Including miasmatic background, management and treatment
Dr Deepak Sharma
- Etiological Classification
- Type 1
- Type 2
- Other Causes
- Evolution of Diabetes Epidemic in India
- Risk factors for Type 2 Diabetes Mellitus
- Type 1
- Type 2
- Clinical Features
- Glycated hemoglobin
- Miasmatic Background
- Indication of Miasm
- Miasmatic Discussion on complications of DM
Diet and Nutrition Exercise Plan
- Preventive measures
|β Cell – Beta Cell of Pancreas||HNF – Hepatocyte Nuclear Transcription Factor|
|DALYs – Disability Adjust Life Year||IDDM – Insulin Dependent Diabetes Mellitus|
|DM – Diabetes Mellitus||IFG – Impaired Fasting Glucose|
|ESRD – End Stage Renal Diseases||IGT – Impaired Glucose Tolerance|
|FPG – Fasting Plasma Glucose||IPF – Insulin Plasma Factor|
|GDM – Gestational Diabetes Mellitus||MODY – Maturity –onset Diabetes Mellitus of Young|
|HDL – High Density Lipoproteins||NIDDM – Non Insulin-dependent Diabetes Mellitus|
Nobody in this country who does not know about the diabetes, commonly called “SUGAR” in Indian community. Diabetes comprises a group of common metabolic disorder that share the phenotype of hyperglycemia (Increase level of glucose in blood plasma). The DRAMATIC WORLDWIDE increase in the prevalence of Type 2 DM is posing a massive health problem in both developed and developing countries. Interestingly in developed countries, lower socioeconomic groups are most affected, while in developing countries, the reverse applies. The magnitude of the healthcare problem of Type 2 DM results not just from the disease itself but also from its association with obesity and cardiovascular risk factors, particularly dislipidiemia and hypertension. Indeed Type 2 DM has now been recognized as one manifestation of the “Metabolic Syndrome”, a condition characterized by insulin resistance and associated with a range of cardiovascular risk factors. Homoeopathy has measureless role in treatment of DM especially of Type 2. In Type 1 when the absolute absence of insulin it is quite difficult to generate a new β Cell to promote the insulin secretion but we know “Miracles” always happen in Homeopathy.
Recent studies in the etiologies and pathogenesis of DM lead to a revised classification. Recent changes in classification reflect an effort to classify DM as the basis of the pathogenesis process leading to hyperglycemia, as opposed to criteria such as age of onset or type of therapy. Some forms of DM are characterized by an absolute insulin deficiency or a genetic defect leading to defective insulin secretion, whereas other forms share insulin resistance as their underlying etiology. DM has two broad categories designated as type1 and type2.
TYPE 1 DM (previously designated as IDDM): Type 1 DM is categorized into two subgroups, i.e., type 1A and type 1B. Type 1A results from autoimmune β cell destruction, which usually leads to insulin deficiency; where as type 1B DM occurs due to lack of immunologic marker inductive of an autoimmune destructive process of the β cells. Type 1 DM is hereditary in character and develops before the age of 30 years. The patient is young, lean and thin, and has an absolute requirement for insulin therapy.
TYPE 2 DM (previously designated as NIDDM): Type 2 DM is characterized by a variable degree of insulin resistance, impaired insulin secretion, and increased glucose production. Type 2 DM more typically develops with increase in age; it also occurs in children, particularly in obese adults. It does not require insulin therapy.
GDM: This type of DM is recognized during pregnancy. It is due to insulin resistance related to its metabolic changes.
MODY: It is a subtype of DM characterized by autosomal dominant inheritance, early onset of hyperglycemia and impairment in insulin secretion. It is also divided into MODY1, MODY2, MODY3, MODY4, and MODY5 according to genetic defect of beta cell function characterized by mutation in Hepatocyte nuclear transcription factor (HNF), glucokinase, HNF1 α, insulin promoter factor (IPF), HNF1 β.
Drug or chemical induced DM: Some drugs such as Nicotinic acid, Glucocorticoids, Thyroid hormones, Diazoxide beta-adrenergic agonists, Thiazides, β blockers etc causes DM.
Endocrinal Diseases: This includes Hyperthyroidism, Hypersecretion of Adrenal cortex, Hyperpituitarism, Cushing’s syndrome, Pheochromocytoma, Acromegaly, Somatostatinoma.
Diseases of Pancreas: This includes Pancreatitis, Cystic Fibrosis, Hemochromatosis, Pancreatopathy, Cancer of pancreas, Pancreactectomy.
Other Genetic Syndrome sometime associated with DM like as Down’s syndrome, Klinefelter’s Syndrome, Turner’s syndrome, Huntington’s corea.
It’s a surprise that India leads the world with largest number of diabetes subjects earning the dubious distinction of being termed the “DIABETES CAPITAL OF WORLD”. Diabetes Atlas 2006 shows the number of people with DM in India currently around 40.9 million is expected to rise to 69.9 million by 2025. The Asian – Indian community shows the certain unique clinical and biochemical abnormalities which includes, greater abdominal adiposity – higher waist circumference despite lower body mass index, lower adiponectine and higher high sensitive C – reactive protein levels – leads to insulin resistance. Even though the prevalence of micro vascular complications of DM like retinopathy and nephropathy are comparatively lower in Indians but the prevalence of premature coronary artery disease (CAD) is much higher in Indians. The prevalence of diabetes is rapidly increasing day by day over the glob at an alarming rate. In past 30 years the status of diabetes has changed from being considered as a mild disorder of the elderly to one of the major cause of morbidity and mortality affecting the youth and middle aged people.
Both Type 1 and Type 2 DM increase in the prevalence but the more common is Type 2. Although both male and female have diabetes but males have slightly higher incidence from females. Among the ethnicity blacks are having three time’s higher incidence then whites.
Evolution of Diabetes Epidemic In India
The first National study on the prevalence of Type 2 diabetes in India was done between 1972 and 1975 by the Indian Council Medical Research (ICMR, New Delhi) shows the prevalence was 2.1 percent in urban and 1.5 percent in rural population. The recent data show very different pictures from different regions.
|Year of Study||City||Percentage|
A recent study from Delhi also reports a high prevalence of insulin resistance in post pubertal children’s which was associated with excess body fat and abdominal adiposity. This is a great concern because if the epidemic shifts to children it could have serious consequences on the health of Nation.
RISK FACTORS FOR TYPE 2 DM
- A strong family history
- Age ≥ 45 years
- Previously identified IFG or IGT
- History of GDM
- Hypertension (Blood pressure ≥ 140/90 mmHg)
- HDL cholesterol level ≤ 35 mg/dl
- Triglyceride level > 250 mg/dl
- Polycystic ovarian syndrome
The pathogenesis of each type of DM is different and discussed separately.
TYPE 1: This type of DM is characterized by an absolute lack of insulin, which is why, patient always wants insulin. It is previously called as IDDM. The absolute lack of insulin is due to the beta cell destruction. There are three main mechanisms responsible for beta cell destruction that is genetic susceptibility, autoimmunity, and environment insult. These factors of genetic predisposition and environmental insult cause unnecessary immune response against normal functioning beta cells. This immune response triggers the auto immunity, which causes beta cell destruction. When complete destruction of beta cells occurs, no insulin secretion occurs in the bloodstream that causes type 1 DM.
TYPE 2: Type 2 DM is characterized by decrease in beta cell secretion of insulin or a decrease response of the tissues to respond to insulin, i.e. insulin resistance. The main factor involved in the pathogenesis of type 2 DM is environmental factor. Obesity is one of the most important cause although genetic predisposition is also important which causes deranged insulin secretion and cause hyperglycemia. This hyperglycemia causes β cell exhaustion and decrease in insulin secretion. Other metabolic disturbances cause reduced responsiveness of tissues to insulin action called as insulin resistance. It is a major factor in the development of type 2 DM
GDM: GDM is a prodromal form of type 2 DM being unmarked by pregnancy. Pregnancy is associated with insulin resistance that necessitates an increase in insulin production to maintain euglycemia (a normal insulin concentration of glucose in blood). Placental hormones that rise late in pregnancy induce the insulin resistance in GDM. GDM itself is typically found late in the second or early third trimester. Some studies suggest that there is an exaggeration of the pregnancy induced insulin resistance in GDM, but it appears that the major determinant of whether a woman develops DM is likely has insulin reserve. This reserve is blunted in women with GDM. In severe GDM an element of glucose toxicity supervenes which may further blunt the insulin sensitivity. The elevated free acids that are also found in GDM may be a further cause of insulin resistance as may be a manifestation of the disease process itself. Thus, GDM is similar to type 2 DM with insulin resistance and impaired insulin secretion, and persistence of these abnormalities postpartum contributes to the increased risk of type 2 DM in the long term.
|Type 1 DM (IDDM)||Type 2 DM (NIDDM)|
|Increase thirst||Increased thirst|
|Increased micturation||Increased micturation|
|Weight loss in spite of Increased/normal appetite||Increased appetite|
|Nausea||Slow healing infections|
New revised criteria for the diagnosis of DM from the expert panel of WHO and National Diabetes Data Group emphasize the FPG as the most reliable and convenient test for diagnosing DM in asymptomatic individual.
Glucose tolerance is classified in to three categories based on the FPG
- FPG < 110 mg/dl is considered as normal
- FPG ≥ 110 mg/dl but < 126 mg/dl is defined as IFG (Impaired Fasting Glucose)
- FPG ≥ 126 confirm the diagnosis of DM
IFG is a new diagnostic category analogous to IGT, which is defined as the plasma glucose level between 140mg/dl and 200mg/dl, 2 hour after a 75gm oral glucose load.
A random plasma glucose concentration ≥ 200 accompanied by classic symptoms of DM, for example polydipsia (increased thirst), polyuria (increased micturation), polyphagia (increased appetite), weight loss is sufficient for the diagnosis of DM.
The two-hour plasma glucose commonly called as post parendial is still a valid mechanism for diagnosing DM but is not recommended as a part of routine screening.
Glycated hemoglobin (also known as Glycohemoglobin, Glycosylated hemoglobin or HbA1c) is used to monitor treatment in patients with diabetes mellitus, however it is not recommended for routine diagnosis of this condition because of a lack of standardization of tests and results.
COMPLICATIONS OF DM
The complication of DM are categorized into two main group i.e. Acute and Chronic complications. The acute complications are due to metabolic disturbances. These include are DKA (Diabetic Ketoacidosis) and Nonketotic Hyperosmolar state.
The chronic complication are also categorized into two broad groups
1.Microvascular complications: These include Ophthalmic Disorders (Retinopathy, Macular edema, Cataract, Glaucoma), Neuropathy (Peripheral neuropathy, Sensory and Motor polyneuropathy), and Nephropathy (ESRD).
2.Macrovascular complications: These include Coronary Artery Diseases (CAD), peripheral vascular disorders, and cerebrovascular diseases.
3.Other complications include Gastroparasis, Diarrhoea, Uropathy, Sexual dysfunction and Dermatologic complications like eczema, cellulites, and gangrene of distal part of limbs (Diabetic foot). Instead of this mechanism of these complications are not known.
When the amount of blood glucose falls below the acceptable normal levels, it is called hypoglycemia. It revels always an emergency. It produces a number of symptoms like
|Symptoms of Hypoglycemia|
|Excessive sweating and Anxiousiness||Blurring of vision|
|Headaches||Faintness/Loss of consciousness|
Generally hypoglycemia accompanied by warning symptoms describe above but in some diabetics, especially those with long standing poorly controlled disease and taking beta-blocker drugs for associated heart problem, sever hypoglycemia may occur without warning symptoms.
DM comprises the pseudopsoric miasm. The pseudopsoric miasm is also known as Tubercular miasm. It is a combination of both Psora and Syphilitic miasm. Tubercular miasm is usually characterized by a “problem child” i.e. slow in comprehension, dull, unable to keep a line of thought, unsocial, morose. He/she getting relief from offensive foot or axillary sweat which when suppressed often induces lung troubles or some other severe disease. The patient always feels better of mental symptoms by an outbreak of an ulcer. The slightest bruise suppurates; the strong tendency is to the formation of pustules. As a general rule, the patient is very intelligent, keen observer and a programmatic planner who wants his life always busy but possesses a sedentary lifestyle.
Indication Of Miasm
As the miasm progress and predominates, weight loss, depreciation and destruction are the first indication of this miasm. Other indications are cosmopolitan habits, mentally keen but physically weak. Symptoms are ever changing. Rapid response to any stimuli (e.g. any slightest change of weather or atmosphere). Emaciation instead of taking proper diet and drink, tendency to cough and cold easily, desire and craving for unnatural things to eat, with desires and cravings for narcotics such as tea, Coffee, tobacco and any other stimulates have often their origin in psoric or tubercular miasm. They sometimes have constant hunger and eat beyond their capacity to digest or they have no appetite in the morning but hunger for other meals.
Miasmatic Discussion On Comlications of DM
As I discuss pseudo psora in the section of miasmatic background; DM has a psorosyphilitic background. As the syphilitic miasm as becomes predominant the complications arises. The acute complications are of the psoric character because they have metabolic disturbances while the chronic complications are associated with syphilitic background or as a result of mixed miasm. As the strong syphilitic character is going to destruction and degeneration it leads to mixed miasmatic diseases. These diseases are more difficult to cure especially when goes to irreversible changes. When the syphilitic miasm is dominant in the condition of chronic complications the condition should become violent. At this stage the individual needs a complete Miasmatic and Therapeutic treatment.
Before we are going to start treatment of DM. It is very essential to know about proper nutrition and exercise plan for diabetic patient to reduce the prevalence and incidence of complications. It also include preventive plan for an individual.
- Diet and Nutrition plan
- Exercise plans
Diet and nutritional plan:
A diabetic can eat almost any food that other people normally eat provided the food is balanced and within the permissible caloric limits. Proper nutritional management or food plan is essential for better glucose control. This in turn helps to reduce the risk of diabetic complications.
The number of factors such as type of diabetic may eat varies on number of factors such as type of diabetics, type of treatment, age of the patient, physical activity etc. The timing and size of the meals would depend on the treatment regimen and your life style. Your physician and dietitian would advice you on these points.
Daily consistency regarding the types of food including in the meal, their nutritional information, and the time at which they are consumed will help to normalize the blood glucose levels.
The common meal planning tips are:
- Avoid saturated fats and oils; instead of that use unsaturated oils found in olive oil, nuts, and canola oil
- Moderate salt and salty food consumption, especially when high blood pressure is present.
- Watch the amount of protein-rich food.
- Incorporate high-fiber food such as grains, raw vegetables and fruits (fruit is better than the fruit juice).
- Spread your daily carbohydrate intake through the day. Don’t eat too much carbohydrate at any time.
When a diabetic often hungry inspite of eating one may take foods which are low in calories. These are called “Free Foods” for e.g. Salads, plain tea or coffee without sugar, plain lemon juice with out sugar.
Physical activity is recommended for everyone. It should take place any time when a person can and is willing. The minimum time recommended is about 30 minutes; three or more times a week. Activity can include moderate walking and household chorus, such as gardening and cleaning as well as jogging, biking, dancing and other sort of exercises.
|The benefits of exercise includes:|
|Improved blood sugar control||Improved muscle strength and tone|
|Weight loss||Improved digestion and appetite control|
|Lower blood pressure||Better sleep|
|Lower cholesterol level||Improved mood, attitude|
|Improved circulation||Increases energy level|
When starting an exercise plan, be sure to warm up, set a comfortable pace, wear good shoes and drink plenty of water. Make it as enjoyable as possible without overdosing it. A good partner will make it easier to commit to it. Be cautious with the duration and intensity of the exercise; then gradually increase the length of the activity by a few minutes every week.
WHEN NOT TO EXERCISE:
- If you are ill.
- In extreme heat or cold.
- During peak insulin action times.
- If your blood sugar is high exercise will usually help bring it down; but if your blood sugar is over 250mg/dl do not prefer exercise.
As Homoeopathy is not a science of therapeutics, it is concerned with totality of symptoms or individuality. As regarding the cure of DM by homoeopathic medicine, the individual needs the complete miasmatic and constitutional therapy in the very early stage. In the later stage of Type 2 DM especially when the complications arises the therapeutic treatment have more value followed by constitutional treatment.
As there is no data suggesting about the prevention through miasmatic treatment, but if we are going through complete miasmatic study of the individual in early stages then we can easily find out about the disease for witch an individual is prone to suffer. Then, we can apply the antimiasmatic therapy as a preventive measure, which causes a decline in the tendency for the progression of the miasm.
The main antimiasmatic remedies for Tubercular miasm are:
“A” Grade: Agar, Ars-i, Aur, Bac, Calc-c, Calc-p, Car, Hep, Iod, Kali-c, Kali-p, Lyc, Med, Nat-s, Phos, Puls, Sep, Sil, Stann, Sulp, Thuj, Zinc.
“B” Grade: All-c, Ant-i, Ars, Bap, Bar-m, Bry, Bufo, Calc-s, Carb-v, Chin, Dulc, Kreos, Nat-m, Nit-ac, Ph-ac, San, Sep.
If family history presents: Carc, Sacch, Thuj.
I found over 50 remedies for DM but when totality of symptom agrees every medicine from Materia Medica can be employed. However, only a smaller group is employed most frequently such as
Acetic acid (Glacial acetic acid) 6, 30: Large quantity of pale urine, unquenchable thirst, and great debility.
Abroma augusta (Olatkambal) θ, 2X, 3X: Frequent and profuse urination, dryness of the mouth and great thirst, urination leads exhaustion, Fishy odour of the urine, Diabetes mellitus and insipidus.
Argentum metallicum (Silver) 6, 30, 200: Polyuria, frequent urination, urine profuse at night, turbid and sweetish odour, restless sleep, frightful dreams, edematous swollen feet, flatulent distention of abdomen.
Arsenicum album (Arsenic trioxide) 6, 30: Urine scanty, burning albuminous, ascites, all prevailing debility, restlessness, burning thirst, drinks often but little at time.
Codeinum (An Alkaloid from Opium) 3X, 3: Sugar in urine, quantity of urine increased, great thirst, it is said to control disease.
Cantharis (Spanish fly) 6, 30: Diabetes complicated with albuminuria, constant desire to urinate Membranous scales looking like bran in water. Urine jelly like, sheddy.
Cephalandra indica (Telakucha) θ, 1X, 3X: DM and insipidus with profuse urination; weakness and exhaustion after urination; sugar in the urine.
Graphitis (black lead) 6, 30: Various complications of diabetes where causes are not known.
Gymnesa sylvestre (Meshasringi or Gurmar) θ, 3x, 6: Is almost specific for DM called as “Sugar Killer” diminishes sugar in urine; Profuse miturition loaded with sugar, extreme weakness after passing large quantities of urine. Polyuria; day and night.
Helleborus (Snow-rose) 3X, 3: Frequent urging to urinate but small quantities emitted, profuse urination, urine pale and watery, dropsical swelling.
Helonias-Chamailirium (Uricorn-root) θ, 6: DM and insipidus, urine profuse and clear, phosphatic and albuminous, great thirst, restlessness, profound melancholy, irritable, boring pain across the lumbar region.
Insulin 3X, 6X: Supposed to be specific and useful in case of carbuncles resulting from DM.
Lacticum acidum (Lactic acid) 6, 30: Frequent passing of large quantities of sugar in urine, great thirst, rheumatic pains in joints.
Murex (Purple Fish) 6: Frequent urine at night, smells like Valerian, constant urging.
Natrum phosphoricum 6X, 12X: They are of great value in diabetes. Profuse urination, urine loaded with bile, lithic deposition in urine, sedentary habits especially when there is a succession of boils.
Natrum sulphuricum (Sulphate of Sodium) 6X, 6, 200: A remedy especially indicated for the so-called hydrogenoid constitution, where the complaints are such as are due to living in damp houses, basements, cellers. Diabetes with nervous origin when due to worry, mental over work and sexual excess.
Phosphoricum acidum (Phosphoric acid) 2X, 30: Frequent and profuse watery urination, milk-like urine, great debility.
Phosphorus 3, 30: DM in phthisis in impotency, urine contain large amount of salt in the morning and excess of sugar in the evening.
Plumbum metallicum (Lead) 6, 30: Urine frequent, scanty, albuminous, low specific gravity.
Rhus aromatica (Fragrant sumach) θ: Large quantity of urine, urine pale, albuminous, specific gravity low.
Squilla maritime (Sea-onion) 3X, 30: Great urging much watery urine, involuntary spurting when coughing, a slow acting remedy correspondence to ailments requiring several days to reach their maximum.
Lac defloratum (Skimmed Milk) 6, 30: Diabetes with faulty nutrition. Albuminuria and other affections of kidney.
Syzygium Jambolanum (Jambol seeds) θ: It has a specific action in diminishing and cause to disappear the sugar in urine, great thirst, and weakness, urine in very large quantities, specific gravity high. Ten drops to be taken twice or thrice daily.
Uranium nitricum (Nitrate of Uranium) 3X, 30: Profuse urination, debility, acid in urine, incontinence, unable to retain urine, excessive thirst, diarrhea of the dyspepticus.
Terebinthinum (Turpentine) 3, 6: Profuse, cloudy, smoky, and albuminous urine, sediments like coffee grounds, haematuria.
Other valuable medicines are: Arsenicum iodatum; Aurum metallicum; Boricum acidum; Bryonia alba; Chamomilla umbellate; Chionanthus virginica; Coca (Erythroxylon coca); Crotalus horridus; Curare; Iris versicolor; Kreosotum; Morphinum; Nux vomica; Pancreatinum; Silicea terra; Strychninum arsenicosum.
- http://www.hpathy.com/diseases/diabetes-mellitus-symptoms-treatment-cure.asp – my first article on Diabetes Mellitus published in 2004.
- The Epidemiology of Diabetes Mellitus: An International Perspective. J-M Ekoé, P Zimmet, R Williams (eds). Chichester: John Wiley, 2001, by Nish Chaturvedi
- Zimmet P, Alberti K, Shaw J. Global and societal implications of the diabetes epidemic.
- Mohan V, Shanthirani S, Deepa R, et al. Intra-urban differences in the prevalence of the metabolic syndrome in Southern India — the Chennai Urban Population study. Diabetic Medicine 2001
- Williams G, Pickup JC. Epidemiology and aetiology of type 2 diabetes. Handbook of diabetes. Oxford: Blackwell Science, 1999: 48-60.
- Reaven G. Banting Lecture 1988. Role of insulin resistance in human disease. Diabetes 1988; 37: 1595-1607
- World Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus. Geneva: WHO Department of Noncommunicable Disease Surveillance, 1999.
- Dunstan D, Zimmet P, Welborn T, et al. The rising prevalence of diabetes and impaired glucose tolerance: the Australian Diabetes, Obesity and Lifestyle Study. Diabetes Care 2002; 25: 829-834.
- Norman RJ, Masters L, Milner CR, et al. Relative risk of conversion from normoglycaemia to impaired glucose tolerance or non-insulin dependent diabetes mellitus in polycystic ovarian syndrome. Hum Reprod 2001; 16: 1995–1998.
- Prentice AM, Jebb SA. Obesity in Britain: gluttony or sloth? BMJ 1995; 311: 437-439.
- International Textbook of Diabetes Mellitus, 2nd edition. In: Alberti K, Zimmet P, DeFronzo R, editors. Chichester: Wiley, 1997.
- Gan SK, Samaras K, Thompson CH, et al. Altered myocellular and abdominal fat partitioning predict disturbance in insulin action in HIV protease inhibitor-related lipodystrophy. Diabetes 2002; 51: 3163-3169.
- Diabetes Prevention Program Study Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346: 393-403.
- L u n d g ren H, Bengtsson C, Blohme G,
- Lapidus L, Sjöström L: Adiposity and adiposetissue distribution in relation to incidence of diabetes in women: results from a prospective population study in Gothenb urg, Sweden. Int J Obes13:413–423, 1989
- Ohlson L-O, Larsson B, Svärdsudd K, Welin L, Eriksson H, Wilhelmsen L, Björntorp P, Tibblin G: The influence of body fat distribution on the incidence of diabetes mellitus: 13.5 years of follow-up of the participants in the study of men born in 1913. D i a b e t e s34:1055–1058, 1985
- Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, Hennekens CH, Speizer FE: Body weight and mortality among women. N Engl J Med 333:677–685, 1995
- Bengtsson C, Björkelund C, Lapidus L, Lissner L: Associations of serum lipid concentrations and obesity with mortality in women: 20-year follow-up of part i c i p a n t s in prospective population study in Gothenb urg, Sweden. B M J 307:1385–1388, 1993
- Boyko E, Fujimoto W, Leonetti D, Newell-M o rris L: Visceral adiposity and risk of type 2 diabetes: a prospective study among Japanese Americans. Diabetes Care2 3 : 4 6 5 – 4 7 1 ,2000 Abate N, Garg A, Peshock RM, Stray-Gundersen
- J, Grundy SM: Relationships of generalized and regional adiposity to insulin sensitivity in men. J Clin Invest9 6 : 8 8 – 9 8 ,1995
- Aspray TJ, Mugusi F, Rashid S, Whiting D, Edwards R, Alberti KG, Unwin NC, Essential Non-Communicable Disease Health Intervention Project: Rural and urban differences in diabetes prevalence in Tanzania: the role of obesity, physical inactivity and urban living. Trans R Soc TropMed Hyg 94:637–644, 2000
- International Diabetes Federation: Diabetes Atlas 2000. Brussels, International Diabetes Federation, 2000
- Barendregt JJ, Van Oortmarssen GJ, Vos T, Murray CJ: Generic model for the assessment of disease epidemiology: the computational basis of DisMod II. Popul Health Metr 1:4, 2003
- Berger B, Stenstrom G, Sundkvist G: Incidence, prevalence, and mortality of diabetes in a large population: a report from the Skaraborg Diabetes Registry. Diabetes Care 22:773–778, 1999
- Morgan CL, Currie CJ, Peters JR: Relationship between diabetes and mortality: a population study using record linkage. Diabetes Care 23:1103–1107, 2000
- Swerdlow AJ, Jones ME: Mortality during 25 years of follow-up of a cohort with diabetes. Int J Epidemiol 25:1250–1261, 1996 The Health of Nations is changing, Nakajima H; World Health, 1991
- WHO & Diabetes, Hiliarg King, World Health, May- June 1991, 3.
- Diabetes in the third world, Johnson TO, World Health May, June, 1991, 8.
- Diabetes Mellitus WHO Tech Report Series 657: WHO, Geneva, 1985 Census India, 1990, Govt of India Press. A pilot study on distribution of glucose intolerance and cardiovascular morbidity in population at high attitude in the Himalayas. Rao P.V, Ahuja M.M.S, Das Gupta J et al Research Project ICMR, 1990.
- Study of glucose intolerance & cardiovascular disease in Mohan Nagar UP, Bhatnagar B, Ahuja M.M.S, ICMR report, 1988.
- Balaji C.N., Problems of Chronic calcific Pancreatitis Thesis, facility of Medicine, AIIMS, New Delhi, 1988.
- Effect of Social Progress on Health Status with reference to Diabetes Mellitus in emegrant Indians in Malaysia, Rao P.V, Zaini A, Ahuja M.M.S, WHO project/RGT/MS/ 72/13.191.90, 1991.
- Principle of Internal Medicine Harrison 15th Edition Vol. 2.
- Illustrated Pathology Robbins 6th Edition
- Preventive and Social Medicine Park 17th Edition
- Treatment from Epitome of Homoeopathic Practice by M. Bhattacharya
- Miasm and their effect on human organism by Raju Subramanium
- Internal Medicine Davidson 19th Edition
- Newer Horizon in Type2 Diabetes Mellitus
- Indication of Miasm Harimohan Chaudhary
- Chronic Miasm J.H. Allen
- Materia Medica Boericke
- Materia Medica J.H. Clark
- Prescriber J.H. Clark
- Prescriber H.C. Allen
- Soul of Remedies by Dr. R. Shankran
- Synthesis Repertory George Vithoulkas 8.0 Version
- Repertory by Robin Murphy Synoptic key by Boger
- Also search at homoeopathy.com; homeopathy.org; diabetesindia.com; medindia.com; and many more.
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