Mark Flanigan,
B.HSc (Nutrition), B.HSc (Herbal Medicine),
Advanced Diploma (Naturopathy).
Diabetes Type I & II
Natural Treatment
1.0 Introduction to Natural Diabetes Treatment:
When reviewing diabetes, it is worthwhile considering the impact of contemporary dietary food choices in Australia - not only on the overall health of Australians, but specifically to the impact it may be having on the increase of the occurence of both type 1 and type 2 diabetes. By reference to the contemporary diet, I have considered that it could include fast food, take away and frozen foods, highly processed and refined food. The contemporary diet may also include guidelines set forth by the food pyramid, which lists as a major food group cereals and grains. (www.nutritionaustralia.org/) Lopez-Ridaura et. al. states that “The western diet is characterized by high intake of saturated and trans fats and refined grains and low intakes of whole grains, vegetables, and fiber, resulting in low micronutrient intake.” (Lopez-Ridaura et. al. 2004)
2.0 Diabetes:
Diabetes is characterised by high blood glucose levels, and associated low levels of insulin production, or normal to high levels of insulin production with accompanying insulin resistance. In some cases both of these conditions of low insulin and insulin resistance may be present. Low levels of insulin production are commonly due to an autoimmune disorder, and this is classified as diabetes type 1. Insulin resistance is classed as type 2. There are believed to be many different causes of the condition, some of which include genetic factors, also diseases such as liver cirrhosis, pancreatitis, malnutrition, haemochromatosis, pancreatic cancer, Cushing’s syndrome, acromegaly, glucagonoma, thyrotoxicosis, and others. It may also be due to dug-induced illnesses from drugs such as thiazide diuretics, and corticosteroids. Here, however, I will be focusing on the effects of diet on the development of the condition. (Kumar & Clark 2002)
3.0 Deficiencies and excesses in the contemporary Australian diet:
Analysis of the contemporary Australian diet would suggest that it is quite deficient in certain essential minerals. Most notable of these in relation to insulin resistance is chromium, zinc and magnesium. (Foodworks program) Dietary analysis would also suggest that many modern foods are high on the glycemic index, and also include a predominance of refined carbohydrates. (www.glycemicindex.com/)
Dietary intake of chromium is believed to be much lower in a modern diet than a traditional diet. This has been reflected in breast milk concentrations of chromium, which have been shown to be 10 times lower than samples measured prior to 1980. A modern diet high in simple sugars also adversely affects chromium levels by increasing requirements of the mineral whilst simultaneously inhibiting absorption. Chromium supplementation of between 200 mcg to 1000 mcg has been shown to be effective for improving the symptoms of the type 2 fom of the condition, insulin resistance and gestational diabetes. The lower doses of supplementation have been shown to be effective only for those with mild insulin resistance, most individuals, however, typically require the higher doses in order for it to be effective. (Anderson 1998) Osiecki lists the following foods as containing chromium: “asparagus, apples, beer, brewer’s yeast, cheese, egg yolk, grape juice, liver, lobster, molasses, mushrooms, nuts, oysters, peanuts, pepper, potato, prunes, raisins, shrimp, wheat, yeast.” (Osiecki 2002 p. 111)
The modern diet which typically includes coffee consumption and other drinks containing caffeine, such as energy drinks containing guarana, cocoa, some soft drinks, tea, chocolate milk, and other chocolate products, has been shown to adversely affect people with type 2 of the condition. (www.afic.org/) Caffeine consumption has been associated with increased blood insulin levels and also increased blood glucose levels, demonstrating an increase in the level of insulin resistance. This study was conducted on type 2 diabetics in a placebo controlled study. (Robinson et. al. 2004)
Dietary consistency was found to be important for patients with the type 1 form of the disease to allow them to regulate blood glucose fluctuations. Glycated hemoglobin, HbA1c, was used as a measure of the variation in blood glucose control. Variations in protein and fat intake had no significant effect on HbA1c, but variations in carbohydrate and starch intake, plus glycemic index variations had the effect of consistently raising HbA1c. To explain this variation, Wolever explained it as thus: “the variability in diet made manipulation of oral hypglycemic agents and insulin difficult and arbitrary.” (Wolever et. al. 1999, p. 245) An increase in HbA1c has also been associated with an increased risk of cardiovascular disease. There has also been found to be a significant correlation with HbA1c and the direct costs of health care for those individuals. (Gilmer 1997) To illustrate the importance of controlling HbA1c levels, Gilmer et. al. state that “medical care charges increased significantly for every 1% increase above HbA1c of 7%. For a person with an HbA1c value of 6%, successive 1% increases in HbA1c resulted in cumulative increases in charges of approximately 4, 10, 20, and 30%.” (Gilmer 1997 p. 1847) Dietary behaviour that helps to regulate these levels of HbA1c are consumption of low GI meals and regular but small meals. In type 1 diabetics, insulin adjustment appropriate to the meal type was also helpful to lower these levels. (Delahanty & Halford 1993)
In addition to there being a strong correlation between sugar and caffeine consumption and the onset of diabetes, an even stronger link has been found with high milk consumption and the development of the condition. A definite conclusion could not be made, but it was determined that a combination of factors may be present, particularly genetics, which predispose certain individuals to an increased likelihood of developing the disease. The same biochemical pathway can, according to Harrison & Honeyman, result in the development of “celiac disease and selective IgA deficiency.” (Harrison & Honeyman 1999 p. 1501) Other reports suggest that the link between milk and the development of the condition is much stronger with the consumption of dairy products containing the A1 b-casein, particularly milk and cream. This same report stated that a diet high in cereal-based products, predominantly wheat, soybean and corn, also promotes the development of diabetes. (Swinburn 2004)
Even neonatal exposure to breast milk from a diabetic parent may predispose the offspring to developmental abnormalities. In a rat study, Fahrenkrog et. al. state that “exposure to milk from diabetic mothers, causes a complex malorganization and malprogramming of hypothalamic orexigenic and anorexigenic neuropeptidergic systems in the offspring. This could contribute to the development of hyperphagia, obesity, and diabetogenic disturbances in infancy and in later life.” They continue with the following statement: “Hypothalamic malprogramming due to altered organization of neuropeptidergic regulatory systems may initially lead to more or less discrete functional consequences, such as moderate hyperphagia, hyperglycemia, hyperinsulinemia and hyperleptinemia, and insulin and leptin resistance.” (Fahrenkrog et. al. 2004 p. 653) This is a compelling reason that diabetic mothers should, as much as possible, try to avoid breast feeding their babies. Or at the very least, attempt to regulate the bodies levels of blood glucose levels through dietary control.
Intracellular magnesium deficiency has been linked with the development of type 2 diabetes. A factor that can induce such a magnesium deficiency, despite apparently normal serum magnesium levels, are excessively high levels of intracellular calcium. High levels of insulin can result in such high levels of intracellular calcium, thereby setting up a self-perpetuating cycle of insulin resistance. Contributing to this effect is the fact that magnesium absorption is impaired under states of insulin resistance. (Alzaid et. al. 1995) Studies have shown, however, that supplementing with magnesium has increased serum magnesium levels, and improved insulin resistance. (Rodriguez-Moran & Guerrero-Romero 2003) (Lima et. al. 1998) Osiecki states that the following foods are high in magnesium: “almonds, brewer’s yeast, cashews, cocoa, mineral water, molasses, parsnips, soy beans, wholegrain cereals, kelp, eggs, seeds.” (Osiecki 2002 p. 111)
According to a Melbourne study, an excessive consumption of foods that have a high glycemic index has been shown to be a contributing factor to the development of diabetes type 2. Total carbohydrate intake had no effect on the development of the condition, and of the high GI foods white bread was found to be most strongly correlated to the onset of the condition. It was suggested that simply a change from white to wholegrain bread could reduce the risk of developing the condition. This is due to both the lower GI and also the higher magnesium content of the wholegrain bread. (Hodge et. al. 2004)
Consumption of eggs has typically been on the decline for over 30 years, but the health benefits of consuming eggs are starting to be recognised once again, and so consumption has been on the increase in recent years. Consumption of these may make a valuable contribution to many people’s diets, and particularly in the case of diabetics. They are a good source of several nutrients such as selenium, vitamin K, and choline. They are a complete protein, and have a very low GI. Recent studies have shown that consumption of more than 4 eggs per week has resulted in lower cholesterol levels than people who ate one or less eggs per week. (Hasler 2000)
According to a recent report in the Journal of Nutrition, vitamin D supplementation can help reduce the risk of developing type 1 form of the disease. Harris states that “all infants and children should receive between 5 µg/d and 25 µg/d of supplemental vitamin D, particularly if they have limited sun exposure, live in northern areas, are exclusively breastfed, or are dark skinned.” (Harris 2005, p. 323)
4.0 Effects of diabetes:
Diabetes and its associated conditions such as hyperglycaemia and hyperinsulinaemia, have been associated with an increased risk of Alzheimer’s disease. (Kuusisto 1997) To reduce the risk of developing Alzheimer’s, and also to provide support against a host of other complications that may occur from the disease, it is advisable to eat a diet high in fruits and vegetables. (Joseph et. al. 2005)
Those who have the condition also have an increased rate of retinal destruction due to increased oxidative stress, and subsequent capillary cell apoptosis. (Kowluru & Abbas 2003) In order to slow the development of this condition, it would be beneficial to consume certain antioxidant foods. These may include potatoes, which are a source of lipoic acid. Osiecki lists lipoic acid as being in increased demand in diabetics, and it has several other useful properties as well. Some of these include improved glucose metabolism, reducing insulin resistance, improve ATP synthesis, and acts as a fat-soluble and water soluble antioxidant. Other nutrients and minerals that are listed as being useful for sufferers of the condition are potassium, vanadium, zinc and co enzyme Q10. Food sources of these include the following: vegetables, apricots, avocado, banana, beef, black pepper, chicken fat, citrus fruit, corn, dates, dill, egg yolk, ginger, herring, lamb, linseed, liver, mushroom, nuts, oysters, parsley, pumpkin seeds, raisins, rye, sardines, shellfish, seafood, soy beans, sunflower seeds, whole grains and yeast. (Osiecki 2002)
Other phytochemicals that help support the retina and prevent destruction are lutein and zeaxanthin. Dietary sources of these two nutrients include carrots, especially yellow carrots, leafy green vegetables such as spinach, egg yolk and corn. (Molldrem et. al. 2004)
Both type 1 and type 2 forms of the condition are strong risk factors for the development of cardiovascular disease. Conjugated linoleic acid (CLA) is one of the compounds that may be beneficial in reducing the risk factors associated with cardiovascular disease. Animal studies have shown that CLA has the ability to lower elevated cholesterol levels. It has also been associated with weight loss in obese individuals due to an effect on leptin levels. A common source of CLA is butter. (Aminot-Gilchrist & Anderson 2004) Other reports about CLA have not been as positive, however, with an article by the American Journal of Clinical Nutrition concluding that although it had positive effects on CVD risk factors, it did have an adverse effect on glucose metabolism and insulin sensitivity. (Moloney et. al. 2004)
5.0 References:
About the healthy eating pyramid [Online. Internet] Available
http://www.nutritionaustralia.org/Food_Facts/Fact_Sheets/about _the_healthy_eating_pyramid.asp Accessed 20 September 2005.
Alzaid et. al. Dinneen S. Moyer T. & Rizza R. 1999. Effects of Insulin on Plasma Magnesium in Noninsulin-Dependent Diabetes Mellitus; Evidence for Insulin Resistance.
Journal of Clinical Endocrinology and Metabolism. 80: p. 1376-1381.
Aminot-Gilchrist D. & Anderson H. 2004. Insulin resistance - associated cardiovascular disease: potential benefits of conjugated linoleic acid
American Journal of Clinical Nutrition. Vol. 79(suppl): p. 1159S-1163S.
Anderson R. 1998. Chromium, Glucose Intolerance and Diabetes.
Journal of the American College of Nutrition. Vol. 17, No. 6, p. 548-555.
Asian Food Information Centre [Online. Internet] Available
http://www.afic.org/Temp/Caffeine.pdf Accessed 20 September 2005.
Delahanty L. & Halford B. 1993. The role of diet behaviors in achieving improved glycemic control in intensively treated patients in the Diabetes Control and Complications Trial.
Diabetes Care. Vol 16, Issue 11, p. 1453-1458.
Fahrenkrog S. Harder T. Stolaczyk E. Melchior K. Franke K. Dudenhausen J. & Plagemann A. 2004. Cross-Fostering to Diabetic Rat Dams Affects Early Development of Mediobasal Hypothalamic Nuclei Regulating Food Intake, Body Weight, and Metabolism.
Journal of Nutrition. 134: p. 648-654.
Gilmer T. O'Connor P. Manning W. & Rush W. 1997. The cost to health plans of poor glycemic control.
Diabetes Care. Vol 20, Issue 12, p. 1847-1853.
Harris S. 2005. Vitamin D in Type 1 Diabetes Prevention.
Journal of Nutrition. 135: p. 323-325.
Harrison L. & Honeyman M. 1999. Cow’s Milk and Type 1 Diabetes
Diabetes. Vol. 48: p. 1501-1507.
Hasler C. 2000. The Changing Face of Functional Foods.
Journal of the American College of Nutrition. Vol. 19, No. 5, 499S-506S.
Hodge A. English D. O’Dea K. & Giles G. 2004. Glycemic Index and Dietary Fiber and the Risk of Type 2 Diabetes.
Diabetes Care. Vol 27, Issue 11, p. 2701-2706.
Home of the Glycemic Index. [Online. Internet] Available
http://www.glycemicindex.com/ Accessed 20 September 2005.
Joseph J, Shukitt-Hale B, Casadesus G. 2005. Reversing the deleterious effects of aging on neuronal communication and behavior: beneficial properties of fruit polyphenolic compounds.
American Journal of Clinical Nutrition. Vol. 81, No. 1, 313S-316S.
Kowluru R. & Abbas S. 2003. Investigative Ophthalmology and Visual Science.
Diabetes-Induced Mitochondrial Dysfunction in the Retina. 44: p. 5327-5334
Kumar P. & Clark M. 2002 Clinical Medicine, fifth edition.
London: W.B. Saunders Company.
Kuusisto J. Koivisto K. Mykkänen L. Helkala E. Vanhanen M. Hänninen T. Kervinen T. Kesäniemi A. Riekkinen P. Laakso M. 1997. Association between features of the insulin resistance syndrome and alzheimer's disease independently of apolipoprotein e4 phenotype: cross sectional population based study
British Medical Journal. 315: p. 1045-1049.
Lima M. Cruz T. Pousada J. Rodrigues L. Barbosa K. Cangucu V. 1998. The Effect of Magnesium Supplementation in Increasing Doses on the Control of Type 2 Diabetes.
Diabetes Care. 21 (5): p. 682-686.
Lopez-Ridaura R. Willett W. Rimm E. Liu S. Stampfer M. Manson J. & Hu F. 2004. Magnesium Intake and Risk of Type 2 Diabetes in Men and Women.
Diabetes Care. 27 (1): p. 134-140.
Molldrem K. Li J. Simon P. & Tanumihardjo S. 2004. Lutein and b-carotene from lutein-containing yellow carrots are bioavailable in humans.
American Journal of Clinical Nutrition. Vol. 80: p. 131-136.
Moloney F. Yeow T. Mullen A. Nolan J. & Roche H. 2004. Conjugated linoleic acid supplementation, insulin sensitivity, and lipoprotein metabolism in patients with type 2 diabetes mellitus.
American Journal of Clinical Nutrition. Vol. 80, No. 4, 887-895
Osiecki H. 2002. The Nutrient Bible.
Eagle Farm: BioConcepts Publishing.
Robinson L. Savani S. Battram D. McLaren D. Sathasivam P. & Graham T. 2004. Caffeine Ingestion Before an Oral Glucose Tolerance Test Impairs Blood Glucose Management in Men with Type 2 Diabetes.
Journal of Nutrition. 134: p. 2528-2533.
Rodriguez-Moran M. & Guerrero-Romero F. 2003. Oral Magnesium Supplementation Improves Insulin Sensitivity and Metabolic Control in Type 2 Diabetic Subjects.
Diabetes Care. 26 (4): p. 1147-1152.
Swinburn B. 2004. Beta casein A1 and A2 in milk and Human Health. [Online. Internet] Available
http://www.nzfsa.govt.nz/policy-law/projects/a1-a2-milk/a1-a2-report.pdf Accessed 20 September 2005.
Wolever T. Hamad S. Chiasson J. Josse R. Leiter L. Rodger W. Ross S. Ryan E. 1999. Day-to-Day Consistency in Amount and Source of Carbohydrate Intake Associated with Improved Blood Glucose Control in Type 1 Diabetes.
Journal of the American College of Nutrition. Vol. 18, No. 3, p. 242-247.
6.0 Additional Information:
Association of Triglyceride–to–HDL Cholesterol Ratio With Heart Rate Recovery
PDF version of above article
Triglycerides and TG-HDL Ratio Help Identify Insulin Resistance in Overweight Patients
Triglycerides and relative health risk
The ratio of fasting serum triglycerides to high-density lipoprotein (HDL) cholesterol is a predictor of insulin resistance in polycystic ovary syndrome (PCOS) which is improved by rosiglitazone.
Use of Common Laboratory Tests To Identify People with Insulin Resistance
Glossary of Heart Disease Risk Medical Terms: LDL, HDL, VLDL, cholesterol, triglycerides, lipids, lipoprotein
Life Extension Foundation report - Metabolic Syndrome
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