What is diabetes?
Type I diabetes
Type II diabetes
Long-term complications from diabetes
Prevention / remedies / treatment for diabetes
What is diabetes?
Diabetes mellitus is a chronic condition in which a person has a high blood sugar (glucose) level. It occurs when either the body doesn't produce enough insulin, or because body cells don't properly respond to the insulin that is produced. Insulin is a hormone produced by the pancreas which tells cells to absorb glucose and store energy. If glucose is not stored it remains in the blood (hyperglycemia) and gradually causes complications.
The optimal blood glucose range is 85-105 mg/dl, rising to the 120-140 after eating a meal and back into the optimal range within a couple of hours. Doctors regard the normal fasting blood sugar level as 80-120 mg/dL. A typical diabetic's level is 160 mg/dL two hours after a meal containing carbohydrates.
Over 6% of the world's population has diabetes, and it is "one of the biggest health catastrophes the world has ever witnessed". (5) It is not only a rich country disease, and is rapidly increasing in developing countries. in 2000 the five countries with the greatest number of people with diabetes were India (31.7 million), China (20.8 million), USA (17.7 million), Indonesia (8.4 million), and Japan (6.8 million). (6)
It is recognized as a global epidemic by the World Health Organization. (7) It causes massive human suffering, disability and socioeconomic cost.
Diabetes is a preventable disease caused by eating too much sugar, refined carbohydrates (things made with flour), sweet and dried fruits, and other sweet things.
Type one diabetes
Type 1 diabetes (insulin-dependent or juvenile diabetes): the pancreas does not produce sufficient insulin. This causes an increased level of glucose in the blood and urine.
This condition is eventually fatal unless treated with insulin. Usually the person injects insulin for the rest of their life. When managed correctly, the person can remain healthy. However, with imperfect management similar symptoms to type 2 diabetes can occur. In addition, the sufferer has an increased risk of vehicle and other accidents.
Incidence of type 1 diabetes
The incidence ranges from 0.8-1.7% in the USA and northern Europe to 3.5% in Scandinavia to a low of 0.1% in Japan and China. (1) Less than 10% of all cases of diabetes are type I.
Causes of type 1 diabetes
- Diet. Cow's milk and other dairy products introduced too early, before the age of two.
- Congenital. Type 1 diabetes has a congenital risk. With identical twins, when one twin has type 1 diabetes the other twin has it only 30%-50% of the time.
- Breastfeeding, insufficient. None, or weaned too soon.
- Vitamin D deficiency during pregnancy or infancy.
- Toxic chemicals. Agricultural chemicals, environmental pollution.
- Environmental. There is a 10-fold difference in occurrence between Caucasians living in different areas of Europe. (9)
Symptoms of type 1 diabetes
The hallmark symptoms of type 1 diabetes are listed below. See also symptoms of type 2 diabetes.
- Frequent urination (polyuria).
- Weight loss.
- Dry mouth.
- Dry skin.
- Rapid, deep breathing.
- Abdominal pain.
Other possible symptoms of type 1 diabetes
Type two diabetes
Type 2 diabetes (noninsulin-dependent diabetes or adult-onset diabetes) is caused by eating too much sugar, refined carbohydrates (things made with flour), sweet and dried fruits, and other sweet things. It occurs when the cells in the body fail to properly respond to insulin (insulin resistance).
Incidence of type 2 diabetes
Approximately 90-95% of all cases of diabetes are Type 2. It is increasing at an alarming rate. In the USA, 11% of people over the age of 20 have Type 2 diabetes, and 24% of those over the age of 60 (Source: CDC). It is estimated that 28% of people with diabetes in the USA do not realise that they have the disease, leading to terrible consequences five years later - loss of limbs, blindness, kidney failure, heart disease, strokes and nerve damage. Diabetes used to be an adult disease, but now it is also common in children.
Two thirds of the population suffers from metabolic syndrome, sometimes referred to as pre-diabetes, with symptoms of aches, pains, tiredness, a tendency to overweight and a general feeling of malaise. Diabetes has increased in line with obesity. It is also increasingly diagnosed in children, again in parallel with obesity.
Causes of type 2 diabetes
- Sugar. (17) It is primarily caused by a diet high in refined, processed foods providing a high level of sugar (especially fructose). (14, 15, 16) Polyunsaturated vegetable oils and MSG are also involved.
- Relentless snacking on sugar and refined carbohydrates. The continual use of sweet foods and drinks for most of the day causes a sustained blood glucose level that never has a chance to go down to normal. Eventually this sugar assault overwhelms and damages the pancreas and the entire insulin-glucose storage system.
- Artificial sweeteners. (22)
- Lack of exercise, lack of movement during the day.
- Obesity increases risk of diabetes, but thin people can also be diabetic. Those who are not obese often have a risky high waist-hip ratio.
- Sleep. 1. Lack of, 2. irregularity, and 3. being a night owl rather than an early bird.
- Chronic stress. (29)
- Pharmaceutical drugs including glucocorticoids, thiazides, beta blockers, atypical antipsychotics, and statins. (2, 3)
- Testosterone deficiency is associated with type 2 diabetes.
- Genetic factors. (minor cause).
Symptoms of type 2 diabetes
In the first year or two, there may be few symptoms.
- Increased thirst.
- Frequent urination, especially at night.
- Oedema (edema).
- Hunger. Increase in appetite / constant hunger, especially for sugar and other carbs.
- Blurred vision, other degenerative eye ailments.
- Acetone smell in breath.
- Fatigue and lethargy, especially after eating.
- Reduced intelligence.
- Unexplained weight loss.
- Micronutrient deficiencies caused by sugar and by poor eating, particularly vitamin C, vitamin D, potassium and zinc. Sugar is an antagonist to vitamin C and potassium.
- Fatty liver.
- Erection problems, female sexual dysfunction.
- Tingling or numbness in hands and feet. Nerve damage leading to weakness and poor sensitivity.
- Mood swings (hostility through to mania), confusion, brain fog.
- Abdominal pain.
- Vaginal infections (recurrent).
Gestational diabetes mellitus (GDM) is a condition in which occurs in pregnant women who have not previously been diagnosed with high blood glucose levels. The insulin receptors on cells do not function properly. If affect about 3-10% of pregnancies, and is most common in the third trimester. It usually has few obvious symptoms, and usually resolves after delivery.
However, the infant is at increased risk of problems such as being large for gestational age (which may lead to delivery complications), low blood sugar, jaundice and an increased risk of obesity and diabetes later in life.
GDM can be treated with the same recommendations, including diet and exercise, as type 2 diabetes.
Long-term complications from diabetes
- Life-expectancy reduced by 10 years. (12)
- Cardiovascular disease, hardening of arteries (risk increased 2-4 times). (12, 13)
- Stroke. (12, 13)
- Chronic renal failure. (12, 13) A study showed that diabetes and its consequent kidney disease were healed after two months on a ketogenic diet. (20)
- Retinal damage, blindness. (12)
- Circulatory problems leading to damage to limbs and organs. Damage can be so severe that amputation is necessary. (12, 13)
- Frequent infections.
- Cognitive dysfunction, dementia, Alzheimer's disease. (10, 11)
- Autism. Risk of autism or other ASD in children of diabetics.
- Nerve damage occurs when blood sugar is above 140mg/dl. (10, 11) Diabetics, and people who regularly consume sweet foods and drinks are slowly poisoning their brain and nerves.
Prevention / remedies / treatment for diabetes
- Diet. A ketogenic diet in which you eliminate all sugars, refined carbohydrates, and especially fructose. (14, 15, 16, 17, 19, 20, 21) A ketogenic diet can permanently heal diabetes. (20, 21, 28)
- Lose weight. If you are overweight, get back to normal. Removing excess fat from the liver and pancreas (fatty liver) is a key to complete remission of type 2 diabetes. (26, 27, 28)
- The conventional medical model and the American Diabetes Association recommend treating diabetes with insulin. The ADA recommends that type 2 diabetics eat carbohydrates every day! This recommendation is seriously flawed. (17, 19, 21)
This study (19) shows that insulin therapy does more harm than good.
A ketogenic diet is a more effective, faster and permanent treatment for diabetes than standard medical treatment. (21)
- Intermittent fasting. Do not snack between meals! Extend the size of the window when you do not eat anything. At first this window may be when you are sleeping, but start having dinner earlier or breakfast later. Eventually move to having two meals per day, and eventually your long term goal is one meal per day. These are long term goals, but you will notice a big and quick improvement just when you stop snacking.
- Micronutrients. Vitamin C, vitamin D, potassium, magnesium and zinc may be low.
- Exercise. A minimal level of aerobic exercise. The exercise should be pleasant and not exhausting while the diabetes heals. Recommended - walking every day (30 minutes or a lot more), gardening, housework, gentle sports and so on. Resistance training (strength training, weights, building up muscle) is also necessary. (4)
- Apple cider vinegar. ACV improves insulin sensitivity. (24, 25) Take ACV in a glass of water a couple of times each day.
- Methylene blue.
- Eliminate dairy products, especially if you suffer from type I diabetes. A likely cause of type I diabetes is too early exposure to milk and other dairy products while breastfeeding and during the first two years of life.
- Citrus (lemon) bioflavonoids.
- Fecal transplant. (18)
- White Chinese mulberry. (23)
- See details of remedies recommended by Grow Youthful visitors, and their experience with them.
1. Kasper, Dennis L; Braunwald, Eugene; Fauci, Anthony; et al.
Harrison's Principles of Internal Medicine (16th ed.)
2005, New York: McGraw-Hill. ISBN 0-07-139140-1.
2. Izzedine, H; Launay-Vacher, V, Deybach, C, Bourry, E, Barrou, B, Deray, G. Drug-induced diabetes mellitus. November 2005, Expert opinion on drug safety 4 (6): 1097-109. doi:10.1517/147403184.108.40.2067. PMID 16255667.
3. Sampson, UK; Linton, MF, Fazio, S. Are statins diabetogenic? July 2011, Current opinion in cardiology 26 (4): 342-7. doi:10.1097/HCO.0b013e3283470359. PMC 3341610. PMID 21499090.
4. Shoback, edited by David G. Gardner, Dolores. Greenspan's basic & clinical endocrinology (9th ed.) 2011. New York: McGraw-Hill Medical. pp. Chapter 17. ISBN 0-07-162243-8.
5. Meetoo D, McGovern P, Safadi R. An epidemiological overview of diabetes across the world. Br J Nurs. 2007 Sep 13-27;16(16):1002-7.
6. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. May 2004, Diabetes Care 27 (5): 1047-53. doi:10.2337/diacare.27.5.1047. PMID 15111519.
7. Diabetes Fact sheet No. 312. World Health Organization. Aug 2011. Retrieved 9 January 2012.
8. OMIM. DIABETES MELLITUS, INSULIN-DEPENDENT; IDDM. Retrieved 4 December 2012.
9. Knip, M.; Veijola, R.; Virtanen, S. M.; Hyoty, H.; Vaarala, O.; Akerblom, H. K. Environmental Triggers and Determinants of Type 1 Diabetes. 2005, Diabetes 54: S125-S136. doi:10.2337/diabetes.54.suppl_2.S125. PMID 16306330.
10. Singleton JR et al. Increased prevalence of impaired glucose tolerance in patients with painful sensory neuropathy. Diabetes Care. 2001 Aug; 24(8):1448-53.
11. Ziegler D. et al. Prevalence of polyneuropathy in pre-diabetics and diabetes is associated with abdominal obesity and macroangiopathy: the MONICA/KORA Augsburg Surveys S2 and S3. Diabetes Care. 2008 Mar; 31(3):464-9.
12. UK Prospective Diabetes Study Group (UKPDS). Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. UKPDS 33. Lancet. 1998 Sept 12; 352(9131):837-53.
13. Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N. Association of hemoglobin A1c with cardiovascular disease and mortality in adults: the European prospective investigation into cancer in Norfolk. Ann Intern Med. 2004 Sep 21;141(6):413-20.
14. Perez-Pozo SE, Schold J, Nakagawa T, Sanchez-Lozada LG, Johnson RJ, Lillo JL. Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response. Int J Obes (Lond). 2010 Mar;34(3):454-61. Epub 2009 Dec 22.
15. Johnson RJ, Perez-Pozo SE, Sautin YY, Manitius J, Sanchez-Lozada LG, Feig DI, Shafiu M, Segal M, Glassock RJ, Shimada M, Roncal C, Nakagawa T. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. 2009 Feb;30(1):96-116. Epub 2009 Jan 16.
16. Bray GA. How bad is fructose? Am J Clin Nutr. 2007 Oct;86(4):895-6.
17. Nita G Forouhi, Fumiaki Imamura, Laura O'Connor, Zheng Ye, Jaakko Mursu, Yasuaki Hayashino, Shilpa N Bhupathiraju. Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction. BMJ 2015;351:h3576 (Published 21 July 2015).
18. Vrieze A, Van Nood E, Holleman F, Salojarvi J, Kootte RS, Bartelsman JF, Dallinga-Thie GM, Ackermans MT, Serlie MJ, Oozeer R, Derrien M, Druesne A, Van Hylckama Vlieg JE, Bloks VW, Groen AK, Heilig HG, Zoetendal EG, Stroes ES, de Vos WM, Hoekstra JB, Nieuwdorp M. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology. 2012 Oct;143(4):913-6.e7. doi: 10.1053/j.gastro.2012.06.031. Epub 2012 Jun 20.
19. Michal M. Poplawski, Jason W. Mastaitis, Fumiko Isoda, Fabrizio Grosjean, Feng Zheng, Charles V. Mobbs. Reversal of Diabetic Nephropathy by a Ketogenic Diet. Published: 20 April 2011. doi.org/10.1371/journal.pone.0018604.
20. Michal M. Poplawski, Jason W. Mastaitis, Fumiko Isoda, Fabrizio Grosjean, Feng Zheng, Charles V. Mobbs. Reversal of Diabetic Nephropathy by a Ketogenic Diet. Published: 20 April 2011. doi.org/10.1371/journal.pone.0018604.
21. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ, Westman EC, Accurso A, Frassetto L, Gower BA, McFarlane SI, Nielsen JV, Krarup T, Saslow L, Roth KS, Vernon MC, Volek JS, Wilshire GB, Dahlqvist A, Sundberg R, Childers A, Morrison K, Manninen AH, Dashti HM, Wood RJ, Wortman J, Worm N. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition. 2015 Jan;31(1):1-13. doi: 10.1016/j.nut.2014.06.011. Epub 2014 Jul 16.
22. Brian Hoffmann et al. Why zero-calorie sweeteners can still lead to diabetes, obesity: Common artificial sweeteners shown to change how the body processes fat and energy. Experimental Biology 2018. 23 April 2018.
23. Hunyadi A, Liktor-Busa E, Marki A, Martins A, Jedlinszki N, Hsieh TJ, Bathori M, Hohmann J, Zupko I. Metabolic effects of mulberry leaves: exploring potential benefits in type 2 diabetes and hyperuricemia. Evid Based Complement Alternat Med. 2013;2013:948627. doi: 10.1155/2013/948627. Epub 5 Dec 2013. PMID: 24381639; PMCID: PMC3870074.
24. Ostman E, Granfeldt Y, Persson L, Bjorck I. Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. Eur J Clin Nutr. 2005 Sep;59(9):983-8. doi: 10.1038/sj.ejcn.1602197. PMID: 16015276.
25. Leeman M, Ostman E, Bjorck I. Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects. Eur J Clin Nutr. 2005 Nov;59(11):1266-71. doi: 10.1038/sj.ejcn.1602238. PMID: 16034360.
26. Roy Taylor, Ahmad Al-Mrabeh, Sviatlana Zhyzhneuskaya, Carl Peters, Alison C. Barnes, Benjamin S. Aribisala, Kieren G. Hollingsworth, John C. Mathers, Naveed Sattar, Michael E.J. Lean. Remission of Human Type 2 Diabetes Requires Decrease in Liver and Pancreas Fat Content but Is Dependent upon Capacity for B Cell Recovery. Cell Metabolism, Volume 28, Issue 4, 2018, Pages 547-556.e3, ISSN 1550-4131, doi.org/10.1016/j.cmet.2018.07.003.
27. Dominic Santoleri, Paul M. Titchenell. Resolving the Paradox of Hepatic Insulin Resistance. Cellular and Molecular Gastroenterology and Hepatology, Volume 7, Issue 2, 2019, Pages 447-456, ISSN 2352-345X, doi.org/10.1016/j.jcmgh.2018.10.016.
28. Raja Gopal Reddy Mooli, Sadeesh K. Ramakrishnan. Emerging Role of Hepatic Ketogenesis in Fatty Liver Disease. Front. Physiol., 04 July 2022. Sec. Metabolic Physiology, Volume 13 - 2022.
29. Verberne AJ, Korim WS, Sabetghadam A, Llewellyn-Smith IJ. Adrenaline: insights into its metabolic roles in hypoglycaemia and diabetes. Br J Pharmacol. 2016 May;173(9):1425-37. doi: 10.1111/bph.13458. Epub 2016 Mar 8. PMID: 26896587; PMCID: PMC4831313.