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Wednesday, August 8, 2012

Homeopathic treatment in diabetes

Contributed by Dr.George
Diabetes mellitus, the most common endocrine disease, is characterized by metabolic abnormalities and by long-term complications involving the eyes, kidneys, nerves, and blood vessels. 

CLASSIFICATION and CHARACTERISTIC
Type 1 diabetes:
·      Polyuria, polydipsia, and weight loss associated with random plasma glucose  200mg/dL.
·      Plasma glucose of 126 mg/dL or higher after an overnight fast, documented on more than one occasion.
·      Ketonemia, ketonuria, or both.
·      Islet autoantibodies are frequently present.



This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less than 10%. The rate of pancreatic B cell destruction is quite variable, being rapid in some individuals and slow in others. Type 1 diabetes is usually associated with ketosis in its untreated state. It occurs at any age but most commonly arises in children and young adults with a peak incidence before school age and again at around puberty. It is a catabolic disorder in which circulating insulin is virtually absent, plasma glucagon is elevated, and the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose.

Type 2 diabetes:
·      Most patients are over 40 years of age and obese.
·      Polyuria and polydipsia. Ketonuria and weight loss generally are uncommon at time of diagnosis. Candidal vaginitis in women may be an initial manifestation. Many patients have few or no symptoms.
·      Plasma glucose of 126 mg/dL or higher after an overnight fast on more than one occasion. After 75 g oral glucose, diagnostic values are 200 mg/dL or more 2 hours after the oral glucose.
·      Hypertension, dyslipidemia, and atherosclerosis are often associated.

This represents a heterogeneous group of conditions that used to occur predominantly in adults, but it is now more frequently encountered in children and adolescents. More than 90% of all diabetic persons are included under this classification.
Circulating endogenous insulin is sufficient to prevent ketoacidosis but is inadequate to prevent hyperglycemia in the face of increased needs owing to tissue insensitivity (insulin resistance).
Obesity is the most important factor causing insulin resistance. The degree and prevalence of obesity varies among different racial groups with type 2 diabetes. Visceral obesity, due to accumulation of fat in the omental and mesenteric regions, correlates with insulin resistance; subcutaneous abdominal fat seems to have less of an association with insulin insensitivity.

Other Specific Types of Diabetes Mellitus

Maturity-onset diabetes of the young (MODY)
This subgroup is a relatively rare monogenic disorder characterized by non–insulin-dependent diabetes with autosomal dominant inheritance and an age at onset of 25 years or younger. Patients are nonobese, and their hyperglycemia is due to impaired glucose-induced secretion of insulin. Six types of MODY have been described. Except for MODY 2, in which a glucokinase gene is defective, all other types involve mutations of a nuclear transcription factor that regulates islet gene expression.

Diabetes due to mutant insulins
This is a very rare subtype of nonobese type 2 diabetes, with no more than ten families having been described. Since affected individuals were heterozygous and possessed one normal insulin gene, diabetes was mild, did not appear until middle age, and showed autosomal dominant genetic transmission.

Diabetes due to mutant insulin receptors
Defects in one of their insulin receptor genes have been found in more than 40 people with diabetes, and most have extreme insulin resistance associated with acanthosis nigricans

Diabetes mellitus associated with a mutation of mitochondrial DNA
Since sperm do not contain mitochondria, only the mother transmits mitochondrial genes to her offspring. Diabetes due to mutations of mitochondrial DNA occurs in less than 2% of patients with diabetes. The most common cause is the A3243G mutation in the gene coding for the tRNA (Leu,UUR). Diabetes occurs even when a small percentage of the mitochondria in the cell carry the mutation; the heteroplasmy levels in the leukocytes range from 1% to 40%. Diabetes usually develops in these patients in their late 30s, and characteristically, they also have hearing loss (maternally inherited diabetes and deafness [MIDD]). In some patients, the beta cell failure can be rapidly progressive and patients require insulin soon after diagnosis. Other patients can be managed by diet or oral agents for a while but most eventually require insulin. MIDD patients are not usually overweight; they resemble patients with type 1 diabetes mellitus but without evidence for autoimmunity.

Wolfram syndrome


Wolfram syndrome is an autosomal recessive neurodegenerative disorder first evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD. It is due to mutations in a gene named WFS1, which encodes a 100.3 KDa transmembrane protein localized in the endoplasmic reticulum. The diabetes mellitus usually presents in the first decade together with the optic atrophy. Cranial diabetes insipidus and sensorineural deafness develop during the second decade in 60–75% of patients. Ureterohydronephrosis, neurogenic bladder, cerebellar ataxia, peripheral neuropathy, and psychiatric illness develop later in many patients.

Laboratory Findings

Urine analysis
1.Glucosuria
A specific and convenient method to detect glucosuria is the paper strip impregnated with glucose oxidase and a chromogen system (Clinistix, Diastix), which is sensitive to as little as 0.1% glucose in urine. Diastix can be directly applied to the urinary stream, and differing color responses of the indicator strip reflect glucose concentration.
A normal renal threshold for glucose as well as reliable bladder emptying is essential for interpretation.
2.Ketonuria
Qualitative detection of ketone bodies can be accomplished by nitroprusside tests (Acetest or Ketostix). Although these tests do not detect  -hydroxybutyric acid, which lacks a ketone group, the semiquantitative estimation of ketonuria thus obtained is nonetheless usually adequate for clinical purposes. Many laboratories now measure  -hydroxybutyric acid, and there is now a meter available (Precision Xtra, Abbott Diabetes Care) for patient use that measures  -hydroxybutyric acid levels in capillary glucose samples.

Blood testing procedures
1.Glucose tolerance test
Methodology and normal fasting glucose
Plasma or serum from venous blood samples has the advantage over whole blood of providing values for glucose that are independent of hematocrit and that reflect the glucose concentration to which body tissues are exposed. For these reasons, and because plasma and serum are more readily measured on automated equipment, they are used in most laboratories. If serum is used or if plasma is collected from tubes that lack an agent to block glucose metabolism (such as fluoride), samples should be refrigerated and separated within 1 hour after collection. The glucose concentration is 10–15% higher in plasma or serum than in whole blood because structural components of blood cells are absent.
2.Criteria for laboratory confirmation of diabetes mellitus
If the fasting plasma glucose level is 126 mg/dL or higher on more than one occasion, further evaluation of the patient with a glucose challenge is unnecessary. However, when fasting plasma glucose is less than 126 mg/dL in suspected cases, a standardized oral glucose tolerance test may be done


Secondary causes of hyperglycemia.
Hyperglycemia due to tissue insensitivity to insulin  
·      Hormonal tumors (acromegaly, Cushing syndrome, glucagonoma, pheochromocytoma)
·      Pharmacologic agents (corticosteroids, sympathomimetic drugs, niacin) Liver disease (cirrhosis, hemochromatosis)
·      Muscle disorders (myotonic dystrophy)
·      Adipose tissue disorders (lipodystrophy, truncal obesity)
·      Insulin receptor disorders (acanthosis nigricans syndromes, leprechaunism)

Hyperglycemia due to reduced insulin secretion 
·      Hormonal tumors (somatostatinoma, pheochromocytoma)
·      Pancreatic disorders (pancreatitis, hemosiderosis, hemochromatosis)
·      Pharmacologic agents (thiazide diuretics, phenytoin, pentamidine)

Homeopathy

complete repertory-urine sugar

complete repertory-diabetes mellitus

 

Homeopathy has a great role in diabetes . The constitutional remedy is the answer. The finely selected silimimum can restore the person to normal. Homeopathic medicines do act for long time and that we can see in our practice.I personally had good results with PHOS ACID; CAUST, PHOS and LYC. In some instances was even able to completely remove the need of allopathic medicines. Some palliative like syzygium tinctures help to suddenly reduce the blood sugar effectively, but in some these do not respond.
Good case taking and good knowledge of the repertory and material medica is the key.
The importance of good physical exercise has a big role in the treatment of diabetes especially the type 2 variety
Ref:Harrison’s Principle of internal medicine
       :Current medical diagnosis and treatment 2010

10 comments:

  1. I heard lot about the Homeopathic treatment for diabetics and after reading your blog i totally sure about it.

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  2. Thanks for sharing information about Homeopathy treatment of Diabetes. Your post was really very informative to me. Keep the blog updated in same way.
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  4. Type 1 accounts for around 10% to 15% of all people with diabetes. It is one of the most serious and common chronic diseases of childhood, with about half of the people with this form of diabetes developing the disease before age 18. It is also known as insulin dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. how to lower a1c

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