DIAGNOSTIC HOMOEOPATHIC DOCTOR
Licence No.KZN00041D Practice No. 0805033 Reg No: A01252
Diabetics must learn to cope with a life-long disease which is allopathically treatable, presently homoeopathically treatable, but not curable. Worldwide there are probably 60 million people who suffer with diabetes.
Most cases are primary, and relatively few are secondary to identifiable causes. Primary diabetes can be divided into two groups namely insulin dependent and non-insulin-dependent. [IDDM AND NIDDM]
|PRIMARY DIABETES||- IDDM||25%|
|- Pancreatic disease|
|- Endocrine disease|
|- Gestational diabetes|
|- Drug induced|
The critical difference in the degree of insulin deficiency, which is so profound in IDDM that even a low insulin concentration which prevents lypolysis and ketogenesis cannot be sustained, without insulin replacement.
By contrast, NIDDM patients have enough endogenous insulin to prevent ketosis and will survive without insulin therapy. Many NIDDM patients are treated with insulin as this is the only way to lower glycaemia effectively but these insulin-dependent patients can be distinguised from the truly insulin-dependent patients because they have a measurable C-peptide level and do not become ketonic if insulin is withdrawn.
The frequency of IDDM shows striking geographical and racial variations. `in Finland it is 35 times more common that in Japan. In the UK the highest frequency is found in Scotland. In South Africa the Natal Indian community had the highest incidence in the world. There is also a seasonal variance, most cases presenting in the autumn and winter. Any age can be affected but most present before the age of 20 years and the incidence peaks at 13 years.
The genetic component of IDDM is less important than in NIDDM as shown by studies of identicl twins of whom one becomes diabetic. In the case of IDDM the chances of the unaffected twin developing the disease are about 50%, whereas the average risk in NIDDM exceeds 95%.
As association of IDDM with organ-specific overall diseases has long been recognized e.g. Schmidts syndrome [adrenal/thyroid failure] in type 2 poly-glandular endocrinopathy syndrome. Like thyroid, adrenal and other tissues which are the target of autoimmune disease, the pancreatic islets of newly diagnosed IDDM patients are infiltrate with immunologically active cells [mostly cytotoxic T-lymphocytes] termed insulitis. With time the intensity abates but the remaining islets were depleted of beta-cells, implying that this was a result of the auto-immune attack.
Many viruses target the pancreas and some selectively attack the beta-cells, where they alter the cells activity or antigenicity. Many IDDM patients have serological evidence of previous encounters with viruses such as Mumps and Coxsakie B series. IDDM develops in 20% of children with congenital Rubella but there is little evidence of diabetics if acquired after birth. Certain chemicals destroy beta-cells.
Young patients typically have a short history [a few weeks or days] of the classic symptoms of :
Hypoglycaemic - Most IDDM patients suffer occationally from this condition. The following are contributing factors.
This appears to be due to two separate defects :
both of which are inherited. No predictive HLA types or other genetic markers have yet been identified.
This is the inability of insulin at physiological concentration to exert its normal metabolic action. It has been demonstrated that the action of insulin is reduced by about 40% in NIDDM.
Liver, skeletal muscle and fat are all insensitive, so that increased hepatic glucose output and reduced peripheral uptake both contribute to hyperglycaemia. The causes of defective insulin uptake are unknown. Possible factors are :
Resting insulin levels may be normal, high or even low in NiDDM patients. There seems to be an infiltration of beta-cells with amyloid deposits containing a peptide name amylin. Amylin is synthesised by the beta-cells but its role is uncertain.
Two-thirds of all NIDDM patients are obese.
There may be marked weight loss and women present with pruritis vulvae due to candidiasis. Certain patients present with:
Nephropathy is one facet of generalized microvascular damage and is always associated with retinopathy. An extremely important association is with hypertension.
|Neuropathy -||impaired sensation
sensory, motor and autonomic nerves involved
|Ischaemia -||microcirculation, cold, pulse abscent,
death of tissue, gangrene
|Trauma -||pressure damage, tight shoes, metatarsal
|Infection -||ulcers or cracks in skin, tissue & bones
infected, fungal infections
Diabetic ulcer - poor periferal circulation
Started treatment 5/3/2010 - Healed 28/10/2011
Diagnosis Gangrene - Action Amputation
Started treatment 19/08/2009 - Healed 16/06/2011
Defined as flood glucose being <2.2 mmol⁄1t. It occurs when glucose taken up into the tissues exceeds that entering the circulation. Reactive hypoglycaemia - after meals high insulin stimulated by increase hormones released from the gut by eating, which outlasts the absorption of glucose from the intestine.
We are able to treat diabetes and the many complications. Patients respond very well to homoeopathic medication.
The two examples were treated only with homoeopathic medicine.