Type 2 DM results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency. This form was previously referred to as non insulin-dependent diabetes mellitus (NIDDM) or “adult-onset diabetes”.
The third main form, gestational diabetes occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. It may precede development of type 2 DM.
Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.
Type 2 diabetes mellitus is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. In the early stage of type 2, the predominant abnormality is reduced insulin sensitivity. At this stage, hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver.
INSULIN RECEPTORS are transmembrane receptors that are activated by insulin, IGF-I, IGF-II and belongs to the large class of tyrosine kinase receptors. Metabolically, the insulin receptor plays a key role in the regulation of glucose homeostasis, a functional process that under degenerate conditions may result in a range of clinical manifestations including diabetes and cancer.
Endogenous ligands of INSULIN RECEPTORS include insulin, IGF-I and IGF-II. The binding of ligand to the receptor induces a chain of biochemical processes leading to blood glucose homeostasis.
Insulin receptors, work by causing the addition of a phosphate group to particular tyrosines on certain proteins within a cell, which eventually leads to an increase in the high affinity glucose transporter molecules on the outer membrane of insulin-responsive tissues, including muscle cells and adipose tissue, and therefore to an increase in the uptake of glucose from blood into these tissues. In other words, the glucose transporter molecules are transported from cellular vesicles to the cell surface, where it then can mediate the transport of glucose into the cell.
THIS IS THE EXACT MOLECULAR MECHANISM BY WHICH INSULIN CONTROLS SUGAR METABOLISM WITH IN THE CELLS
The main activity of activation of the insulin receptor is inducing glucose uptake. For this reason “insulin insensitivity”, or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia or an increase in circulating glucose, and all the sequelae that result from diabetes.
There is a group of diabetic cases, where the defect is purely related with a GENETIC DISORDER, resulting in a totally non-functional insulin receptor. They present with fluctuations of the glucose level: After a meal the glucose is initially very high, and then falls rapidly to abnormally low levels. HOMEOPATHY HAS NO SCOPE IN THESE CASES.
Pre-diabetes indicates a condition that occurs when a person’s blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 DM. Many people destined to develop type 2 DM spend many years in a state of prediabetes which has been termed “America’s largest healthcare epidemic.”:10–11
Latent autoimmune diabetes of adults (LADA) is a condition in which type 1 DM develops in adults. Adults with LADA are frequently initially misdiagnosed as having type 2 DM, based on age rather than etiology.
Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function.
Abnormal insulin action may also have been genetically determined in some cases.
Any disease- CHRONIC PANCREATITIS, CYSTIC FIBROSIS- that causes extensive damage to the pancreas may lead to diabetes
Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed).
Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, leading to DIABETES.
The following is a comprehensive list of other causes of diabetes:
1. Genetic defects of β-cell function- Maturity onset diabetes of the young- Mitochondrial DNA mutations
2. Genetic defects in insulin processing or insulin action- Defects in proinsulin conversion- insulin gene mutations- Insulin receptor mutations
3. Exocrine pancreatic defects- Chronic pancreatitis- Pancreatectomy- Pancreatic neoplasia- Cystic fibrosis- Hemochromatosis- Fibrocalculous pancreatopathy
4. Endocrinopathies- Growth hormone excess (acromegaly)- Cushing syndrome- Hyperthyroidism- Pheochromocytoma- Glucagonoma
5. Infections- Cytomegalovirus infection- Coxsackievirus B
6. Drugs- Glucocorticoids- Thyroid hormone- β-adrenergic agonists- Statins
My method of managing DIABETES:
SIMILIMUM is selected using PHYSICAL GENERALS, MENTALS and PARTICULARS. In certain cases, it may not be single, but multiple, depending upon symptoms. Doses repeated daily for long period.
CORTISONE 30, PITUTRIN 30, PANCREATINUM 30, INSULINUM 30, ACTH 30, THYROIDINUM 30, CARCINOCIN 30, ADRENALIN 30, SULPHUR 30 etc are also used ALONG WITH selected similimum.
In persons with genetic disposition for cancers, especially if there is such a family history, ANTIBODIES against proteins synthesized by mutant genes will be existing in their body- whether they have cancer or not. These cancer antibodies work as chronic miasm, by attacking various off-target biological molecules. In my opinion, we should consider CARCINOCIN to be included in all chronic prescriptions, especially METABOLIC diseases such as DIABETES and various AUTOIMMUNE DISEASES.
Pancreatic enzymes play a big role in destroying beta cells and producing a state of diabetes. Hence, molecular imprints of constituent molecules of pancreatic extract is expected to reverse it, if used before total destruction of beta cells. That is why PANCREATINUM 30 is incorporated in the prescription.