(Article with Diet chart according to Indian Vegetarian and Non vegetarian Diet ) By Dr Anmol Arora
The prevalence of diabetes is on the rise, more alarmingly in the developing nations. Ranked 7th among leading causes of death, it has been rated third when all its fatal complications are taken into account. Besides multiplying the risks for coronary heart disease, diabetes enhances the incidence of cerebrovascular strokes. Moreover, it is the leading cause of acquired blindness and accounts for over 25 percent of cases with end-stage renal failure as well as 50 percent of non-traumatic lower limb amputations.
HISTORY
Reference to disorders with polyuria can be traced back to Egyptian papyrus (1550 BC). Charak and Sushruta of ancient India (600-400 BC) were versed with many of the currently known facets of the disease and named it madhumeha (rain of honey) as they noticed that urine tasted sweet and attracted ants. Madhumeha (diabetes mellitus) was distinguished from udak (water) meha (diabetes insipidus) and ikshu (sugarcane) meha (renal glycosuria) by its genetic origin and intractable course. Two types were recognised, one associated with stout build, glutonny and indolence and the other characterised by leanness, severe polyuria, thirst and dehydration.
In the second century AD, Arataeus of Cappadocia coined the term ‘diabetes’ (running through, a siphon). Claude Bernard (1850) was the first to note hyperglycaemia as the cardinal feature of diabetes. Description of islets in the pancreatic tissue by Langerhans (1869) and discovery that extirpation of pancreas resulted in diabetes (Von Mering and Minkosky, 1889) led Laguesse (1893) to speculate on an internal secretion of the islets, named ‘insulin’ by Mayer (1909), in later years. Opie (1901) established the link between diabetes and lesions in the islets.
By the end of 1921 Banting and Best could obtain an extract from pancreatic islets which, on purification by Collip (1922), was effective in reviving a patient ill from juvenile diabetes.
Insulin remained the sole antidiabetic drug until the introduction of oral hypoglycaemic agents by Franke and Fuchs in 1955.
PREVALENCE
The number of diabetic patients in the world has been estimated at 110 million by 1994. This is likely to rise to 175 million by the turn of the century. Such leaps in numbers are contributed more by populous developing countries such as India and China.
Non-insulin dependent diabetes (NIDDM) is by far the most common, accounting for 85 to 99 percent of patients depending on geography and ethnicity. Previously known as maturity-onset type, NIDDM, as a rule, occurs in adults, more so over 35 years of age.
Insulin-dependent diabetes (IDDM) accounts for 0.2% to 15% of patients. It is more common in Caucasians of North European origin. Once known as juvenile-onset type of diabetes, IDDM especially afflicts children and young adults. Presently, a relatively larger proportion of patients are older adults due to longer life expectancy and recognition of latent autoimmune diabetes in adults (LADA).
In the developed countries, IDDM is for all practical purposes the lone type of diabetes among older children and adolescents. In contrast, in several developing countries, as in some parts of India and Bangladesh, a high proportion (40-60%) of such patients may have either malnutrition-related diabetes or fibrocalculous pancreatic diabetes (FCPD), while over 85% of children with onset before 15 years have typical IDDM.
INSULIN AND METABOLISM
In diabetes mellitus, there is disturbance of intermediary metabolism, mainly manifesting as chronic hyperglycaemia, primarily due to relative or absolute lack of insulin. Insulin (i) facilitates transport of glucose and amino acids at the membrane site, (ii) increases RNA synthesis at the nuclear site, (iii) promotes translation at the ribosomes for protein synthesis and (iv) decreases the intracellular level of cyclic AMP. In the muscle and adipose tissue, the primary effect of insulin is to facilitate the transport of glucose and amino acids. However, in the liver these are freely permeable into the hepatocytes, and the major effect of insulin is on intracellular metabolic pathways rather than on the transport mechanism
Metabolic effects of lack of insulin
|
Functions of insulin |
Consequences of insulin deficiency |
|
Increases activity of glycolytic enzymes |
Activity of glycolytic enzymes decreases |
|
Decreases activity of gluconeogenic enzymes |
Activity of gluconeogenic enzymes increases (gluconeogenesis |
|
Increases glycogen synthesis |
Glycogen breakdown into glucose increases (gluconeogenesis |
|
Increases uptake of glucose by skeletal and cardiac muscle |
Decreased glucose transport into skeletal and cardiac muscle |
|
As a result of first four functions, decreases blood glucose level |
Increase in blood glucose level |
|
Increased lipid synthesis |
Lipolysis (raised plasma free fatty acids), ketogenesis |
|
Increases transmembrane K+ transport |
Decrease in movement of K+ into the cell |
|
Decreases cyclic AMP level in adipose tissue and liver |
Increased cyclic AMP levels in adipose tissue and liver |
|
Enhances tissue uptake of amino acids and accelerates protein synthesis |
Decrease in tissue uptake of amino acids and reduced protein synthesis |
There are two facts of clinical relevance which need emphasis: (i) There is a time-relationship of the molecular effects of insulin. The effects on transport of glucose and amino acids, and alterations in ion fluxes, manifest within minutes of the binding of insulin to its receptor sites. In contrast, effects related to enzymatic regulation and protein synthesis may take 3-6 hours. (ii) There is a dose-related differential effect on glucose and lipid metabolism; insulin concentrations of about 55 µU/ml are required to decrease the activity of gluconeogenic enzymes while a concentration of 5-15 µU/ml is adequate to regulate lipolysis. These facts provide the basis for non-occurrence of ketosis in the presence of even smaller than normal amounts of insulin in circulation, which are otherwise inadequate to control postprandial hyperglycaemia.
REGULATORY ACTION OF HORMONES ON HOMEOSTASIS OF METABOLIC FUELS
The human system needs endogenous energy which is generated by combustion of the metabolic fuels, glucose and free fatty acids (FFA).
Glucose is the preferred fuel for most tissues, especially the brain. Plasma levels of glucose are normally maintained within 70 to 140 mg/dl (3.9 – 7.8 mEq/L). Ingestion of a meal should lead to transient hyperglycaemia but this is prevented by hepatic extraction and uptake by the large mass of skeletal muscles and adipose tissue. These activities are mediated by raised levels of insulin. Insulin promotes hepatic glycogen synthesis and facilitates entry of glucose into muscle and fat cells with consequent increase in synthesis of glycogen and triglycerides for storage. Pari passu there is inhibition of glycogenolysis, gluconeogenesis and lipolysis so as to restrict hepatic production of glucose and release of FFA from adipose tissue.
During the remote post-prandial period, plasma level of glucose tends to fall. Lipolysis is stepped up in order to provide enough FFA as alternative fuel. Also, breakdown of the limited store of hepatic glycogen (75 g) and accelerated hepatic gluconeogenesis occurs. These processes are promoted by counter-regulatory hormones, viz. glucagon and catecholamines facilitated by tapering down of insulin secretion
Anti-insulin hormones (glucagon, growth hormone, glucocorticoids, catecholamines, thyroid hormones) and their actions
|
1. |
Hepatic gluconeogenesis : Increased by all (except growth hormone) |
|
2. |
Glucose uptake in muscle : Decreased by all (except glucagon and thyroid hormones) |
|
3. |
Lipolysis : Increased by all (except glucagon) |
|
4. |
Ketogenesis : Increased by all |
|
5. |
Insulin release : Decreased only by catecholamines |
CLINICAL FEATURES
The presenting features of diabetes vary widely. Age and nature of symptoms at onset may be broadly indicative of the clinical type. Almost all children, adolescents and underweight young adults (IDDM, MRDM) as well as a variable proportion (20-30%) of older patients (NIDDM) present with the classical triad of
1. polyuria (nocturia)
2. polydipsia and less commonly
3. polyphagia.
4. Fatigue, lassitude
5. weight loss follow inspite of good appetite and adequate food intake.
6. Aches, pains,
7. cramps,
8. paraesthesiae (mostly in the lower limbs),
9. dizziness and blurring of vision occur when treatment is delayed.
10. Some children may have a stormy onset and seek medical aid for the first time with symptoms of ketoacidosis (IDDM) such as persistent enuresis, abdominal pain, vomiting, dehydration, prostration, drowsiness or even coma.
Most middle aged and elderly patients (NIDDM) have an indefinite or insidious onset. In a number of subjects glycosuria and hyperglycaemia are detected during a routine check-up. Others get investigated for
• unexplained weakness,
• weight loss,
• aching or cramps in the legs.
• Delayed healing of wounds,
• recurrent crops of boils or
• appearance of a carbuncle
• pruritus vulvae in women
• and balanoposthitis in men.
• Not infrequently, poor obstetric history or impotence indicates the possibility of diabetes.
Investigations in cases presenting with neurological deficits, visual disturbances, or premature coronary, peripheral or cerebrovascular disease may reveal diabetes for the first time.
In endemic areas classical symptoms of hyperglycaemia in young patients may be preceded by
1. recurrent attacks of abdominal pain,
2. indigestion and
3. bulky stools (FCPD).
Not all patients with FCPD give history of abdominal pain; routine skiagram of the abdomen may lead to the diagnosis in most cases.
1. Stunted growth,
2. emaciation,
3. extreme asthenia
4. , ravenous hunger,
5. dermatitis,
6. paraesthesiae,
7. cramps and
8. Amenorrhoea
are common features in young patients who invariably hail from the poor socioeconomic strata of the rural population (PDDM). Enlarged parotid glands is a common feature in both these situations. The characteristics of common clinical types of diabetes are:
Characteristics of common clinical types of diabetes
| IDDM | NIDDM | PDDM | FCPD | ||
| 1. | Usual age at onset (years) | 5-30 | 35-65 | 10-30 | 10-30 |
| 2. | Sex | M:F = 1:1 | F > M
India: M > F |
M > F | M > F |
| 3. | Prevalence | More in populations of European origin, Caucasoids (5-8% of all diabetics).
1% in India, Japan |
90-95% of all diabetics.
Highest in Pima Indians, Naurans. Low in Eskimoes, tribals |
Tropical developing countries 50% of young-onset diabetes | Within the tropics more in cassava-growing areas |
| 4. | Genetic | Heredity + strong HLA association | Heredity + + + No HLA association | Not established | Not established |
| 5. | Nutrition (build) | Non-obese | Often obese, may be non-obese or lean, particularly Indians | Invariably emaciated | Lean, emaciated |
| 6. | Usual onset | Rapid | Slow, insidious | Intermediate | Slow, abdominal colic in many |
| 7. | Ketosis | Prone | Not prone | Not prone | Not prone |
| 8. | Islet cell antibodies | Present within 1 year of onset | Absent | Not established | Absent |
| 9. | Insulin lack | + + + + | +(-) | + + | + + |
| 10. | Insulin resistance | Rare, secondary when present | + + + particularly in obese | + + + | + + |
| 11. | Insulin requirement | Low to moderate | Low, moderate to high | High | Moderate |
| 12. | Sulphonylurea | Unresponsive | Responsive | Unresponsive | Rarely responsive |
| 13. | Common causes of death | Nephropathy, CHD, ketoacidosis, stroke, gangrene hypoglycaemia | CHD, nephropathy, | Infection, lack of treatment | Lack of treatment |
Physical examination includes measurements of height and weight in all patients and assessment of body mass index (kg/m2), skinfold thickness and waist: hip ratio in special situations. Skin and mucosal surface are to be surveyed for evidences of avitaminosis, infection and dehydration. Pulse rate and blood pressure are to be recorded and heart size assessed regularly. Volume of pulse and thickness of walls are to be noted in peripheral arteries, including the dorsalis pedis and posterior tibials. The liver may be palpable in 20-30 percent of cases with uncontrolled diabetes. Tenderness or wasting of muscles, diminished ankle and knee jerks, and blunting of touch, pain and vibration senses are to be looked for carefully. The eyes need to be examined in all aspects at regular intervals.
Management of Diabetes Mellitus (by Dr Anmol Arora )
A well-balanced, nutritious diet remains a fundamental element of therapy. However, in more than half of cases, diabetic patients fail to follow their diet. In prescribing a diet, it is important to relate dietary objectives to the type of diabetes.
In obese patients with mild hyperglycemia, the major goal of diet therapy is weight reduction by caloric restriction. Thus, there is less need for exchange lists, emphasis on timing of meals, or periodic snacks, all of which are so essential in the treatment of insulin-requiring nonobese diabetics. This type of patient represents the most frequent challenge for the clinician. Weight reduction is an elusive goal that can only be achieved by close supervision and education of the obese patient.
- Cholesterol-The current recommendations for both types of diabetes continue to limit cholesterol to 300 mg daily and advise a daily protein intake of 10-20% of total calories. They suggest that saturated fat be no higher than 8-9% of total calories with a similar proportion of polyunsaturated fat and that the remainder of caloric needs be made up of an individualized ratio of monounsaturated fat and of carbohydrate containing 20-35 g of dietary fiber. Poultry, veal, and fish continue to be recommended as a substitute for red meats for keeping saturated fat content low.
- Dietary fiber – Plant components such as cellulose, gum, and pectin are indigestible by humans and are termed dietary “fiber.” Insoluble fibers such as cellulose or hemicellulose, as found in bran, tend to increase intestinal transit and may have beneficial effects on colonic function. In contrast, soluble fibers such as gums and pectins, as found in beans, oatmeal, or apple skin, tend to retard nutrient absorption rates so that glucose absorption is slower and hyperglycemia may be slightly diminished. Although its recommendations do not include insoluble fiber supplements such as added bran, food such as oatmeal, cereals, and beans with relatively high soluble fiber content as staple components of the diet in diabetics. High soluble fiber content in the diet may also have a favorable effect on blood cholesterol levels.
3. Artificial sweeteners – Aspartame (NutraSweet) has proved to be a popular sweetener for diabetic patients. It consists of two amino acids (aspartic acid and phenylalanine) that combine to produce a nutritive sweetener 180 times as sweet as sucrose. A major limitation is that it cannot be used in baking or cooking because of its lability to heat.
The nonnutritive sweetener saccharin continues to be available in certain foods and beverages despite warnings by the Food and Drug Administration (FDA) about its potential long-term carcinogenicity to the bladder. The latest position statement of the ADA concludes that all nonnutritive sweeteners that have been approved by the FDA (such as aspartame and saccharin) are safe for consumption by all people with diabetes. Two other nonnutritive sweeteners have been approved by the FDA as safe for general use: sucralose (Splenda) and acesulfame potassium (Sunett, Sweet One, DiabetiSweet). These are both highly stable and, in contrast to aspartame, can be used in cooking and baking.
Nutritive sweeteners such as sorbitol and fructose have increased in popularity. Except for acute diarrhoea induced by ingestion of large amounts of sorbitol-containing foods, their relative risk has yet to be established. Fructose represents a “natural” sugar substance that is a highly effective sweetener and induces only slight increases in plasma glucose levels. However, because of potential adverse effects of large amounts of fructose (up to 20% of total calories) on raising serum cholesterol and LDL cholesterol, the ADA feels it may have no overall advantage as a sweetening agent in the diabetic diet. This does not preclude, however, ingestion of fructose-containing fruits and vegetables or fructose-sweetened foods in moderation.
Points to be taken into consideration while planning the diet
- Avoid roots and tubers e.g.: potato, sweet potato, colocasia, yam, tapioca but carrot and radish can be consumed.
- Avoid sugar, glucose, jams, jaggery, honey, sweets, nuts, Horlicks, Bournvita, etc.
- Avoid fried foods.
- Include salads but no salad dressing like mayonnaise.
- Include plenty of green leafy vegetables.
- Quantity of oil should be restricted.
- Dietary exchanges should be taken into consideration.
- Avoid alcohol.
- Include food rich in fiber.
- Avoid fruits such as mango, banana, chickoo, custard apple etc
DAILY DIET SCHEDULE
| Vegetarian |
Non vegetarian |
||||
| Time |
Menu |
Quantity |
Time |
Menu |
Quantity |
| Early morning | Tea/coffee
(without sugar) |
1cup | Early morning | Tea/coffee (without sugar) | 1cup |
| Breakfast | Skim milk
Roti Sabji |
1 glass
2 nos. 1cup |
Breakfast | Skim milk
Bread Egg |
1 glass
2 slices 2nos. |
| Mid-Morning | Musambi/Orange
Buttermilk |
1 nos.
1 glass |
Mid-Morning | Musambi/Orange
Buttermilk |
1 nos.
1 glass |
| Lunch | Rice
Roti Chana Dhal Methi Sag Curd Salad (radish, onion, cucumber, tomato) |
1 1/2 cup
2 nos. 1 cup 1 cup 1 cup 1 serving |
Lunch | Rice
Roti Cauliflower sabji Fish curry Curd Salad |
1 1/2 cup
2 nos. 1 cup 1 cup 1/2 cup 1 serving |
| Evening tea | Tea/coffee
(without sugar) Marie biscuit |
1 cup
2 nos. |
Evening tea | Tea/coffee
(without sugar) Marie biscuit |
1 cup
2 nos. |
| Dinner | Roti
Moong whole Karela sabji Salad |
2 nos.
1 cup 1 cup 1 serving |
Dinner | Roti
Palak sabji Chicken curry Salad |
2 nos
1 cup 1 cup 1 serving |
| Bedtime | Skim milk
Without sugar |
1 cup | Bedtime | Skim milk
Without sugar |
1 cup |
Homoeopathic Medicines
Homoeopathy has a great role to play in lifestyle disorders and its efficacy is well proven for DM . When the dietary restrictions alone doesn’t prove to be effective for controlling DM then there is the need for consulting a doctor .
Homoeopathic Medicines found efficacious clinically are Cephlendera , Gymnema , Uranium Nit, Syszgium Jamb, Phos acid ( For Doctors ) along with the dietary restrictions.
We are running a special clinical OPD for lifestyle disorder at ARORA MULTISPECIALITY CLINIC on every Saturday. (+91-9810097591 for consultation) .
Home Remedies
- Diabetes can be controlled by consuming fenugreek seeds. It is soaked in about a glass full of water and left overnight. Now these seeds are crushed and sieved from a fine cloth. Now this mixture is being drunk to se the wonderful result in 2 months.
- Half cup juice of karela (bitter gourd) is very effective in treating diabetes.
- Grape juice is very helpful in controlling diabetes.
- Mango tree leaves boiled in water and the juice is taken helps in curing diabetes.
- Leaves, seeds and fruit of jamun tree (Syszgium cumini) is very help full in preventing diabetes.
- Consuming leaves of neem and bilva in mornings and evening is very effective in regulating sugar level un blood.
- Almonds soaked overnight in water and then consumed early morning empty stomach is very effective in treating diabetes.
- Amla (Indian goose berry) has also proven its worth in treating diabetes.
- Bel patra (leaves), tulsi (holy basil) leaves and neem leaves each taken ten in number and then consumed early morning empty stomach is very beneficial in curing diabetes.
- For making chapatti use dough made from flour by mixing of wheat, barley and gram is useful in preventing diabetic condition.
- Soya bean that is rich in proteins and minerals like calcium, iron and vitamin like retinol (vitamin A) is quite effective in treating diabetes.
- Consumption of Bengal gram helps in preventing diabetes.
- Morning and evening walk is very important in diabetic condition.
- Yogic asana like shashank asana is very effective in curing diabetes.
- Diet control by in taking low calorie diet, low fat food and consuming high fiber diet is very effective means to prevent diabetes.
- Garlic, ginger and onions are best options in curing diabetes.

September 7th, 2008

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