|Yoga therapy for Diabetes
Diabetes mellitus is one of the most common endocrine diseases in all populations and all age groups. It is also a chronic metabolic disorder in which the body cannot metabolize carbohydrates, fats and proteins because of a lack of or ineffective use of the hormone insulin. The basic defect is in utilization of sugar by the body.
Glucose is the main source of energy for all the bodily functions. After digestion, it passes into the blood stream where cells use it for energy and growth. For its utilization, a hormone, Insulin must be present in proper quantity, which is produced by the pancreas. The defect in pancreas to produce proper amount of Insulin leads to decreased uptake of glucose from the blood and hence increased level of blood sugar.
Diabetes Mellitus (DM) is not a single diseases entity, but rather a group of metabolic disorders sharing the common underline feature of hyperglycemia. Hyperglycemia in diabetes results from defect in insulin secretion, insulin action or most commonly, both. The chronic hyperglycemia and attendant metabolic dysregulation may be associated with secondary damage in multiple organ systems, especially the kidneys, eyes, nerves and blood vessels.
Blood glucose values are normally maintained in a very narrow range, usually 70-120mg/dl. The diagnosis of diabetes is established by noting elevation of blood glucose by any one of three criteria:
1. A random glucose > 200mg/dl, with classical signs and symptoms (discussed below)
2. A fasting glucose > 126 mg/dl on more than one occasion.
3. An abnormal oral glucose tolerance test (OGTT), in which the glucose > 200 mg/dl. 2 hours after a standard carbohydrate load.
The vast majority of cases of diabetes fall into one of two broad classes.
Type 1 : Diabetes is characterized by an absolute deficiency of insulin due to pancreatic beta cell destruction. It accounts for approximately 10% of all cases.
Type 2 : Diabetes is caused by a combination of peripheral resistance to insulin action an inadequate secretory response by the pancreatic beta cells (relative insulin deficiency). Approximately 80% to 90% of patients have type 2 Diabetes.
Another reason for Diabetes mellitus is that the cells cannot use insulin properly, which is known as Insulin resistance.
1) Polyuria : Excessive urination
2) Polyphagia : Increased appetite
3) Polydypsia : Excessive thirst
4) Loss of body weight
5) Dehydration due to excessive urinary output
6) Decreased resistance
Problems, which Diabetics encounter more often are
1) Heart Attacks, Strokes
2) Gangrene of foot
3) Repeated attacks of infections/boils
4) Rapid Deterioration of Vision & Blindness
5) Sexual Problems
6) Kidney diseases
7) Blurring of vision or double vision (Diplopia)
LONG TERM COMPLICATIONS WITH DIABETES MELLITUS
1) Retinopathy - The blood vessels and lens of the eyes are swollen and dilated due to increase in blood glucose level, resulting in distorted vision. It has damaging effect on the optic nerve also.
2) Nephropathy-Impaired kidneyfunction
3) Neuropathy - When blood sugar goes very high, nerves can produce pain specially in legs.
EFFECTIVE DIABETES MANAGEMENT
The chief tools in the treatment of diabetes are diet, exercise and suitable medication to keep the symptoms in control.
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 monosacch- aride glucose, the principal carbohydrate found in blood and used by the body as fuel. The most significant exceptions are fructose, most disaccharides (except sucrose and in some people lactose), and all more complex polysaccharides, with the outstanding exception of starch. Insulin is released into the blood by beta cells (3-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 lackthe necessary export mechanism.
Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
Ifthe amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance) or ifthe 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.
PATHOGENESIS OF TYPE 1 DIABETES MELLITUS
This form of diabetes results from a severe lack of insulin caused by an immunologically medicated destruction of beta cells.
Type 1 diabetes is an autoimmune disease in which islet of langerhans destruction is caused primarily by T-lymphocytes reacting against the poorly defined beta-cell antigens.
PATHOGENESIS OF TYPE-2 DIABETES MELUTUS
Environmental factors, such as a sedentary lifestyle and dietary habits, evidently play a role in occurrence of diabetes. Nevertheless, genetic factors are even more important than in Type 1 diabetes.
The two metabolic defects that characterize Type 2 diabetes are:
(1) Adecreased ability of peripheral tissuesto respond to insulin (insulin resistant).
(2) Beta cell dysfunction that is manifested as inadequate insulin secretion in the face of insulin resistance is the primary event, and is followed by increasing degrees of beta-cell dysfunction.
Insulin resistance leads to decreased uptake of glucose in muscle and adipose tissue and an inability of the hormone to suppress hepatic gluco-neogenesis. Functional studies in individuals with insulin resistance have demonstrated numerous quantitative and qualitative abnormalities of the insulin signaling pathway.
Beta Cell Dysfunction: Beta cell dysfunction in Type 2 diabetes reflects the inability of these cells to adapt themselves to the long-term demand of peripheral insulin resistance and increased insulin secretion.
Several mechanisms contribute to beta cell destruction
1) T-lymphocytes react against beta cell antigens and cause cell damage.
2) Locally produced cytokines damage beta cells.
3) Auto-antibodies against islet cells and insulin are also detected in the blood of 70% to 80% of patients.
Obesity and Insulin Resistance:
The link between obesity and diabetes is mediated via effects on insulin resistance. Insulin resistance is present even in simple obesity unaccompanied by hyperglycemia, indicating a fundamental abnormality of insulin signaling in states of fat excess. The risk of diabetes increases as the body mass index (a measure of body fat content) increase. It is not only the absolute amount but also the distribution of body fat that has an effect on insulin sensitivity. Central obesity (abdominal fat) is more likely to be linked with insulin resistance than are peripheral obesity (gluteal/ subcutaneous).
MANAGEMENT OF DIABETES MELLITUS
I. DIETARY MANAGEMENT
It varies according to the severity of the disease, activity and metabolic needs. There are certaingeneral principlesforall diabetic diets:
1) The caloric intake should allow the patient to loose or to gain weight as required.
2) The protein recommended in the diet is normal
3) Carbohydrates should be sufficient to prevent Ketosis.
4) High fiber in diet helps in controlling diabetes by preventing excessive rise in blood glucose helps in decreasing blood cholesterol and triglycerides and also helps in reducing weight.
Foods to be avoided
1) Root Vegetables: Potato, Yam etc.
2) Fried foods and sweets
3) Soft drinks and alcoholic drinks
4) Fruits like Mango, Banana, Chiku, Custard Apple, Grapes & Dates
5) Oily, fried, frozen and fast foods should be avoided.
II. YOGIC MANAGEMENT
In both IDDM and NIDDM physiologically demanding stressful situations like infection, pregnancy
etc. are known to increase the demand for insulin. Similarly emotional stresses also contribute to
the irregular control of diabetes. Relaxation therapies using biofeedback or taped instructions have
been reported to be useful in better control of diabetes (Me grady et al. 1991). Jobson et al (1991)
in a well planned controlled study showed that although there was demonstrable physiological rest
(reduced muscle activity and skin resistance) the progressive relaxation training and biofeedback
given once a week did not help in improving diabetic control in 20 patients with type II diabetes.
Monro et al (1992) carried out a controlled trial on 21 subjects with NIDDM. Fasting blood glucose
and glycosylated haemoglobin reduced significantly [p < 0.05] in the group of 11 who practised the
integrated programme of yoga as compared to a matched control group of 10 who did not practice
yoga. Several other studies (Sahay et al 1986, Jain et al 1993) have shown the beneficial effects of
yoga in NIDDM through reduction in hyperglycemia and the need for oral hypoglycemic agents. Rice
et al (1992) observed increased peripheral blood circulation in lower extremities as measured
through toe temperature and blood volume pulse in 40 diabetes in the age range of 17 to 73 years
after biofeedback assisted relaxation training.