (October 2000), 163–175.
Lindström, J., M. Peltonen, J. G. Eriksson, et al. “Improved Lifestyle and Decreased Diabetes Risk Over 13 Years: Long-Term Follow-up of the Randomised Finnish Diabetes Prevention Study (DPS).” Diabetologia, 56 (February 2013): 284–293. Retrieved from http://link.springer.com/article/10.1007/s00125-012-2752-5.
Muller, Y. L., R. L. Hanson, W. C. Knowler, et al. “Identification of Genetic Variation That Determines Human Trehalase Activity and Its Association with Type 2 Diabetes.” Human Genetics, 132 (June 2013): 697–707. DOI: 10.1007/s00439- 013-1278-3. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23468175.
Novak, M. “Perceived Stress and Incidence of Type 2 Diabetes: A 35-Year Follow- up Study of Middle-Aged Swedish Men.” Diabetic Medicine, 30 (January 2013), e8–e16.
Paul-Labrador, M., D. Polk, J. H. Dwyer, I. Velasquez, S. Nidich, M. Rainforth, R. Schneider, and C. N. Merz. “Effects of a Randomized Controlled Trial of Transcendental Meditation on Components of the Metabolic Syndrome in Subjects with Coronary Heart Disease.” Archives of Internal Medicine (June 12, 2006).
Pilkington, K., E. Stenhouse, and G. Kirkwood. “Diabetes and Complementary Therapies: Mapping the Evidence.” Practical Diabetes, Wiley Online Library (2007).
Purnell, Jonathan Q. “The Effect of Excess Weight Gain with Intensive Diabetes Mellitus Treatment on Cardiovascular Disease Risk Factors and Atherosclerosis in Type 1 Diabetes Mellitus.” Results from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Study (DCCT/EDIC) Study. Circulation, 127 (2013): 180–187.
Tuomilehto, J., J. Lindstrom, J. G. Eriksson, et al. “Prevention of Type 2 Diabetes Mellitus, by Changes in Lifestyle Among Subjects with Impaired Glucose Tolerance.” New England Journal of Medicine, 344 (May 3, 2001): 1343–1350.