All About Diabetes

 14 Novermber is the world Diabetic day
Diabetes in General

Diabetes mellitus—often referred to as diabetes—is a condition in which the body either does not produce enough, or does not properly respond to, insulin, a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. This causes glucose to accumulate in the blood, leading
to various potential complications.


Many types of diabetes are recognized: 


Prediabetes is the state in which some but not all of the diagnostic criteria for diabetes are met .It is often described as the “gray area” between normal blood sugar and diabetic levels. While in this range, patients are at risk for not only developing type 2 diabetes, but also for cardiovascular complications. It has been termed "America's largest healthcare epidemic," affecting more than 57 million Americans. Prediabetes is also referred to as borderline diabetes, impaired glucose tolerance (IGT), and/or impaired fasting glucose (IFG).

Impaired Fasting Glycemia

Impaired fasting glycemia or impaired fasting glucose (IFG) refers to a condition in which the fasting blood glucose is elevated
above what is considered normal levels but is not high enough to be classified as diabetes mellitus. It is considered a pre-diabetic state, associated with insulin resistance and increased risk of cardiovascular pathology, although of lesser risk than impaired glucose tolerance (IGT). IFG sometimes progresses to type 2 diabetes mellitus. There is a 50% risk over 10 years of progressing to overt diabetes. A recent study cited the average time for progression as less than three years. IFG is also a risk factor for mortality.

Fasting blood glucose levels are in a continuum within a given population, with higher fasting glucose levels corresponding to a higher risk for complications caused by the high glucose levels. Impaired fasting glucose is defined as a fasting glucose that is higher than the upper limit of normal, but not high enough to be classified as diabetes mellitus. Some patients with impaired fasting glucose can also be diagnosed with impaired glucose tolerance, but many have normal responses to a glucose tolerance test.


WHO criteria for impaired fasting glucose differs from the ADA criteria, because the normal range of glucose is defined differently. Fasting glucose levels 100 mg/dL and higher have been shown to increase complication rates significantly. However, WHO opted to keep its upper limit of normal at under 110 mg/dL for fear of causing too many people to be diagnosed as having impaired fasting glucose, whereas the ADA lowered the upper
limit of normal to a fasting glucose under 100 mg/dL.

WHO criteria: fasting plasma glucose level from 6.1 mmol/l (110 mg/dL) to 6.9 mmol/l (125 mg/dL).

ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL).

Impaired Glucose Tolerance

Impaired glucose tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.

According to the criteria of the World Health Organization and the American Diabetes Association, impaired glucose tolerance is defined as:
Two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol) on the 75-g oral glucose tolerance test. A patient is said to be under the condition of IGT when he/she has an intermediately raised glucose level after 2 hours, but less than would qualify for type 2 diabetes mellitus. The fasting glucose may be either normal or mildly elevated.

From 10 to 15 percent of adults in the United States have one of these conditions.


The risk of progression to diabetes and development of cardiovascular disease is greater than for Impaired fasting glycaemia

Although some drugs can delay the onset of diabetes, lifestyle modifications play a greater role in the prevention of diabetes. Patients identified as having an IGT should exercise regularly and limit sugar intake. And follow the advice of their doctor.

Diabetes Type I
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas leading insulin deficiency. This type of diabetes can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, where beta cell loss is a T-cell mediated autoimmune attack.There is no known preventive measure against type 1 diabetes, which causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed “juvenile diabetes" because it  represents a majority of the diabetes cases in children.

Diabetes Type II
Diabetes mellitus type II 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. However, the specific defects are not known. Diabetes mellitus due to a known defect are classified separately. Diabetes type II is the most common type.
In the early stage of diabetes type II, 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. As the disease progresses, the impairment of insulin secretion occurs, and therapeutic replacement of insulin often becomes necessary.

Gestational Diabetes
Gestational diabetes mellitus (GDM) resembles diabetes type II in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop diabetes type II later in life. A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future. Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.

Signs and Symptoms
Overview of the most significant symptoms of diabetes. The classical symptoms of DM are:

Polyuria (frequent urination),
Polydipsia (increased thirst)
Polyphagia (increased hunger).
Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes symptoms usually develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible mental fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled, although unexplained weight loss may be experienced at the onset of the disease. Final diagnosis is made by measuring the blood glucose concentration. When the glucose concentration in the blood is raised beyond its renal threshold (about 10 mmol/L, although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.

Patients (usually with type 1 diabetes) may also initially present with diabetic etoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires immediate hospitalization.

1. Lifestyle
There are numerous theories as to the exact cause of diabetes type II. Obesity is found in approximately 55% of patients diagnosed with diabetes type II. This is believed to be due to its role in increasing insulin resistance. In the last decade, diabetes type II has affected more children and adolescents, probably in connection with the increased prevalence of childhood obesity.

Environmental exposures may contribute to recent increases in the rate of diabetes type II. A positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of polycarbonate plastic from some producers, and
The incidence of diabetes type II. 2. Medical Conditions
Subclinical Cushing's syndrome (cortisol excess) may be associated with DM type 2. The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%. Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal of these microadenomas.

Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with diabetes mellitus type 2, even if the exact mechanism by which testosterone improve insulin resistance is still not known.

3. Genetics

Both type 1 and type 2 diabetes are partly inherited. Type 1 diabetes may be triggered by certain infections, with some evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.

There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Moreover, obesity (which is an independent risk factor for Diabetes type II) is strongly inherited.
Gene expression promoted by a diet of fat and glucose as well as high levels of inflammation related cytokines found in the obese results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.


Pancreas is the primary organ which controls the blood sugar levels. It is made up of different cells. One of the cell types is Beta cells which releases Insulin.

Whenever we eat, the food enters into our mouth and reaches our stomach through the food pipe called esophagus. Right at the mouth, the digestion of food is started and food is broken down into smaller particles by the help of the chewing action of teeth as well as enzymes(chemicals that act on food and digest it) present. More enzymes are present in stomach to digest food. From the stomach the food enters into intestines and into the blood stream.

The food that has entered the blood stream is in the form of sugar. With the rise of sugar in the blood stream ,Insulin is released from the beta langerhan cells of the pancreas. Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus. Most of the carbohydrates in food are converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel.Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.

Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage.

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.


Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
  • Fasting plasma glucose level at or above 7.0 mmol/L (126 mg/dL).
  • Plasma glucose at or above 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load as in a glucose tolerance test.
  • Symptoms of hyperglycemia and casual plasma glucose at or above 11.1 mmol/L (200 mg/dL). About a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis (a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids) by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
  •  A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) is considered diagnostic for diabetes mellitus.
    Patients with fasting glucose levels from 100 to 125 mg/dL (6.1 and 7.0 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/L, but not over 200, two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
    While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin (termed glycated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately) which is the average lifetime of red blood cells which contain hemoglobin in most patients. However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is 6.5%.
    We at Miracles recommend our patients to bring down their HbA1c to 5.5% which is as good as in non -diabetics. And if such a good control of blood glucose is maintained then the patients can enjoy the healthy life equal to having no diabetes. We have a special offer of free consultancy for all our valuable patients whose HbA1c is equal to 5.5% or less than that. So educate yourself to have a better control of your diabetes and get benefited from our offer.
Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells. Some research has suggested that breastfeeding decreased the risk in later life; various other nutritional risk factors are being studied, but no firm evidence has been found. Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes, though the causal relationship is obscure.
Children with antibodies to beta cell proteins (ie at early stages of an immune reaction to them) but no overt diabetes, and treated with vitamin B-3 (niacin), had less than half the diabetes onset incidence in a 7-year time span as did the general population, and an even lower incidence relative to those with antibodies as above, but who received no vitamin B3. Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity. The American Diabetes Association (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (several brisk sustained walks appear sufficient), having a modest fat intake, and eating sufficient fiber (e.g., from whole grains). There is inadequate evidence that eating foods of low glycemic index is clinically helpful despite recommendations and suggested diets emphasizing this approach. Diets that are very low in saturated fats reduce the risk of becoming insulin resistant and diabetic. Study group participants whose "physical activity level and dietary, smoking, and alcohol habits were all in the low-risk group had an 82% lower incidence of diabetes." In another study of dietary practice and incidence of diabetes, "foods rich in vegetable oils, including non-hydrogenated margarines, nuts, and seeds, should replace foods rich in saturated fats from meats and fat-rich dairy products. Consumption of partially hydrogenated fats should be minimized."
There are numerous studies which suggest connections between some aspects of Type II diabetes with ingestion of certain foods or with some drugs. Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin, rosiglitazone, or valsartan. In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77% though causal mechanisms are unclear. Breastfeeding may also be associated with the prevention of type 2 of the disease in mothers. Clear evidence for these and any of many other connections between foods and supplements and diabetes is sparse to date; none, despite secondary claims for (or against), is sufficiently well established to justify as a standard clinical approach.

Homoeopathic Remedies
Homoeopathy attempts to treat NIDDM or Type 2 diabetes taking the totality of symptoms and the constitution of the person suffering from diabetes. Some of the most commonly used homoeopathic remedies in clinical practice are
Acetic Acid: Emaciation and weakness is marked in patients needing this remedy. Severe burning thirst and copious pale urination is marked in this patient. Patient is sensitive to cold.
Argentum Metallicum: there is gradual emaciation in the patient; Urine is profuse and turbid in appearance with a sweet odor. Swelling of ankles is seen.
Arsenicum Album: Severe marked exhaustion, restlessness, aggravations at night are keynote features of individuals who need this remedy. Urine is albuminous and scanty. Unquenchable thirst is seen.
Cephalandra Indica (Tincture) - in diabetics who have severe thirst for large quantities of water and have dry skin with severe itching and boils.

Homeopathic Remedies for Diabetes
Homeopathy remedies for the management of diabetes can help to control diabetes, improve the quality of life and control complications of diabetes.

Homeopathic drugs treatment for diabetes
The homeopathy drug treatment used in diabetes can be classified in to six groups namely acids, metals, other minerals, vegetables, drugs from animals, and organo therapic remedies.
The acids used for treatment of diabetes are acetic acid, lactic acid, phosphoric acid, nitric acid, picric acid, carbolic acid, and flouric acid. Acids are often used in patients with debility or persistent weakness. Acid can prevent acidosis one of the greatest danger of diabetic mellitus
Metals Aurum met, Argentum met, Argentum nitricum, Uranium nitricum, Vanadium, Plumbum met, Cup ars are used as a homeopathic treatment for diabetes.
Other minerals (such as Ars alb, Sulphur, Silicea, Iodum, Natrum sulph),
vegetables (such as Cephalandra indica, Chimaphilla, Chionanthus, China, Curara, Nux vom, Helleborus niger), and products from  
Animal kingdom (such as Moschus, Crotalus horridus, Lachesis, Tarentula, Lac defloratum) are prescribed based on the individual characteristics and symptoms of the patients.
Insulin an organo therapic remedy is prescribed in critical cases of diabetes, in lean and thin consumptive patients and also in coma. Pancreatin, adrenalin, urea, lecithin are the other organo therapic remedies.
Biochemic remedies for diabetes mellitus are Nat mur, Nat sulph, Kali phos, Kali mur and Kali sulph.

The metals are used for treatment of patients with hypertension, diabetic nephropathy, arteriosclerosis, mentally and physically exhausted and various other symptoms. The minerals, vegetables and animal products are used to manage symptoms such as weakness and prostration, gangrene, diabetes complicated with digestive troubles, impotence, ocular troubles and other complications of diabetes. The homeopathic remedy prescribed to a patient depends on his/her symptoms and characteristics. Hence two patients may have diabetes but their prescriptions may be completely different.

Homeopathic treatment with drugs can improve the general well being of the person with diabetes. In patients with poor general health it can be very difficult to achieve good control of diabetes. Improvement of general health improves the general sense of well-being, decreases the dose and number of drugs needed to control blood glucose and improves blood glucose control. Remedies such as Syzygium, Uranium nitricum, Phloridzin (obtained from the root of the apple and other fruit trees) are given to improve the general health of the patient.

Caution with Homeopathy
To use homeopathic remedies and homeopathic treatment if you are a diabetic is a personal decision, but use them with caution. These drugs do have effect on the body and may help to control your blood sugar. However even if they benefit you, consult your physician before you stop regular insulin or other medication for diabetes. Monitor your blood sugar closely if you take these remedies to find out how effective the remedy is. In case of emergency like diabetic coma the homeopathic remedies may not be effective as the primary therapy. In these conditions consult your physician for conventional medicine and you may use homeopathic remedies as a complementary therapy.
If you are a diabetic and intend to use homeopathic treatment for diabetes, please let your physician know about it. Consult a homeopath physician to decide on the drugs that you would need for management of your symptoms and control of diabetes.

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