Problems of diabetes have been growing in leaps and bounds. The Greek word diabetes means siphon, which first was given by Aretaeus of Cappadocia (150 A.D). Willis first observed that urine in diabetes is honey like (1674). Mathew Dobson demonstrated that sweetness of urine is sugar which is excreted from blood (1784).
The pancreas secretes exocrine digestive enzymes & endocrine hormones. The total islets are about 2 million. Gastrin, glucagon and insulin are secreted by A1, A2, and B cells respectably. The total beta cells weight is about 1.2 gm. The Islets of Langerhans stores insulin 150 units (about 6mg). Pro-insulin has 84 amino acids and its molecular weight is 9045. Insulin has 51 amino acids (A chain = 20, B chain= 31 amino acids), its molecular weight is 5000. Daily insulin requirement: 1mg=24 units (sufficient for 200 gm carbohydrates). Pancreas wt: 60 gm. Length: 15 cm. Shape: lady finger. Color: ash.
It is a constitutional disease affecting the entire body. It is a poly-endocrine gland disorder due to a multi-enzymes defect. It is a metabolic disorder related to inadequate production of insulin or insulin insensitivity of cells.
DM -Positive view
It is not a contagious disease. The major types are of lifestyle origin. Less than 4% of the total population is affected. Mild adult onset is easy to cure. All complications are preventable. Diabetes mostly occurs after middle age and comes on slowly.
Each human being (approx. 649 crores= 6.49 billion) has one disease or another.
DM -negative view
It is a chronic degenerative disorder involving almost all vital organs. It may be stable throughout one’s life. It is a disease of civilization (consumption of refined white starchy food, kola, consumption of sucrose >150gm/day, etc. raises the triglyceride levels and later leads to atherosclerosis). It may occur suddenly after a mental or any physical stress.
It may change to overt or to brittle type or even to coma suddenly by a precipitating factor like pregnancy, fracture or infection. It may persist as sub- clinical even for 15 years. It is a terrible disorder, responsible for 1 in every 8 deaths, 1 in every 3 cases of blindness.
Pregnancy risks: Chance of miscarriage, difficult labor, birth of over-weight baby, insufficient breast milk, neonatal death, developmental diseases, childhood headache, recurrent infection, increased hair growth, height gain, blindness, early development of glaucoma, premature cataract, etc.
Racial: Pima Indians, Fiji Indians, and Jews. Geographical: Mauritius (Coconut-Phosphorus, fish-high iodine). Nauru island (Phosphorus), Finland (Tobacco), East India (Arsenic-mustard, Argemona mexicona, Ergot contamination), south India (milk, Phosphorus), South Kerala (minerals-tapioca), north India (wheat -Uranium contamination, Ergot). It is calculated that > 8% of population in Kerala (India) are affected.
People in civilized societies are more susceptible to diabetes.
TYPE I- Insulin dependent.
A. Insulin dependent in children & juvenile
B. Insulin dependent in adult (thin build)
TYPE II– Non insulin dependent (adult onset)
Other non specific categories are genetic, latent, thin diabetic, obese diabetic, gestational, chemical, clinical, stable, brittle, overt, secondary pancreatic, secondary endocrinal, hepatic, dysenzymatic intercellular, auto immune diabetic, nutritional (protein -cystine) deficient, geographical (the pancreatic fibrocalcinosis- consuming the food items amara, tapioca, cassava, food containing hydrocyanic acid, phosphorus) etc.
Old Indian classification
Kafa (10 types): symptoms: sweet in mouth, running of nose, desire for sugar, distaste, dyspepsia, sleepiness, hair growth, etc.
Pita (6 types): symptoms: high BMR, dry throat, bladder pain, loose motion, etc.
Vata (4 types): symptoms: flatulence, tremor, pain, weight loss etc.
Diabetes is considered a chronic degenerative disease. Hyperglycemia occurs due to deficiency of insulin or difficulty in entry of glucose into the cell. The two major factors which stand out distinctly in causing diabetes are genetics and homoeostasis (life style). Many contributing factors may present in one individual.
The most frequent causes are heredity, gestational changes, obesity (80%), lack of exercise, consuming excess of refined carbohydrates and saturated fat; Nutritional deficiency (Vitamin B1, B12, C, A, E; Niacin, Chromium, Zinc, Mg, K, Mn, selenium); Pancreatic insufficiency (coffee, alcohol, tobacco, stress through adrenal over activity); Sudden sympathetic over activity, spinal T6 -T10 lesion; Severe infection; Hepatic insufficiency-fatty liver, liver damage, cirrhosis, insulin antibodies-anti insulin liver enzymes; Renal insulin loss, poor toxin elimination; Endocrinal imbalance-excess of thyroxin (rapid glucose absorption from Gastro intestinal tract- >1.84 gm / hour / kg), Growth hormone with low liver hexokinase, GH with low insulin (low entry to cell- < 1.84 gm / hour / kg), glucagon (liver glycogenolysis) and adrenaline (neoglucogenesis- protein); Chemical contamination: tobacco, alloxan, uric acid, urate, acetate, sulphate, phosphate, lactate, citrate; Drugs: toxicity of beta blockers and calcium blocker (inhibit insulin secretion) etc.
Digestion and metabolism
Intake of high fat in childhood creates over stress on the pancreatic digestive enzyme system. Thus it causes depression on both digestive & hormonal cells.
Mal digestion is occurs first due to insufficient production of pancreatic enzymes. The fat molecules (large size) formed by insufficient fat digestion are involved later in the genesis of atherosclerosis. The protein molecules formed by insufficient protein digestion cause both the production of organic acid and auto immune reactions. Diabetes is not simply a disorder of the pancreas.
The Lens, RBC’s, myelinated nerves, cells of kidney, testis etc. receive more sugar passively and are more sensitive to insulin. This excess of glucose is converted partly to insoluble fructose and sorbitol. Later it is crystallized locally. Thus the oxygen caring capacity of RBC is reduced. Oxygen and glucose are essential to RBC.
Glycogen is formed from Glucose-6-Phosphate which is primarily synthesized inside the cells from glucose with hexokinase. The liver stores glycogen, about 50 gm to 300 gm. Glucose is also formed from ketones (G-6-P via lactic acid) at muscle with insulin.
Diabetes is not just a disorder of carbohydrate metabolism. It affect lipid and protein metabolism also. It affects all organs of the body. The body utilizes energy in diabetes poorly from carbohydrate and more from fat and protein. The items promoting the anaerobic glucose metabolism are glucagon (liver glycogenolysis), insulin, hexokinase, and vitamin C. Vitamins like niacin, B12, B1 and some enzymes are essential for aerobic metabolism
Other factors promoting glycogenolysis are starvation, hypoglycemia, adrenalin (muscle), lack of insulin (muscle) and glucagon.
Lactic acid, Ketones & Cholesterol
Lactic acid formed by glycogenolysis enters into blood circulation. Lactic acid is produced by heavy exercise also. Cardiac muscles use it for aerobic metabolism. The liver takes it for glucose formation. Lactic acidosis is usually developed in starvation, hypoxia, liver damage and high muscular exertion.
1/3 glucose and 2/3 fatty acids are formed from catabolism of fat and that enter into circulation. ¼ of these fatty acids go to the liver and combine with apoprotein (from ribose sugar) and finally reach adipose tissues (as HDL- low molecular size). Fatty acids, Alcohol, acids etc more quickly enter into adipose cells than glucose. The remaining 3/4 of fatty acids persists in circulation and may deposit in liver cells and on vessel walls or excrete through bile.
Fat, protein and carbohydrates jointly participate in metabolism at the liver with oxygen. Improper metabolism of any one will cause the production of metabolites like ketones, cholesterol and organic acids. Ketones produced in the liver normally enter inside the muscle cell with insulin. Ketones are water soluble, so a large portion is lost through urine. More ketones and cholesterol are formed within liver cells by deficiency of insulin, coenzyme A and oxygen.
Arteriosclerosis denotes sclerosis of the middle coat of the artery. The fat molecules formed by insufficient fat digestion are primarily involved in the development of atherosclerosis. Injected insulin quickly enters the circulation and produces hypoglycemia and local vascular changes more than endogenous insulin in the presence of hyperlipidemia.
Coronary artery disease occurred in > 15% of total heart diseases. Central obesity promotes ischemia and atheroma of pancreatic vessels and thus it may cause hyperglycemia.
Vascular degeneration is also developed by continued consumption of sympatholytics. Atherosclerosis is also related to changes in haemostasis: Items promoting clotting are cold, coffee, Ca++, vitamin K (alfalfa), protamine (trout fish) etc.
Items promoting bleeding are heat, insulin, urea, melilotus, dicoumarol, acids, salicylates (China, aloes, and salix nigra), tea -xanthonine etc.
Potassium exists inside as the cell constant. 1/3 of Potassium is in ionic form and involved in interchanges across the cell with insulin.
Tachycardia may occur in hypokalemia developed by either high insulin (tissue entry) or proteinuria. Chest discomfort with bradycardia occur more in hyperkalaemia (renal failure, infarction, tissue damage).
SIGNS AND SYMPTOMS
Glucose Tolerance Test: Take low caloric diet with 150-250 gm carbohydrate for 10 days. Test plasma glucose and urinary sugar after 10 hour fasting. Take carbohydrate 1.75/kg with 300ml water. Test plasma glucose and urinary sugar after ½ hour and after 2 hour. The test is considered negative if fasting < 126 %, PPBS after 1/2 hours < 180% and PPBS after 2hour < 126%.