Everybody needs sugar in their diet, primarily for providing our cells with the energy they need to do their jobs. Insulin is also very important because it is needed to escort sugar into our cells via the insulin receptors on each of our cells. However, a serious problem can be created if there is too much sugar or insulin in the body.
Too much sugar: Excess sugar circulates in the body causing oxidative damage to arteries, nerves and other cells. This leads to diabetes, heart disease, arthritis, brain disorders, blindness, amputations and even cancer.
Too much insulin: Excess insulin causes the insulin receptors on our cells to lose their sensitivity, which means cells cannot function properly and sugar circulates doing its damage. In a normal, healthy person, only one unit of insulin is needed to help10 mg of glucose to enter into a cell group.
As cells lose their insulin sensitivity, more units of insulin are needed to get glucose into cells. Eventually, it may require 10 units of insulin to get 10 mg of glucose into a cell group. This is called hyperinsulinemia. When this occurs, the body's response leads to elevated triglycerides, low HDL cholesterol, Type 2 diabetes and obesity.
Insulin in excess can also impair sodium balance in the body, leading to high blood pressure (hypertension). Too much insulin can also harm the kidneys and the vascular system. In addition, insulin is a catalyst for cell growth, which can increase the risk for certain cancers. High insulin levels promote the formation of beta amyloid in the brain cells. This has been recognized as a causal factor in Alzheimer's disease.
Overproduction of insulin has also been associated with prostate enlargement, and thus prostate cancer. In one study, people with hyperinsulinemia were at twice the risk of dying than people without hyperinsulinemia. In spite of these amazing facts about the danger of high insulin levels, it is almost never included as a regular part of blood diagnostic testing by insurance companies. Why not?
The Cause of High Insulin Levels
High insulin levels are nearly always related to high sugar or glucose levels. Now we know that high sugar levels are due just as much to the high intake of starch, as it is to the high intake of sugar. Foods, such as bread, pasta, rice and potatoes are converted into sugar very quickly in the body (15-20 minutes).
This can cause a serious spike in sugar levels, which in turn causes the pancreas to produce high levels of insulin because sugar is not allowed to be in the body by itself. At least that is not supposed to happen.
It does happen if the pancreas cannot make insulin quickly enough, or if the insulin receptors on our cells become exhausted and cannot take the insulin and glucose into the cell in an efficient manner.
How Much is Too Much Sugar?
The level of sugar in the body is usually measured after fasting for 12 hours and can be either a total sugar reading or an AIc reading. Most doctors use 100 mg/UL as the beginning level for pre-diabetes with levels above 120 mg /UL constituting diabetes. In reality, these levels are too high. Fasting glucose or blood sugar levels should be less than 85 mg/UL, and even then, problems can exist.
AIc levels of 5.7 or above are said to be problematic. AIc measures the amount of glucose that has attached to hemoglobin over the past 3 to 4 months. Hemoglobin is a protein in blood that can become modified or glycosylated when exposed to glucose.
It is this level of exposure over a period of time that supposedly gives doctors an even better picture of glucose levels than the total glucose level test. However, even the AIc test is flawed because the amount of glucose consumed over the past 30 days may dominate the reading and it still requires 12 hours of fasting, which can lead to deceptive analysis.
The Post Meal Test is the Best
A far better test than either total glucose or AIc is probably the post-meal glucose challenge test. In this test, readings are taken for three hours after a meal. This measures the rate that glucose increases, as well as the rate that it declines after eating. This provides a much more accurate picture of how efficient the pancreas is at making insulin, as well as how efficient the insulin receptors on the cells are at taking insulin and glucose into the cells.
Because all meals are not equal in their level of sugar and starch, it is actually better for someone to fast for twelve hours and take some baseline readings of insulin and glucose. Then the doctor provides a glucose solution to drink with 75 mg of glucose. Every 30 minutes new readings are taken for glucose and insulin. Ideally, fasting glucose levels should be 85 mg/dL and fasting insulin levels should be 5MIU/ml (micro international unit per milliliter).
Post consumption glucose levels
- one hour-200 mg/dL
- two hours-140 mg/dL
- three hours-100 mg/dL
Post consumption insulin levels
- one hour-10 mlu/ml
- two hours-8 mlu/ml
- three hours-5 mlu/ml
The post meal glucose tolerance test is the best because it provides the most timely and accurate measurement of your bodies ability to react to the presence of glucose. A person could have normal readings of total glucose or AIc levels but still be suffering blood sugar damage due to high glucose levels after a meal. In fact, someone could have good total glucose and AIc readings for 5 years before a fasting blood test would register at a high level.
The blood glucose tolerance test will not allow this to happen because it will immediately measure any difficulty the body is experiencing in the processing of sugar. In fact, insulin levels will increase before glucose levels will. That means that a potentially diabetic person can see their risk 5 to 7 years before the total glucose or AIc test will see anything, and, the earlier this situation is found, the easier it is to reverse it.
Less pancreatic cells will have been damaged and fewer insulin receptors will have suffered reduction in their efficiency levels. The health benefits and the cost savings possible from the use of the glucose tolerance test are astronomical.
Some Disturbing Health Facts
- A study in 2012 found a strong relationship between hyperinsulinemia and chronic kidney disease in metabolic syndrome patients. In the US, 40 percent of people over age 65 show some sign of kidney failure.
- Another study found that people with the highest insulin levels had a 63 percent increased risk of cancer mortality.
- Hyperinsulinemia creates chronic inflammation and the generation of free radicals that damage our DNA. This leads to many chronic illnesses, as well as premature aging.
- Two studies in 2013 identified a causative relationship between hyperinsulinemia and non-alcoholic fatty liver disease.
- When sugar binds to protein, it produces advanced glycation end products (AGES), which is one of the most dangerous free radicals in the body. Cooking at high temperatures creates these molecules.
A Sugar/Insulin Strategy
It has been estimated that over 90 percent of the population consumes too much sugar and starch. This may be the number one health challenge facing our country. Here are some of the best strategies for addressing this very serious health challenge.
- Get the right tests. Everyone should get tested for their insulin levels, as well as their glucose tolerance levels. Having C-reactive protein tested is also important because this is a measure of inflammation.
- Try to reduce your level of carbohydrates from the current average level of 65-70 percent to less than 50 percent of total calories. Ensure that a vast majority of these carbohydrates come from non-starchy vegetables.
- Increase your level of fiber consumption from currently low levels of 20g/day for the average person to 40g/day.
- Eat in accordance with glycemic load guidelines. About 40g/day of glycemic load is recommended. Glycemic load is calculated by multiplying the glycemic index value of a food times the grams of the food being eaten.
- Reduce or eliminate if you can, foods such as soft drinks, cookies, pastry, ice cream, maple syrup, potatoes, molasses, corn syrup, high fructose corn syrup, pasteurized honey, white bread, white rice and white pasta.
- Seriously limit your consumption of fruit juices, whole grain bread, whole grain pasta and brown rice.
- Increase your level of exercise in all categories, including aerobic, weight bearing and flexibility.
Muscle burns more calories than fat tissue. Exercise increases insulin receptor efficiency.Exercise can be detoxifying. Exercise improves cardiovascular performance. Take supplements, such as enzymes, green powder drinks, magnesium, CoQ10, multiple vitamin, Vitamin B complex, Vitamin D3, fish oil and Curcumin.
Conclusion
This reduction of sugar or starch consumption will not be easy for most people to achieve and one of the reasons is that many people are actually addicted to sugar. There are very strong cravings generated in the brain due to the demand for neurotransmitters such as dopamine or serotonin. The body, and especially the brain, needs certain nutrients to make these transmitters.
Here is a list of the most commonly craved foods and the nutrients actually needed by the body and the brain. Amino Acids + Methylation B Vitamins = Neurotransmitters
This basic formula can be expanded to cover specific foods that we crave, what the body really is looking for and which foods can best satisfy these needs. These cravings are mostly in the brain, but can be caused by nutritional deficiencies throughout the body.
Written by:
Charles K. Bens, PhD.Healthy at Work Sarasota, Florida.
References
- Cochran E. Musso C, Gorden P. The use of U-500 in patients with extreme insulin resistance. Diabetes Care. 2005 May; 28(5):1240-4.
- Godsland IF, Corrk D, Walton C, Wynn V, Oliver MF. Influence of insulin resistance, secretion and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol and blood pressure in healthy men. Arterioscler Thromb. 1992 Sep; 12(9):1030-5.
- Salonen JT, Lakka TA, Lakka HM, Volkonen VP, Everson SA, Kaplan GA. Hyperinsulinemiwa is associated with the incidence of hypertension and dyslipidemia in middle-aged men. Diabetes. 1998 Feb;47(2):270-5.
- Stannard SR, Johnson NA. Insulin resistance and elevated triglyceride in muscle: more important for survival than thrifty genes? J Physiol. 2004 Feb 1;554(Pt 3):595-607.
- Mykknen L. Kuusisto J, Haffner SM, Pyrl K, Laakso M. Hyperinsulinemia predicts multiple atherogenic changes in lipoproteins in elderly subjects. Arteriorscler Thromb. 1994 Apr;14(4):518-26.
- Karhap P, Malkki M, Laakso M. Isolated low HDL cholesterol. An insulin-resistant state. Diabetes. 1994 Mar;43(3):411-7.
- Ko GT, Cockram CS, Woo J, Chan JC. Obesity, insulin resistant and isolated low high-density-lipoprotein cholesterol in Chinese subjects . Diabet Med. 2001 Aug; 18(8):663-6.
- Goldstein BJ. Insulin resistance as the core defect in type 2 diabetes mellitus. AM J Cardoil. 2002 Sep 5;90(5A):3G10G.
- Haffner SM, Stern MP, Mitchell BD, Hazuda HP, Patterson JK. Incidence of type II diabetes in Mexican Americans predicted by fasting insulin and glucose levels, obesity, and body-fat distribution. Diabetes. 1990 MR;39(3):283-9.
- Hansen J, Rinnov A, Krogh-Madisen R, et al. Plasma follistatin is elevated in patients with type 2 diabetes: relationship to hyperglycemia, hyperinsulinemia, and systemic low-grade inflammation. Diabetes Metab Res Rev. 2013 Apr 6.
- Despres JP, Pascot A, Lemieux I. Risk factors associated with obesity: a metabolic perspective. Ann Endocrinol. 2000 Dec;61 Suppl 6:31-8.
- Modan M. Haklin H, Almog S, et al. Hyperinsulinemia. A link between hypertension obesity and glucose intolerance. J Clin Invest. Mar;75(3):809-17.
- Feuers RJ, Desai VG, Chen FX, Hunter JD, Duffy PH, Oriaku ET. Effects of dietary restriction on insulin resistance in obese mice. J Am Aging Assoc. 2000 Apr;23(2): 95-101
- Chu N, Spiegelman D, Hotamisligil GS, Rifai N, Stampler M, Rimm EB. Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. Atherosclerosis. 2001 Aug;157(2):495-503.
- Hano T, Nishio I. Treatment of hypertension in the patients with obesity. Nippon Rinsho. 2001 May;59(8):929-35.
- Kopf D, Muhlen I, Kroning G, Sendzik I, Huschke B, Lehnert H. Insulin sensitivity and sodium excretion in normotensive offspring and hypertensive patients. Metabolism. 2001 Aug;50(8):929-35.
- Noda M, Matsuo T, Nagano-Tsuge H, et al. Involvement of angiotensin II in progression of renal injury in rats with genetic non-insulin-dependent diabetes mellitus (Wistar fatty rats). Jpn J Pharmacol. 2001 Apr;85(4):416-22.
- Hegele RA. Premature atherosclerosis associated with monogenic insulin resistance. Circulation. 2001 May 8;103(18):2225-9.
- Burnol AF, Morzyglod L, Popineau L. Cross-talk between insulin signaling and cell proliferation pathways. Ann Endocrinol (Paris). 2013 Apr 9. [Epub ahead of print]
- Balkau B, Kahn HS, Courbon D, Eschwege E, Ducimetier P. Hyperinsulinemia predicts fatal liver cancer but is inversely associated with fatal cancer at some other sites. Diabetes Care. 2005 May;28(5):1240-4.
- Kaaks R. Plasma insulin, IGF-I and breast cancer. Gynecol Obstet Fertil. 2001 Mar;29(3):185-91.
- Czyzyk A, Szczepanik Z. Diabetes mellitus and cancer. Eur J Intern Med. 2000 Oct;11(5):245-52.
- Bruce WR, Wolever TM, Giacca A. Mechanisms linking diet and colorectal cancer: the possible role of insulin resistance. Nutr Cancer. 2000 37(1):19-26.
- Cook DG, Leverenz JB, McMillian PJ, et al. Reduced hippocampal insulin-degrading enzyme in late-onset Alzheimer's disease is associated with the apolipoprotein E-epsilon4 allele. Am J Pathol. 2003 Jan;162(1):313-9.
- Hammarsten J, Hogstedt B. Hyperinsulinaemia as a risk factor for developing benign prostatic hyperplasia. Eur Urol. 2001 Feb;39(2):151-8.
- Ceriello A. The postprandial state and cardiovascular disease: relevance to diabetes mellitus. Diabetes Metab Res Rev. 2000 Mar-Apr;16(2):125-32.
- Hoffman-Snyder C, Smith BE, Ross MA, Hernandez J, Bosch EP. Value of the oral glucose tolerance test in the evaluation of chronic idiopathic axonal polyneuropathy. Arch Neurol. 2006 Aug;63(8):1075-9.
- Chien KL, Lee BC, Lin HJ, Hsu HC, Chen MF. Association of fasting and post-prandial hyperglycemia on the risk of cardiovascular and all-cause death among non-diabetic Chinese. Diabetes Res Clin Pract. 2009 Feb;82(2):e47-50.
- Ceriello A. Impaired glucose tolerance and cardiovascular disease: the possible role of postprandial hyperglycemia. Am Heart J. 2004 May;147(5):803-7.
- Lebovitz HE. Effect of the postprandial state on nontraditional risk factors. Am J Cardiol. 2001 Sep 20;88(6A):20H-5H.
- Available at:http://www.a4m.com/assets/pdf/bookstore/thera6_ch4.pdf?SESSION _MAIN=dap3mjgnb96luhbje8tcklgp75. Accessed April 29, 2013.
- Hurjui DM, NiO, Graur LI, Mihalache L, Popescu DS, Graur M. The central role of the non-alcoholic fatty liver disease in metabolic syndrome. Rev Med Chir Soc Med Nat Iasi. 2012 Apr-Jun;116(2):425-31.
- Titov VN, Ivanova KV, Malyshev PP, Kaba SI, Shiriaeva IuK. The unity of pathogenesis of insulin resistance syndrome and non-alcoholic fatty disease of liver. The metabolic disorder of fatty acids and triglycerides. Klin Lab Diagn. 2012 Nov;(11):3-12.
- Yang WS, Shu XO, Gao J, et al. Prospective evaluation of type 2 diabetes mellitus on the risk of primary liver cancer in Chinese men and women. Ann Oncol. 2013 Feb 13.
- Available at: http://kidney.niddk.nih.gov/kudiseases/pubs/kustats/. Accessed April 25, 2013.
- Perseghin G, Calori G, Lattuada G, et al. Insulin resistance/hyperinsulinemia and the 15th year of follow-up. Acta Diabetol. 2012 Dec;49(6):421-8.
- Available at: http://www.huffingtonpost.com/2013/03/06/alzheimers-health-united-states-america-threat_n_2820887. Html. Accessed April 18, 2013.
- Jovanovi Z. Mechanisms of neurodegeneration in Alzheimer's disease. Med Pregl. 2012 July-Aug;65(7-8):301-7.Brand-Miller JC, Stockmann K, Atkinson F, Petocz P,
- Denyer G. Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1,000 foods. Am J Clin Nutr. 2009 Jan;89(1):97-105.
- Ao Z, Simsek S, Zhang G, Venkatachalam M, Reuhs BL, Hamaker BR. Starch with a slow digestion property produced by altering its chain length, branch density, and crystalline structure. J Agric Food Chem. 2007 May 30;55(11):4540-7.
- Available at: gtty://www.madsci.org/posts/archives/2000-12/978293375.Bc.r.html. Accessed Feb 26, 2013.
- Liljeberg HG, Akerberg AK, Bjrck IM. Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects. Am J Clin Nutr. 1999 Apr;69(4):647-55.
- Cerf ME. Beta cell dynamics: beta cell replenishment, beta cell compensation and diabetes. Endocrine. 2013 Mar 13.
- Kuhl, H. Breast cancer risk in the WHI study: the problem of obesity . Maturitas. 2005 May 16;51(1) :83-97.
- Sandovici I, Hammerle CM, Ozanne SE, Constancia M. Developmental and environmental epigenetic programing of the endocrine pancreas: consequences for Type 2 diabetes. Cell Mol Life Sci. 2013 Mar 6.