Clinical Study

Rushi Medohar :
Introduction : Ayurveda the Ancient Indian Medicine , Based on terminology established after minute observation and on scientific goruns and medical experience. These knowledge led to a high level of differentiation and a wide spectrum of differentiation and a wide spectrum of therapeutical experience. Ayurveda medicine treat the patient rather the disease. These are not enough but it is towards the goal of happiness that the entire activity of every creature is held to be directed. On account, however, of the divergent conditions of knowledge and ignorance there is seen divergence of the right and the wrong approaches to the goal of happiness. It is also said that, the whole of suffering which cleaves to mind and body has ignorance for its basis and conversely all happiness is founded in clear scientific knowledge. It suggests that to overcome the Dukha, clear knowledge of Ayurveda and ultimately knowledge of Dravyaguna is most essential. As regards these substances (Dravyas), properties (Guna) and actions (Karma). Some of which are promotive of life and some not, the instruction is given throughout the entire treatise. Dravyaguna forms an integral part of all the branches all the branches of Ayurveda. It is clearly mentioned in Dhanvantary nighantu.

Modern Aspect of obesity : ( Link name) Definition and Incidence : The term obesity implies an excess of adipose tissue, but the meaning of excess is hard to define. Aesthetic considerations a side, obesity is best defined as any degree of excess adiposity that imparts a health risk. Visual inspection of a patient can give a subjective but fairly accurate estimate of the degree of obesity. Obesity can be assessed in several ways. The direct methods of measuring body fat include underwater weighing (Densitometry) estimation of total body water, estimation of total body potassium and estimation of fat cell mass by isotope dilution method. Both computed topography and nuclear magnetic resonance imaging can be used to distinguish between the fat and lean tissue of the body. These methods are unsuitable for routine use. Thus indirect methods of measuring body fat are commonly utilized in clinical and field practice, and they have the advantage of use of less sophisticated equipment's. Most Commonly Used Parameters Are: BMI= Weight (Ib) X 703.1 Height (Inches) This simple measurement correlates quite highly with other estimates of obesity and thus pore particular from above BMI to grade of obesity. According to the BMI, patients can be divided into different degrees of obesity as below. Grade 0 = <25 Grade 1 = 25 to 29.9 Grade 2 = 30 to 40 Grade 3 = >40 Health risks increases as BMI increases above 25.The national institute of health consensus panel on obesity agreed with the definitional and concluded that a 20 percent increase in relative weight or a BMI above the 85th for young adults constitutes a health risk; by the use of these criteria, 20 to 30 percent of adult men and 30 to 40 percent of adult women are obese, with the highest rates among the poor and minority groups. A simple but fairly good index of obesity consists in grasping the skin on the side of the body just below the ribs between the thumb and index finger if the thickness of the fold

exceeds one inch, a person is obese. Assessment of skin fold thickness over various areas of body together with height, weight and age can be used to assess the degree of adiposity. More precise assessment of obesity can be made with measurements of body density or with isotopic methods but these are unsuitable for routine use. To estimate ideal body weight simple way is assuming a base line of 49.5 kg. (110 1b) for 150 cm (5Ht) individual and adding 2 kg. (5 Lb) for each 2.5 cm. (1 INCH) over 150cm. Plus 2kg. For a medium frame or 4.5 kg. (101b) for heavy frame. The qualifier '' Morbid" is applied to the condition when the amount of over id 49.5 kg. or more or when the patient is more than twice ideal weight. The use of height - weight tables based on averages to assess the severity of a given patient over weight dose not take into account the distribution of body fat, which as will be explained below, influences the morbidity from excess weight, as well as other important factors such as age and social, economic and ethnic status. PREVALENCE: The prevalence of obesity has been studied using body mass index as well as the height and weight standard tables; A prevalence rate of 10-12 % in the adult population of USA has been reported. Racial and socioeconomic conditions influence the development obesity. ETIOLOGY: Hyperphagia is a striking cause of obesity. When caloric intake exceeds expenditure, the excess calories are stored in adipose tissue, and if this net positive caloric balance is prolonged obesity results. I.e. there are two c omponents of weight balance, and an abnormality on either side (intake or expenditure) Can lead to obesity. An individual gradually increases his caloric intake, and the pounds accumulate. The effect is cumulative second one due to some endocrine disorder or pathological condition. In first type many have a physiological imbalance which accounts foe their overeating. Thus, '' Obesity is an outcome of race between energy input and energy output where energy input always WINS'' Energy intake : the regulation of eating behaviour is incompletely understood. To some extent, appetite is controlled by discrete areas in the hypothalamus: VLH: Centre at ventrolateral hypothalamus it id called feeding centre is stimulates eating. VMH : Centre at ventromedial hypoth alamus it is called satiety centre which stop eating by sending inhibitory impulse to feeding centre. In addition some gut hormones play a role in an (enteroneural) Axis that may affect eating behavior this integrated system can be overridden by psychology factors.

MECHANISH OF EATING BEHAVIOUR: 1. CEREBRAL CORTEX: The satiety centre VMH insulin receptors and is insulin sensitive. It is activated by the increases in glucose and/or insulin that follow a meal. Meal induced gastric distention is another p ossible inhibitory factor. The cerebral cortex receives positive signals from the feeding center that stimulates eating and the satiety center modulates this process by sending inhibitory impulses to the feeding centre. In animals destruction of the feeding centre results in decreased food intake, and destruction of the satiety centre leads to overeating and obesity. Ultimately, the cerebral cortex controls eating behaviour, and impulses from the feeding centre to the cerebral cortex are only one input. 2. EXTERNAL SIGNALS: Psychological, social, and genetic factors also influence food intake. In many obese

subjects these influences are overriding ; indeed, obese subjects usually responds to external signals such as time of day, social setting, and smell o r taste of food to a greater extent than do persons of normal weight. The sight of desirable food leads to a rise in the level of insulin in the blood the ''anticipatory insulin response''. It is of interest in this connection that external responders have a large anticipatory insulin response, but this is usually not large enough to case any detectable change in blood sugar''. 3. DAILY CALORIC NEED: Although overeating is the usual cause of obesity other factors may participate. Daily caloric needs range between 31 and 35 Kcl per kilogram of body weight; this is higher in active and lower in sedentary individuals. 4. EMOTIONAL STATE: It is generally held that emotional perturbation can affect our desire to eat, some people are more affected in this way than others. In 1965, Silverstone proved when the appetitive response to emotional distress is in the direction of eating more (comfort eating) it may lead to obesity. 5. ADIPOSE TISSUE MASS: The total adipose tissue mass may also influence the activity of the hypothalamic centres; there is a relatively fixed 'set point' is established and how the hypothalamus senses total fat stores are unknown. Glycerol release from far cells and ascending neural impulse may be signals of adipose tissue size. Additionally, the hypothalamic centres are sensitive to catecholamines, and beta-adrenergic stimulation inhibits eating behaviour. This provides at least one relational for the anorexiant effects of amphetamines.

ENERGY OUTPUT (EXPENDITURE) : Expenditure of energy is by 3 ways :

A1 - Resting metabolic rate B - Thermo genesis C - Physical exertion A. RESTING METABOLICRATE: Even while resting, the body needs at least that ma calories for its various functions. The ny metabolic rate is the energy required to maintain the normal processes of the body like breathing and heart beat. The basal metabolic rate, measured at a time of complete rest in thermo neutral, varies from individual to individual. In women the resting metabolic rate is around 1400 calories, while it is about 1800 in men. In few cases, obese patients eat only as much as their friends, but still tend to weight gain. This can only mean that their metabolic rate is sluggish-slower than that of their lean friends. But exercise can help such patients. The metabolic rate continues to increase for a while after the exercise. So that even while the body is resting, calories are being burned. The rate of metabolism at basal conditions has been found to vary in different individuals and therefore the B. M. R. varies with different factor . FACTORS AFFECTING BASALMETABOLIC RATE: 1) AGE 2) SEX 3) SURFACE AREA 4) CLIMATE 5) HABIT 6) DIET 7) HORMONES 8) BEROMETRIC PRESSURE 9) PREGNANCY 10) BODY 11) DRUGS 12) RACIAL VARIATION PATHOGENESIS: Obesity may result from primary defects in adipose tissue in a way, whereby lipolysis is diminished and/or lipogenesis is enhanced. But no convincing evidence is there to blame on dimished lipolysis. Bray (1969) reported decreased oxidation of glycerophosphate in the mitochondria of fat cells in fatty tissue, so more of glycerophosphate is spared for further synthesis of triglyceride and this may favour lipogenesis. Glycerophosphate oxidation efficiently regulates the mechanism to couple the oxidation and phosphorylation reactions. On the other hand, increased oxidation of glycerophosphate in mitochondria occurs in normal persons on high calorie diet, whereby more heat and energy is produced, and energy expenditure become more. Therefore this system favors prevention of weight gain even with excess caloric intake. Conversely, a deficiency in the related oxidative enzyme system at the mitochondria level cannot oxidise glycerophosphate in obese people causing impairment in calorie, heat or energy expenditure favouring obesity. MANIFESTATION: SIGN: 1) Weight - 20% increased above desired weight. 2) B.M.I. - above 30 in males and above 28.6 in females are called obese. 3) Skin fold thickness - obesity is indicated by a reading by a above 20 mm in a man, and above 28 mm in woman. 4) Waist hip ratio - when W. H. R. is above 0.9 in males and above 0.8 in females, the type of obesity is aneroid; i.e. man pattern obesity and when W.H.R. is below this it suggest gynoid type i.e. female pattern obesity. Waist circumference Hip circumference.

SYMPTOMS: 1) General lassitude 2) Day time hypersomnalism 3) Dyspnoea on exertion. TYPE OF OBESITY AND DIFFERENT DIAGNOSIS: 1) According to severity: (a) mild (b) moderate (c) Severe 2) According to distribution of fat a) Generalized b) Central - involving only the trunk and neck c) Superior (Buffalo type) - involving the face, neck arms and upper part of trunk. d) Inferior type - involving lower part of trunk a nd legs. e) Girdle type - involving hips, buttocks, abdomen and with a fatty apron. f) Breaches or trochanteric type - involving only the buttocks. g) Lipomatous type - multiple lipomatosis with localized deposits of fat over the body. 3) HISTOPATHOLOGICAL CLASSIFICATION. a) Hyperplastic obesity - the total number of fat cells is increased in hypereplastic obesity. b) Hypertrophied obesity - involves enlargement of Fat cells, hypertropic obesity tends to correlate with an android or truncal fat disorders such as diabetes mellitus, hypertention, coronary artery disease and hyperlipidaemia. 4) ACCORING TO ETIOLOGY: a) Physiological - observed temporarily during pregnancy Delivery and Lactation. b) Idiopathic - an obesity is labelled idiopathic after all p ossible cause of weight gain have been investigated and ruled out. c) Water Salt retention - Characterized by sudden increases of body weight which responds promptly to diuretic therapy. d) Derumis disease- obesity associated with symmetrical tender and painful lumps over the body. e) Hyper insulinism -obesity observed in cases of pancreatic tumor associated with attacks of spontaneous hypoglycemia or in diabetic children overrated with insulin. 5) According to a) Exogenous - due to over eating. The distribution of fat id uniform, although somewhat excessive under the and over the abdomen. b) Endogenous (1) Cushing 's syndrome - Rounded pelthoric appearance central obesity, buffalo lump accumulation of fat at the lower part of the back & neck.) (2) Forhlich's syndrome - Damage to certain areas of the hypothalamus greatly decreases the secretion of gonadotropin releasing hormones and there is a corresponfding decrease in the secretion of gonadotropin hormones by the anterior pituatary. If this occurs p rior to puberty, it causes typical eunuchism. (3) Hypothyroidism: these include fatigue and extreme sleep (14 to 16 hrs. / day) extreme muscular sluggishness; slowed heart rate, decreased cardias output, decreased blood volumes, constipation, mental slugi shness, development of an edematous appearance throughout the body called myxedema. (4) Menopausal obesity - Associated with a mild degree of virilism hersutism, hypertension. The fat is deposited mainly over the neck, trunk and arms.

COMPLCATION: (1) LIFE EXPECTANCY: (2) PSYCHOLOGICAL: (3) MECHANICAL DISABILITIES : (4) METABOLIC DISORDERS: (5) CARDIOVASCULAS DISORDERS : (6) HYPERTENTION : (7) DLABETES MELLITUS: (8) PULMONARY DISEASE : EFFECT OF OBSITY ON OVARY AND SEX STEROID: (1) EFFECT OF OBSITY ON INSULIN: (2) EFFECT OF OBESITY ON THYROID FUNCTION: (3) EFFECT OF OBESITY ON GH AND STOMATOSTAIN:

LIPID
Lipid comprise a heterogenous gorup of water inoluble organic substances occuring mostly in association with fatty acids. Depending on their source and composition, lipids are classified as simple,compound and derived. Five categories of lipid viz. Triglycerides (TG), free fatty acid (FFA) phospholipids (PL) glycolipids and cholesterol occurs as physiologially important constituents of the body. Triglycerides, fatty acid esters of glycerol, constitute the bulk of simple lipids (Fat) stored in the adipose tissue. In the postabsorptive and fasted states,50-90% of the energy demand is met by FFA released from the adipose tissue on hydrolysis of triglyceri des. The sources of TG are both exogenous from dietary fat and endogenous by synthesis in the liver. Free fally acids derived from hydrolysis of dietary, stored and endogenous TG are metabolically most active, hence plasma level at any given time remains l ow (820mg/di)although around 25 g is transported per hour. Choledterol, an exclusive product of animals metabolism is very widely distributed in the human system. All nucleated cells, except in the CNS, can synthesis cholesterol while dietary sources contributes 200 to 500 mg per day. An essential component component of plasma membranes in all cells, cholesterol is in great demand by rapidly proliferating tissues. Assessment of cholesterol status has assumed great clinical significance as cholesterol is the major constituent of atheromatous plaques and biliary calculi. TRANSPORT OF LIPID: The active involvement of lipids in cellular metabolism necessitates and efficient mechanism for their transport in plasma. Two thirds of FFA circulates as reversible complexes with albumin, where as TG, PL and cholesterl, both free (FC) and esterified (CE), combine with specific glycoproteins called apoproteins (Apo-A, B,C,D and E) to form specialised i.e. PL and FC, are placed on the surface while nonpolar ones (TG and CE) the bibding of the same to specific receptors present on surfaces of approriate cells and thus facilitate the metabolism of the macromolecules. Some of the apoproteins also act as enzyme catalysts. Depending on the size, constituents, specific gravity, apoprotein content and electrophoretic mobility, lipoproteins are classified into 4 major classes, viz. Chylomicrons, very low density lipoproteins (VLDL) low density lipoprotein (LDL) and high density lipoproteins are also present in circulation.

These are known as chylomicron remnants. Or VLDL remnants (IDL) Intermediate density lipoprotein) A new group has been identified, referred to as lipoprotein a (LP- a) or medium density lipoprotein (M.DL). The sources, transport and metabolism of lipids and lipoproteins may be considered under two heading major and minor. Major: FFA being metabolically most active, transport of FFA and TG is considered as the 'major transport task' 1. Exogenous : Monoglycerides and FFA derived from hydrolysis of dietary fat along with cholesterol are processed in the intestinal mucosal cell to from triglycerides and CE. These combine mostly with ApoB48 and some amounts of ApoC ApoE synthesised i n the mucosal cell to from "chylomicrons'' the largest of all lipoproteins chylomicrons pass through the lacteals, lymphatics and the thorasic duct to reach venous blood. During circulation, these arehydrolysed by the enzyme lipoprotein lipase (LPL) at the capillary endothelial interface of tissues such as muscles and fat. APoCII Catalyses the process of hydrolusis so that the degradation occurs rapidly. Insulin also facilitates the action of LPL. Chylomicrons normally disappear from circulation within 1 of 5 hrs. following food intake while their remnants are taken up by the liver (hepatocytes), through specific receptors having affinity for ApoE, for final disposal. 2. Endogenous : triglycerides synthesised by the liver combine with ApoB100 as well as AP0C, APoE, and cholesterol to from VLDL. The VLDL molecules accept further APoC form HDL in circulation and follow a similar path as ehylomicrons except that the process is less efficient and much slower. On losing part of the TG by the action of LPL, VLDL gets reduced to remnant particles or IDL. A portion of these remnants are further processed during circulation and during passage through the liver to loss nearly all TG and all apoproteins except. B100 and become cholesterol rich, Thus forming LDL.The rest aretaken up by hepatocytes and catabolised through hepatic endothelial lipase (HEL). The FFA librated from hydrolysis of TG in chylomisrons and VLDL are utilised by muscles for geberation of energy, taken up by adipose tissue to be converted into storage fat, or pass on to the liver for beta-oxidation or resunthesis of VLDL. Minor: Absorption, synthesis, transport, utilisation and excretion of cholesterol and its eslers constitute the minor lipid circuit. 1. Sources of cholesterol : Cholesterol in cricul ation is mostly derived from diet and from denova synthesis by hepatocytes and mucosal cells of the small gut. carried from the intestine in chylomicrons,cholesterol is rapidly removed from the circulatio and does not produce immediate hypercholesterolaemis. Cholesterol synthesised by the liver is incorporated into VLDL. 2. Cholesterol transport: Cholesterol is present is variable amount in all type of lipoproteins. Yet LDL is by far the major carrier of cholesterol in circulation. As LDL contains only one

apoprotein, it is taken up by those cells that possess the corresponding receptors. Thus LDL delivers cholesterol to the liver and to a variety of peripheral tissues including fibroblasts and cells in the vascular wall. However if the amount of cholesterol in these cells is adequate from prior acquisition or denova synthesis, there occurs a reduction in the number of specific receptors (down regulation ) As a result, there is a reduction in the delivery of cholesterol from circulation to the intracellular compartment. Cholestrol rich LDL is mostly catabolised, after receptor binding and internalization, by intracellular lysome. A small proportion is phagocytosed and broken down by macrophages (scavengers). 3. Reverse Cholesterol Transport : Normally the cholesterol content of cells is in a state of dynamic equilibrium where influx from circulating lipoproteins denovo synthesis and efflux into the circulation are maintained by a sensitive receptors for Apo-B-E, the efflux is encouraged by ApoA, contained in H DL. Further HDL provides the carrier for centripetal transport of cholesterol released from the tissues. HDL originates as a nascent disc shaped molecule (HDLn) formed mostly in the liver and partly in the intestinal endothelium. In the circulation, HDLn recives ApoA, Lecithin and Fe, while it tranxfers Apoe to triglyceride - rioch lipoproteins. Esterification of the cholesterol content of HDL occurs by the action of an enzyme lecithin; Cholesterol acyltransferase (LCAT) Thus, HDLn gets converted to a spherical molecule termed HDL3 further acceptance of cholesterol from the peripheral tissues and ApoE from circulation converts HDL3 into a larger molecule (HDL2)this transfers part of its CE content to VLDL and to remnant particles in the course of their conversion to LDL and is finally taken up by tissue possessing APoE receptors. In the liver, HDL regulates the hydrolysis of cholesterol, HDL2 gets reconverted to HDL3 and reenters the circulation. Cholesterol thus released from internalized HDL2as well as from remnant perticles and LDL is utilised for the synthesis of bile acids which is excreted into the gut along with FC. Anprmalities in synthesis, transport, deposition, metabolism, dissimilation and excretion of lipids are associated with disoeders charact erised by obesity, premature atherosclerosis, xanthome, pancreatitis, cholelithiasis and hepatosplenomegaly, for premature athersoclerosis, excess of certain types of lipoproteins (hyperlipidaemia/hyperlipoproteinaemia) as well as improper distribution of cholesterol and TG among the lipoproteins (dyslipoproteinaemia) constitute the most important risk factors.

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(1) VYITPATI & NIRUKTI: Sthula: It is derived from the root ''sthul brimhane '' w ith an addition of ac pratyaya. Which stand probably be thick or solid or strong.'' The person who is huge is called sthula; word sthula is also used as one of the name of bhagvan visnu, one type of kanda, priyangu, raktalasuna,iksu (sabdakalpadrum) Increment of udaradi organs is called sthula

Sthaulya: Sthaulya is an adjective of the word ''sthula'' (Vacaspatyam 6th part of Caturthoadhyaya P.No. 5356). DEFINITION: A person in whome excessive and abnormal increase of Meda along with Mamsa Dhata is found, which results into pendulous appearance of sphika, udara, and Stana and whose increased bulk is not matched by a corresponding increase in energy. CLASSIFICATION: In Ayurvedic literature, systematic classification of the disease Sthauly is not availabl e. Vagbhatta has mentioned three types of sthaulya while describing the efficacy of Langhana therapy (AH.Su.14/12-14) this classification as follows: I. Hina Sthaulya: Mild degree of overweight. II. Madhyama Sthaulya: Moderate degree of overweight. III. Adhika Sthaulya: Excessive state of overweight. NIDANA OF STHAULYA: Only a particular factor is called as Nidana when it has the capacity to develop a complete disease process in the body either immediately or after a certain period (Madhav Nidana 1 -4 Madhu Kosa). In Ayurvedic classics of diagnosis that in Madhav Nidana there is reference of sudanta sen in which while describing the types of Nidanas as the Bahya Nidana and Abhyantra Nidana are included separately they are just like the exogenous and endogenous causes. The exogenous causes are those which affect the body from outside like unwholesome diets and regiments while the endogenous factors are those which are concerned with the maintenance of health. i.e. Dosa, Dhatu, Mala, Agni and Srota which are closely interrelated and vitiated by the exogenous causes to produce the disease which is the nearest cause of the disease and also called as Samavayi karana. All the Nidanas, mentioned by various Acaryas can be classified under four groups as follows: 1. Aharatmaka Hetus 2. Viharatmake Hetus 3. Manas Vyaparatmaka Hetus 4. Other Hetus. For better understanding these causes are being tabulated as follows:

1.
Atibhojana

NIDANA

CA. +

Su. +

Ah. MNi. + -

BH. -

Yr. -

2.

Overeating) Guru Aharasevana (excessive consumption of heavy food ) + -

3.

Madhura Ahrarsevana (sweet food) Sita Aharasevana (Excessive consumption of cold diet)

4.

Snigdha Aharasevana (Excessive consumption of unctuous food)

5.

Navanna Sevana (Usage of fresh alcoholic preparation) Nava Madhyasevana + + + -

6.
(Usage of fresh alcoholic preparetion) Gramya Rasasevana (Usage of domestic animal's meat & Soups) + + -

7.

Paya Vikara Sevana

8.

(Excessive Usage of milk and its preparations) + Dadhi Sevana (Excessive usages of milk and its Preparation) -

9.
+ + -

NIDANA Preparations)

CA.

SU.

Ah.

Mni.

BH.

YR.

1.

Dadhi Sevana (Excessive use of curd) Sarpi Sevana (Excessive use of ghee)

+ + + -

2.

3.

Slesmala Ahrasevana (Kapha increasing food) +

_+

4. 5.

Iksu Ssevana (Usage of Sugarcane) Guda Vikara Sevana (Usage of Jaggery's preparations) Mamsa Sevana + +

6. 7.

(Excessive use of meat) Salisevana(excessive use of basmati rise) +

8. 9.

Masa Sevana (Excessive use of phasilous munga) Godhuma Sevana (excessive wheat) Audak Rasasevana (Usages of aquatic animal's meat & soups) +

10.

VOHARATMAKA NIDANA: NIDANA 1 2 3 4 5 Avayayama Avyvaya Divasvapa Sukha Saiya Gandhamalyanu Sevana CA. + + + + + AH. + + SU. + + Mni. Bh. Yr. + + + + -

Svapna Prasangat

MANASAVYAPARATMAKA NIDANA NIDANA Harsantiyatavat Acintan CA. + + SU. AH. + + Mni. BH. YR. -

Mansonivrti Priyadarsana Saukhyena

+ + -

ANYA NIDANA NIDANA Amarsa Snigdha- Madhura Bastisevana Tailabhyanga Snigdha Udvartana Bijadosas vabhavat SAMPRAPTI: On the basis of satakriyakala the samprapti of sthaulya can be explained. FIRST KRIYAKALA Due to the multiple factors medovrddhi takes place firstly due to Dravyaguna Samanya and Karma Samanya i.e. lack of Pratirodhibhava and secondly by Bijadosa and others. The diet which contains Parthiva and Apamahabhuta in excess-produce. Anarasa which consist of excess Medovardhaka PosakaSubstances. The Hetus like Madhur, Guru etc. and Divasvapa etc. increase the kapha Dose in excess. Thus due to Dravyaguna Samanya there is excess increase in Meda and Kapha . This vitiated Kapha causes hypofunction state of Jatharagni on the other hand function of Saman Vayu is also disturbed due to the Nidana hence can not perform its funcation like stimulation of Jatharagni. SECOND KRIYAKALA: In the hypofunction condition of Jatharagni, if the person continues to indulge in Kapha and Meda increasing aetiological factors, heavy food does not undergo perfect digestion and undigested food material Ama is produced. THIRD & FOURTH KRIYAKALA: Alongwith Kapha the Maduratara Anna rasa is absorbed in the membrane of gastrointestinal track and circulates by Vyanavayu. While circulating in Medovahasrotas Mdadhuratara Ama combines with Medo Dhatu and Dosa-dusya samurshana takes place. This leads to the impairment of Medodhatvagni which causes formation of Apakva ama meda. Further the Vyana Vayu is obstructed by Amameda and this obstructed by Amameda and this obstructed Vayu goes to the kostha. Thus, Jatharagnisandhuksana results in Ksudhadhikya and Sighrajarana of the ingested food thus the person ingests more food which is rapidly digested, and crave for more food. So the person becomes voracious eater now due to the constant incoming of the Medaposakansa the capacity to digest the Medamsa by the Medadhatvagni is hampered and again form ation of Apakvameda takes place. Ca. + + + + Su. Ah. + Mni. BH. + YR. -

FIFTH KRIYAKALA: In this stage eight undesirable manifestation of sthaulya takes place. There is the fat alone that keeps increasing and not the other body elements (Uttar Dhatu). Consequently, there is shortening of the lifespan (Ayusohrasa). Saithilya, Saukumarya and Guruta of Meda results in Javoparodha. Sukra-Abahutva and Avruta Marga of its cause Krucchravyavaya. Owing to imbalance of Sapta Dhatu, debility results. Due to excessive sweating, due to vitiation of Meda and also due to the nature of Meda, fetor of the body takes places. By the admixture of Kapha with Meda, Visyandita,bahula and guruta properities of Meda and its inability to bear the strain causes Svedabadha. In the Kostha increased Agni and Vitiated Vayu cause Ksudhatimatra and Pipastiyoga (Ca. Su. 21/4(3). PURVARUP OF STHAULYA : In any Ayurvedic text, the purvarupa of sthaulaya have not been mentioned, but according to Ca.Ci. 28/19 and Ca.Ci. 11/12 where ever Purvarupas are not mentioned weak manifestation of Rupa should be considered as Purvarupas, So in the 1st stage of Sthaulya a some Laksanas are observed due to Kapha Vrddhi which should be considered as Purvarupas of Sthaulya. They are as follows: Alasya,Angasaithily, Madurasya, Atinidra Atipipasa Etc. RUPA OF STHAULYA: No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 Rupa Cala Shika Cala Udara Cala Stana Ayatha Upacaya Anutsaha Ayusohrasa Javoparodha Kricch Vyavaya Daurbalya Daurgandhya Svedabadha Ksudhatimatra Pipasatiyoga Ksudra Svasa Nindradhikya Gatrasada Gadgadvani Krathana Alpaprana Survakriyasu Asamarthata Alpaprana Kasa Svasa Snigdhangat a Udaraparsva Vriddhi Alasya Ama Moha Saukumarata Anga Satihilya Alpabala Aplavega Ca. + + + + + + + + + + + + + + + Su. + + + + + + + + + + + + + + + + + As + + + + + + + + + + + + + + + + + Ah + + + + + + + MNI. + + + + + + + + + + + + + + + + + + BH. + + + + + + + + + + + + + + + + + + + + YR. + + + + + + + + + + + -

(Ca. SU. 21) (Su. Su. 15) (Ah.-14) (As.24) (MA.NI.34) (Y0-Medoroganidana) (Bh.M. -39). The cardinal or Pratyatma Laksana of Sthaulya have been enlisted By Charaka are: Cala sfik, Cala Udara, Cala Stana, Ayatha Upacaya Anutsaha (ca. Su. 21). UPADRAVAS OF STHAULYA: Carak has not described the Upadravas separately but he has reported that if sthaulya is left untreated, many diseases may be arisen out, Upadravas mentioned by other Acarya's are as -follows:

No 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Updrava Prameha Pramehapidika Jvara Bhagandara Vidradhi Vatavikara Udar - Roga Urustambha Svasa Apaci Kasa Sanyasa Kustha Visarpa Atisara Arsa Slipada Kamala Mutrakriccha Ajirna

Su. + + + + -

As. + + + + + + + -

Ah. + + + + + + + + + +

YR. + + + + + + + + + + + -

BH. + + + + + + + + + + + + -

Mni. + + + + + -

(Su.Su.15) (Ah.Su.14) (A.S.C.24) (Bh.M.39) (M.Ni.34) (Yo - Medoroganidana) SADHYATA - ASADHYATA : To know the prognosis is essenial to sketch a plan of the treatment. A physician, even after knowing that the disease is incurable, if undertakes the management, subjects himself to the loss of wealth and fame. This would cast an adverse affect on his reputation. Regarding the Sthaulya, most of Acaryas have described bad prognosis of above said disease. Sahaj or inherited sthaulya is incurable. Acarya Caraka has clearly mentioned the drastic nature of the disease. He described that the gastric fire and the vata are the special workers of havos. They burn up the corpulent man, as the forest fire burs up the forest. The fat element in the body having increased inordinately, the vata and other h umors, breaking out into sudden and fierce disorders rapidly destroy their victim's life (Ca. Su.21/7-8). The treatment of sthaulya is a tedious task, as compared to curing Karsaya, as asserted by Acarya caraka. The treatment of sthaulya should aim at reducing Vata, Agni, Meda, neither Santarpana; nor Apatarpana, mode of treatment is efficacious for combating Sthaulya, because santarpana cliktsa pacifies vayu and agni,but at the same time raises Meda Dhatu on the contrary, Apatarpana Cikitsa reduces Meda on one hand. But elevates the agni and vayu. To achieve desired result, Guru and Apatarpana Dravya have been suggested by Acarya Caraka and such specific drug are very few in number, it can be concluded that sthaulya is a Kastasadhya disease (Ca.Su.21/20)

CHIKITSA SIDDHANTA : The process which balances the disturbed Dhatus of the body, is called cikitsa. Excessively increased Medodhatu disturbs other balabced Dhatus of body and cause imbalance of other Dhatus also. This imbalabced state is the main factor for the pathogenesis of sthaulya, other factors involved are Meda, Kapha, Agni and Ama.

In ayurvedic text, Clikits Sutra has been given for the disease are (I) Nidana Parivarjana (ii) Sodhana (iii) Samana NIDANA PARIVARJANA In Nidana (Aetiological factors) of particular disease avoiede at proper time, may help in arresting the pathogenesis of the disease. So, the first step to be taken by the sthlaputusis to forsake Nidana i.e.Atisampurana, Madhur, Sita, Snigdha, Guru ahara, Abhyasana. Not only these but Viharatmaka Nidana should be a avoided. SODHANA: In this therapy, evacution of aggravated Dosas is the chief aim. If can be devided into two 1. Bahya Sodhana 2. Abhyantara Sodhana Ruksa Udvartana is one type of Bahya Sodhana,Vaman, Virecana, Asthapana basti are abhyantara Sodhana. These all are useful measures for sthaulya also. Acarya Caraka has mentioned that Atisthula person possessing stamina and strength; should be treated with Vamana and Virecana Karma.Non-unctuous, warm and strong enemata also suggested by AcaryaCaraka (Ca. Su.21/21-23) SAMANA: Samana therapy means, the disease is eradicated by suppresing the vitiated Dosa, without disturbing the other Dhatus. This type of treatment is very effective in primary stage of disease Vyayam Dipan -Pacan, Ksudha,Trsna, Vata Sevan-Atapa Sevana are described as samana therapy.these all can be included under the Langhana (Apatarpana) Dipan - Pacan Dravya Stimulates Jatharagni, Bhutagni and Dhatvagni, thus it will be effective in digesting the Ama and Meda. Fasting (Ksudhanigraha) means administration of Laghu and Ruksa. Ahara in small quantity. This stimulates Agni and digests Ama. Control of thirst (trusa Nigraha) also helps in the digestion. Vata sevan causes Kleda sosana of kapha and Meda. whiLe Atapa Sevan enhances Usma in the body Vyayama builts the stamina, lightens the body,stimulates Agni. According to modern science exercise increases the B.M.R. hence,utilise the stored fat. AUSADHA: Acarya Caraka has mentioned Lekhaniya dasemani Dravyas - a group of 10 drugs, these drugs principally perform the Lekahana Karma of excess and abnormal Meda, causing weight reduction as well as relief in other signs and symptoms. These revu;sives drugs are given below1. Mustaka 2. Kustha 3. Haridra 4. Vaca 5. Atievisa 6. Katu rohini 7. Citraka 8. Citrabilva 9. Daruharidra 10. Haimvati (Karanja) (Ca. Su.4/3/Cakrapani) PATHYAPATHYA: Caraka has mentioned a special type of diet which is guru apatarpana. It acts in two ways. One is the neutralisation of Vayu and Agni by heaviness of the food, another is non-nourishing of the Meds rather it prevents the further formation of fat. Regarding these properties following diet can be used. The ancient Acaryas have listed numberous Pathys and Apathyas for Sthula person. These are as follows PATHYA - APATHYA AHARA: Aharavargag pathya Apathya

Suka Dhanya

Yava, Veuyava,Kodrava Nivar, Jurna, Mudga, Rajmasa,Kulattha Canak,Masur, Adhaki, Vruntak, Partrasaka, Patol

Godhum, Navanna Sali, Masa, Tila

Sami Dhanya

Saka Varga

Madhursaka Kanda. Madhurphala Dugdha, Iksu Navni, Ghrt,

Phala Dravya

Kapitha, Jamun, Amalak Takra, Madhu, Usnodaka Till tail, Sarasap tail, Aristha Asava,Jirnamadya Rohit Matsya

Mamsa

Anupa, Audaka

PATHYA-APATHYA VIHARA: PATHYA Srama Jagarana Vyavaya Nitya Bhramana Cintana Soka Krodha APATHYA Sitala Jalas nana Diva Svapa Avyayam Avyavaya, Svapna Prasanga Sukha Saiya Nityaharsa Acintana, Manso Nivrti

Drug Profile : (Link Name)

INTRODUCTION : From time immemorial, it has been earnest desire of man to lead a happy and healthy life. He has been a victim of innumerable maladies and ailments. In order to get rid of suffering from diseases, he resorts to various therapies the chief being the drug therapy. The treatment without drug would b e same as ciphers without figures. Etymological derivation of the word "DRUG" is from the French word "DROGUE".It may be defined as "any" substance which taken by a living organism may modify one or more functions. Acarya Caraka has asserted that each substance on this earth is useful in combating illness when applied with planning and for a specific purpose. Ayurveda describes four basic factors which are most essential for avocation of proper treatment. Among these, Ausadha (Bhaisa) is graded at the second rank which is the main source of therapeuties. LATIN NAME: Plants have always been useful to man, and plant nomenclature acrose because there was need for names which could serve as vehicles of communication. Modern Botany originated in Europe in the 1 6th century A. D, Since the various languages of different countries could not furnish precise names for all

plants. Botanists all over the world were compelled to invent a vocabulary of their own for consistency and uniformity in scientific names because the use of scientific names rather than of common or vernacular names, has much to commend it. Scientific names do indicate generic and usually genetic relationships, hence they are of biological significance. They are international in scope and are common to all tongues, therefore Latin vocabulary was universally accepted because Latin is specific and exact in its meaning which is particularly pertinent to the needs of descriptive phrases of the biological sciences Latin names of Drugs areDETAILS OF DRUGS 1) Haritaki 2) Trifla Gugglgu Combination of A. Harde B. Amlaki C. Lindi Pipper D. Gugglu 3) Trikatu Combination of A. Sunth B. Mari C. Pipper 4) Panurnava

HARITAKI:
1 Latin Names : Terminalia chebula retz. 2 Family: Combretaceae 3 English Name : Chebulic myobalan. 4 Chemical compound There is 24.6 - 32.5% Tanin in the chebulic fruite . Compound of turlin mainly are (a) Chebulagic acid (b) Chebulinic acid (c) Corilagin also 18 amino -acid and less persentage of Phospharic, quinin,shieimic. 5 According to ayuvedic science property of haritaki A. B. C. D. E. GUNA: Ladhu, Rukhhsu VIPAK: MAdhur RASA: Madhur, Amla, Katu, Atikta, Kashaya VIRYA: Ushana Prabhav: Tridhosh- har Haritaki is mild laxative drug,thus it eliminate the meda (fat) through feaces. 6 Indication : Anti - Obejity Activity, Laxative, Dijestive, etc

TRIFLA GUGGLU : (multiple drug compound)

Prepararation of Trifla Gugglu: A fine powder of (1) Harde (2) Baheda (3) Amlki (4) Lindi Pipper (each same quentity) ADD Four time Gugglu of same quantity. Mix according to tablet formulation and make 500 mg tabel. DISCRIPTION OF TRIFL A GUGGLU CONTAIN : HARDE (Haritaki) Mentioned Above

BAHEDA 1. Latin name : Terminali bellirica Roxb. 2. Family : Combretaceae 3. English Name : Belliric Myrobalam. 4. Chemical Compound : 21.4% tunin in Fruite. Who B-sitosterol, Gailic acide, elgic acid, ethulgeletic chebujelic acid, menital, glucose, gelecose, ectose, remnose. 5. According to ayurvedic science property of BAHEDA 1 GUNA : Rukhsa, Laghu 2 RASA : Kashhay 3 VIPAK: Madhu 4 VIRYA: Ushana This drugs mainly used on kapha and meda(Fat) diseas. Introduction: Anti - Objity Anti - Imflamatary Anti - Dipretion Anti - HElmentic AMLAKI 1 Latin Names : Emblic myrobalan Gaertn. 2 Family: Euphorbiaceae 3 English Name : Emblic myrobalan 4 Chemical compound :Amla is very rich in uitaminc, it is also known as anti -oxi dant drugs, ambla fruite contain gelic acide, Tenic acide, Albumine, Minerals drugs (Mainly Calcium). Moisture - 81.2% Calcium - 0.05% Protien - 0.5% Phosphorus - 0.02%, Fat - 0.1% Iron 1.2 mg Minerals - 0.7%, Nicotenic acide - 0.2 mg, Curbohydrates - 14.1% According to ayurvedic science property of Amlaki 1 GUNA : Rukhsa, Guru, Shit 2 RASA : Kashhay,Madhur, AMla, Katu, Tikta 3 VIPAK: Madhur 4 VIRYA: Shit 5 PRABHAV: Tri-dosh. Har Introduction: Anti - Objity Anti - Oxidant Anti - Diabeter Anti - Rejuvenator Good for eyes, liver, and dijestive It is work as dieuratic, thus it elimanate dosha through urinary systems. LINDI PIPER 1 Latin Names : Piper longum Linn 2 Family: Piperaceae 3 English Name : Long Pepper 4 Chemical compound :Volentine oil-0.7%, Piperine - 4 to 5 % and salt material of piplartine. There are also Piperloguminin, and steroid, glycocide. According to ayurvedic science property of long Pepper 1 GUNA : Laghu, Snigdha, Tikshana 2 RASA : Katu 3 VIPAK: Anushnshit 5 PRABHAV: Pita samak, vat samuk Introduction: Appitiser Improve metabolic system Anti - Obejity

Anti - Helmentic Blood Purifier Dieuretic Rejuvenator GUGGULU 1 Latin Names : Commiphora mukul (hook ex stocks) engl 2 Family: Burseraeae 3 English Name : Gum - guggul, Indian bedellium 4 Chemical compound : Diterpenes Esters Fatty alcohols Ketone fraction composed of steroids e - and z- guggulsterone (chdesterol lowering components) Streds Volatile oil containing cembrene a TOXI CITY "No know Toxicity" According to ayurvedic science property of guggulu 1 GUNA : Laghu, Ruksha, Sar Snigah- Pichchhil, Tikshana, Sushma, 2 RASA : Katu, Tikta 3 VIPAK: Katu 4 VIRYA: Ushna 5 PRABHAV: Tridosh - Har Therapeutic Actions: Activates the thyroid gland Anti - Obejity Anti - Fangal Anti - Inflummatory in acute models, comparable to 1/5 hydrocortisone and equal to Phenylbutazone and ibuprofen, in chronic models, it is more effective than all three. Antioxidant Antiseptic Increase cateeholamine biosysthesis and activity Inhibits Platelet aggregation Lower VLDL, and LDTS while elevating HDLS Stimulates liver metabolism of LDL cholesterl.

TRIKATU

is three drugs compound

1 Shunthi Ginger root 2 Mari Black PePPer 3 PiPPli Pippli berry The traditional uses of trikatu Rasayana are: Anti- Objity To stimulate digestion Promote the flow of gastric juices Stimulate the bodies own enzyme production Improve the metabolism Increase circulation Improve appetite Stimulate the taste buds Improve the immune system Increase absorption of nutrients Used as a chutney to flavor food

It has beenused traditionally to coounteract: Itching Candida Intestinal toxins Worms Mcus congestion Blood impurities Constipation Indigestion Gas Bloating Mucus formation Undigested meals Trkatu Rasayana strengthens digestion. Help to remove stagnated food from the digestive tract and to restore normal functioning of the spleen and stomach in digesesting, transporting and distention, belching, acid regurgitation, stuffiness, anorexia, abdominal pain, nausea, vomiting and irregular bowel movements. Shunthi 1 Latin Names :Zingiber officinale Rose. 2 Family: Zingiberaceue 3 English Name : Ginger 4 Chemical compound : Moisture - 80.6% Protein - 2.3% Fat -0.6% Carbohydrates - 12.3% Minerals 1.2% Calcium 20mg /100gm Phosphorus 60mg/100mg Iron -60mg/100/mg Iodine,clorine Vitamin A-B or C Oil of Ginger Oleo - resin Giggerol, Shogaol, Zingerone. According to ayurvedic science Property of ginger 1 GUNA : Laghu, Shnigdha 2 RASA : Katu 3 VIPAK: Katu,Madhur 4 VIRYA: Ushna 5 PRABHAV: Kapha - vat shamak Therapeutic Actions: Anti- obejity Stimulates liver metabolism of LDL cholesterol Lowers ULDLS and LDLS while elevation HDLS Anti-inflammatory Improve metabolic system Anti- Pyritis used in rinits, asthma,cough,expectorant Marich 1 Latin Names :Piper nigrum Linn 2 Family: Piperaceea 3 English Name : Black Pepper 4 Chemical compound : Piperine 5-10% Piperdine 5% Piprettine Chavicine Volatile oil containing 1-2.6% Fat -7 % Moisture 13.2% Proteine -11.5% Carbohydrattes 41.2% Phosphorus 168mg/100mg Iron -16.8mg/100/mg Vitamin B ,E According to ayurvedic science Property of ginger 1 GUNA : Laghu,Tikshana 2 RASA : Katu 3 VIPAK: Katu 4 VIRYA: Ushna 5 PRABHAV: Kaoha nashak i.e. it works as anti-obejity

Therapeutic Actions: Anti- obejity Lowering VLDLS and LDLS while elevation HDLS used in asthma,Skin Disease Improve metabolic system Rejuvenator Blood Purifier PIPPLI : Indian Long Pepper(Mentipned above)

PUNARNAVA
1 Latin Names :Boerhavia diffuse linn 2 Family: Nyctaginuseae 3 English Name : Spreading hogweed 4 Chemical compound : Punarnavien-0.04% Potesium Nitrate -0.52% Sulphet Nitrate Clorate. According to ayurvedic science Property of ginger 1 GUNA : Laghu,Auksha 2 RASA : Madhur, Tikta, Kashqya 3 VIPAK: Madhur 4 VIRYA: Ushna 5 PRABHAV:Tri -dhose-har Therapeutic Actions: Punarnava is Tri-dhoshar drugs i.e. it work as anti -obejity Anti-inflamatory Heart stimulatar Anti- poisioning Good for eyes, skin

Clinical Study : (Link Name)

In Ayurveda it is stated that Vaidya should apply any type of treatment after examining it from all possible dimensions because if a know drug is not properly administered, will cause disaster and Vaidya won't succeed in his profession. (Ca.Su. 1/126). Every body will agree with the fact that to evaluate the particular action of the drug in the particular symptoms, a clinical study is most essential and keen observation during the clinical study is the final aspect to prove the effect. Tab - Haritaki (TDS), Tab Trifla guglu, Tab - Trikatu (TDS), Tab- Punarnava (TDS) as a Medphara Dravya has been described in various Nighantus but a scientific base of this aspect is still needed. So, the present study has been framed to assess its results on multifold parameters and in this chapter, to get conclusive opinion

regarding the effect of the drug Tab - Haritaki (TDS), Tab - Trifla guglu, Tab - Trikatu (TDS), Tab Punarnava (TDS) on Sthaulya, statistical data of clinical analysisi has been presented. AIMS AND OBJECTS: 1. To study the efficacy of Tab - Haritaki (TDS), Tab - Trifla guglu(TDS), Tab - Trikatu (TDS), Tab - Punarnava (TDS) regarding the disease Sthaulya. 2. To find out suitable mode of administration of Tab - Haritaki (TDS), Tab - Trifla guglu, Tab - Trikatu (TDS), Tab - Punarnava (TDS) 3. To analyse if administration of Tab - haritaki (TDS), Tab - Trifla guglu, Tab - Trikatu (TDS), Tab - Punarnava (TDS) are associated with any side effects or not. 4. To analyse the clinical data statistically. MATERIALS AND METHODS: Patients presenting with the symptomatology of Sthaulya (0BJITY) were selected for the study, from Rushu Herbal pvt. Ltd. (Ashirvad Building ) and also Relief Road (Elora Building ), Ahmedabad Irrespective of age, sex, etc. Patients were subjected to thorough clinical examinations and the relevantdata recorded in a specially prepared Performa. Clinical diagnosis was done according Laksana (Symptoms) samuccaya of the Vyadhi laid down in the classical lierture of Ayurveda and they are fixed as the criteria which had been followed through out the study. Criteria for diagnosis are dealt here. SUBJECTIVE CRITERIA: According to Ayurvedic context.Presence of the clinical signs and symptoms have been considered. OBJECTIVE CRITERIA: It has assessed on a) Body weight. b) Body mass index. c) Measurement of circumference like abdomen chest, hip. d) Skinfold thickness. GROUPING: Randomly selected patients of Sthaulya were treated under only a single group. DIET: Normal diet devoid of high fat and exc ess sweets was sugested. Patients were also advised to avoid day time sleep and recommended for morning or evening walk.

THE BASIC DATA: The basic data of 80 patients of Sthaulya is given as follows Table 1 AGE WISE DISTRIBUTION OF 80 PATIENTS Sr.No. 1 2 3 4 Age in yrs. 15-25 26-35 36-45 46-55 No. of patients 22 28 28 02 Perecentage 27.50 32.50 32.50 02.50

The above table shows that maximum number of patients i.e. 32.50% were from

26-45 yrs age group. While27.50%of patients belonged to15-25 yrs. Age group. Minimum i.e. 2.50% belonged to the age group 46 -55 years. Table 2 GENDER WISE DISTRIBUTION OF 80 PATIENTS Sr.No. 1 2 Gender Female Male No.of patients 56 24 Percentage 70.00 30.00

Maximum incidence of Sthaulya i.e. 70.00%found in female w hile 30.00% in male. Table 3 RELICION WISE DISTRIBUTION OF 80 PATIENTS Sr. no. 1 2 3 4 Religion Hindu Muslim Shikh Jain No.of patients 72 00 00 08 Percentage 90.00 00.00 00.00 10.00

Maximum patients i.e. 36 (90.00%) were Hindu and 4 (10%) patients were Jain. Table 4 OCCUPATION WISE DISTRIBUTION OF 80 PATIENTS Sr. No. 1 2 3 4 5 Occupation Labour House wife Student Service Business No.of patients 04 38 12 20 09 Perecentage 05.00 47.50 15.00 25.00 07.00

Table 5 DISTRIBUTION OF 80 PATIENTS ACCORDINGS TO NATURE OF OCCUPATION Sr. no. 1 2 3 Nature of occupation No.of patients Very light physical 38 work Light physical work 18 Mental work 24 Percentage 47.50% 22.50% 30.00%

The table shows that maximum 47.00% patients done very light physical work, 30.00% of patients performs mental work while, only 22.50% have light physical work. Table 6 SOCIO-ECONOMIC STATUS WISE DISTRIBUTION OF 80 PATIENTS Sr. No. 1 2 3 4 Socio -Economic status Rich Upper middle class Middle class Lower middle class No. of patients 10 24 32 14 Percentage 12.50 30.00 40.00 17.50

Analysis of the socio-economic status shows that majority of patients (40.00%) belonged to the middle class, followed by upper middle class, followed by upper middle class (50.00%) lower middle class (17.50%) and rich (12.50%)

Table 7 MARITAL STATUS WISE DISTRIBUTION OF 80 PATIENTS Sr. No. 1 2 Matital Status Married Unmarried No.of patients 60 20 Percentage 75.00 25.00

The above data reveals that the maximum patients were married i.e. 75.00% while 25.00% were unmarried. Table 8 FAMILY HISTORY WISE DISTRIBUTION OF 80 PATIENTS Sr. No. 1 2 Family History Present Absent No. of patients 32 48 Percentage 40.00 60.00

Family history of Sthaulya was presented in 40% while 60% had no fam ily history. Table 9 MASTICATION WISE DISTRIBUTION OF 80 PATIENTS Sr. No. 1 2 Mastication Proper Improper No. of paints 32 48 Percentage 40.00 60.00

Improper mastication was found in maximum patients i.e. 60.00%. These all patients take very less time for eating while 40% were masticated the diet properly. Table 10 DISTRBUTION OF 80 PATIENTS ACCORDING TO THE RASA DOMINANCE IN THE DIET SR. No. 1 2 3 4 5 6 Dominant Rasa in diet Madhura Amla Lavana Katu Tikta Kasaya No. of patients 36 30 30 14 00 00 Percentage 75.00% 62.50 62.50 17.50 00.00 00.00

Maximum patients (75.00%) reported Madura Rasa dominance followed by Amla and Lavana (62.50%) and Katu Rasa (17.50%) Table 11 DISTRIBUTION OF 80 PATIENTS ACCORDING SARA Sr. No. 1 2 3 Sara Pravara Madhyama Avara No.of patien ts 18 56 06 Percentage 22.50 70.00 07.50

Madhyama sara was noted in maximum i.e. 70.00% of patients while pravara and Avara Sara was noted in 22.50% and 7.50% patients respectively. Table 12 DISTRIBUTION OF 80 PATIENTS ACCORDING TO VYAYAMA SAKTI

SR.No. 1 2 3

Vyayama sakti Pravara Madhyama Avara

No.of patients 02 36 42

Percentage 02.50 45.00 52.50

Avara vyayamsakti was found in maximum patients i.e. 52.50% followed by Madhyama vyayamsakti in 45.00% of patients and pravara Vyayama Sakti was found in minimum patients i.e. 02.50% Table 13 DISTRIBUTION OF 80 PATIENTS ACCORDING TO JATHARAGNI SR.NO. 1 2 3 4 Jatharagni Manda Tiksna Visama Sama No. of patients 04 34 24 18 Percentage 05.00 42.50 30.00 22.50

In maximum patients i.e. 42.50% Tiksna Agni was noted followed by Visama Agni in 30.00% of patients. While Sama Agni was found in 22.50% and Manda Agni in 50.00% of patients. Table 14 DISTRIBUTION OF 80 PATIENTS ACCORDING TO VAYATAH Sr. no. 1 2 3 Vayatah Bala Yuva Madhya No. of patients 04 28 48 Percentage 05.00 35.00 60.00

The above table shows that maximum patients belongs to Madhyama Vaya i.e. 60.00% followed by Yuva and Bala Vaya 35.00% and 05.00% respectively. Table 15 DISTRBUTION OF 80 PATIENTS ACCORDING TO NIDANA SEVANA Sr.no. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Nidana Acintana Adhyasana Atibhojana Atigurudravya sevana Ati Snigdha Sevana Ati Nidra Avyayama Asanasukha Bijadosa Svabava Chestadvesa Dadhisevana Madhura Ahara Sevana Mamsa Sevana Paya vikara Sevana Sarpisevana No.of patients 22 36 56 32 44 44 64 42 28 42 18 36 14 22 12 Percentage 27.50 45.00 70.00 40.00 55.00 55.00 80.00 52.50 35.50 52.50 22.50 45.00 17.50 27.50 15.00

The Nidana Avyayama was reported in maximum i.e.80.00% of patients. Followed by Atibhojana 70.00% while Atinidra and Atisnigdha Sevana was found in 55.00% of patients. Asanasukh and Chestadvesa was found in similar i.e. 52.50% of patients. Adhyasan and Madhura Ahara Sevana was noted in 45.00% of patients followed by Atiguru Dravya Sevana and Bijadosa Svabhava i.e. 40.00% and 35.00% respectively.

The other nidanas like payavikara sevana, mamsa sevana, sarpi sevana were found in 27.50%,22.50%, 17.50% respectively. Table 17 DISTRIBUTION OF 80 PATIENTS ACCORDING TO CHRONICITY SR.NO. 1 2 3 Chronicity 3 months to 1 yrs. 4 yrs. to 5yrs. 6 yrs.to 10 yrs. No.of patients 14 36 30 Percentage 17.50 45.00 37.50

The above data reveals that maximum number of patients i.e. 45.00% were suffering from the disease since 2 to 5 years. Followed by 37.50% of patients suffering since 6 to 10 years. While in 17.50% of patients the chronically was between 3 months to 1 years. Table 18 DISTRIBUTION OD 80 PATIETNS ACCORDING TO WEIGHT RANGE SR. NO. 1 2 3 4 5 Weight In kg. 60 to 70 71 to 80 81 to 90 91 to 100 100 to 110 No.of patients 28 28 16 04 04 Percentage 35.00 35.00 20.00 05.00 05.00

The table shows that maximum 35.00% of patients belonged to the weight range 60 to 70 kgs. Followed by weight range 81 to 90 kgs. In which the patients were 20.00% while 05.00% was found in weight rangs 91 to 100 and 100 to 110kgs. Table 19 DISTRIBUTION OF 80 PATIENTS ACCORDING TO BODY MASS INDEX SR. No. 1 2 3 4 5 6 BMI range kg/m 25-30 >30-34 >34-3 8 >38-4 2 >42-4 6 >46-5 0 No. of patients 46 20 10 00 02 02 Percentage 57.50 25.00 12.50 00.00 02.50 02.50

Maximum i.e. 57.50% of patients have B. M.I between 25 - 30 kg/m while minimum i.e. 02.50% of patients had BMI. In the range >42- 46, and 46-50 kg/m. Table 20 DISTRIBUTION OF 80 PATIENTS ACCORDING TO TIME OF ONSET SR. NO. 1 2 Time of onset Childhood Adulthood No. of patients 12 68 Percentage 15.00 85.00

Table shows that maximum i.e. 85.00% patients have adulthood onset of the disease. Table 21 DISTRIBUTION OF 80 PATIENTS ACCORDING TO AGGRAVATING FACTORS

Sr. No. 1 2 3 4 5 6 7

Aggrivating Over eat Sedentary life style Delivery Oral contra Ceptive IUCD Leproscopy Menopause

No.of patients 26 20 12 09 09 04 02

percentage 37.50 25.00 15.00 07.50 07.50 05.00 02.50

In maximum patients i.e. 37.50 % over eat was noted as aggravating factor followed by sedentary life style (25.00%), delivery (15.00%), oral contraceptive (07.50%), IUCD (07.50%), leproscopy (05.00%) and menopose(02.50%). Table 22 DISTRIBUTION OF 80 PATIENTS ACCORDING TO UPADRAVA SR. NO. 1 2 3 4 5 6 7 8 Upadrava Knee joint pain Depression Backache Hypertation Flat foot Piles and fissure Exertional dyspnoea Sterility No.of patients 28 14 09 09 09 04 04 02 Percentage 35.00 17.50 07.50 07.50 07.50 05.00 05.00 02.50

Table shows that 35.0% of patients had complaint of knee joint pain. While depression had been seen in 17.50 % of patients, backache, hypertention and flat foot was noted similar in 07.50 % of patients minimum patients was complaining for sterility i.e. 02.50% We are at your service since 1981, providing ayurvedic herbal formulations for various ailments. We specialise in weight balancing, that is, either putting up more weight or reducing weight by way of ayurvedic herbal medicines only. From 1994 we started a unique method of providing herbal formulations to weight conscious people by way of post parcel. This way we have been able to successfully provide ayurvedic herbal weight balancing solutions to more than 75,000 weight balancing enthusiasts so far. Our vast experience in the field of preparing ayurvedic herbal products and formulations together with the continued efforts and innovative ideas of our research team has enabled us to provide you with a yurvedic herbal products and herbal cures without any side effects whatsoever.

Effects of Therapy : (Link Name)

Table - 23 EFFECT OF MEDICINE ON SIGNS AND SYMPTOMS Sr Signs & Symptoms mean B.T. A.T. Diff. s.d. s.e. t P

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Anga Gaurava Ati Ksudha Atinidra Ati Pipasa Anga Saithilya Alpa Vyayama Cala Stma Cala Udara Cala Sphika Daurbalya Gatradaurgandhya Ksudrasvasa Snigdhangata Svedadhikya Utsahahani

1.08 2.33 1.78 1.90 1.00 1.33 1.83 3.00 1.70 1.60 1. 25 1.55 1.30 2.91 1.73

0.00 1.53 1.00 1.46 0.40 0.25 1.50 0.78 1.10 0.76 0.50 0.74 0.70 1.73 1.37

1.08 0.8 0.78 0.44 0.60 1.08 0.33 0.78 0.60 0.84 0.75 0.81 0.60 1.18 0.36

0.28 0.77 0.57 0.52 0.54 0.28 0.51 0.57 0.51 0.68 0.46 0.60 0.51 0.75 0.92

0.08 0.05 0.15 0.17 0.24 0.08 0.09 0.04 0.16 0.19 0.16 0.18 0.16 0.22 0.08

13 15.49 5.07 2.52 2.44 13.0 3.87 19.0 3.67 4.42 4.58 4.50 3.67 5.22 16.22

<0.001 <0.001 <0.001 <0.05 >0.05 <0.001 <0.05 <0.001 <0.01 <0.001 <0.01 <0.01 <0.01 <0.001 <0.001

Above table shows that patients had statistically hifhly significant (p<0.001) relief in signs and symptoms like Angagaurava (100%), Alpavyayama and Daurblya (52.50%), Atinidra (42.13%), Svedadhikya (40.55%) Atiksudha (34.33%), Utsahahani (20.80 %) and cala udara (08.67%), Resu;ts were also highly significant (P <0.001) in other sins and symptoms like Gatradaurgandhya (46.55%), Ksudrasvasa (52.46%), Snigdhangata (46.55%), and Cala Sphik (35,29%). While significant result P<0.05 was found in Atipipasand Cala Stana (18.03%). EFFECT OF MEDICINE ON VARIOUS BODY CIRCUMFERENCES BODY Circumferences Chest Abdomen Hip Mid Arm Mid calf B.T. 99.63 100.13 107.70 11.86 2.64 Mean A.T. 96.50 92.00 96.60 11.56 2.13 3.13 3.07 1.44 0.23 0.17 1.42 0.82 0.39 0.56 0.05 8.20 9.93 18.54 3.51 11.19 <0.001 <0.001 <0.001 <0.01 <0.001 S.D S.E. T P

The table shows that statistically highly significant (P<0.001) reduction was observed in body circumferences l Table - 25 EFFECT OF MEDICINE ON ANTHROPOMETRIC PARAMETERS Sr mean S.D. S.E. T P

1 2 3

Body weight B.M.I. TSF Thickness

B.T. 74.46 28.73 2.62

A.T. 71.20 27.70 2.46

1.83 0.64 0.20

1.01 0.17 0.50

3.22 6.25 0.40

<0.01 <0.001 >0.05

Statistically highly significant (P <0.001) reduction was note d in B.M.I. (3.59%). Reduction in body weight (4.37%) was observed highly significant (p <0.01), While insignificant (p>0.05) reduction in TSF Thickness was noted. Table - 26 EFFECT OF MEDICINE ON BLOOD PRESSURE Sr Blood Pressure Mean S.D. T P

B.T. 1 2 Systolic Diastolic 138.13 86.78

A.T. 130.27 80.53 10.05 5.92 2.77 4.38 >0.05 <0.001

The table shows that 5.69% decrease in systolic pressure was noted. It depicts the mild hypotensive activity of the test drug.

Observa tion (Discussion & Conclusion) : Link Name) Total number of patients registered were 80, for the present study. The clinical observation of 80 patients were presented in the study and the effect of therapy was evaluated in the 80 patients who have completed the duration of treatment. Here the basic data of the patients is given followed by the observed Nidana. Rupa, Upadrava of the disease and lastly the effect of the therapy on the patients is being presented. Discussion & conclusion Aim of the study was to assess efficacy of drugs which are given from Rushi Herbal Pvt Ltd by Dr. Amrish Dawada on sathaulya (obesity) Patients were registered from Rushi Herbal Pvt Ltd. Dr. Amrish Dawada. Ahmedabad two main criteria were adopted subject to criteria include symptoms of obesity objective criteria included weight, BMI circumferences. Out of 80 patients studied maximum were females (70%) with gynoid pattern of obesity.

Screening of the history reveals that maximum patients were housewives (47.5%). Adhyasana and Visamasana were noted in 45% and 27.50% respectively. Majority of patients were married (75%) belonged to middle class (40%), vegetarian (82.50%) and performs very light physical work (47.50%). Maximum relife was noted in Angagaurava (100%), alpavyayama (81.20%), ksudhadikya(34.33%), Atinidra(42.13%), Snigdhangata(46.15%), Ksudrasvasa(52.26%). Statistically highly significant reduction was observed in body circumference like chest (3.14%) abdomin (8.13%), hip(8.42%), reduction in BMI (3.59%), and body weight(4.37%) was also statistically highly significant. In the present study on screening of overall effect of test drug showed that maximum patients had moderate improvement(66.66%) and partially improvement in 26.66% of patients. These all proves better efficacy 4 DRUGS sthaulya. Our main criteria was reduction of weight in obesity patient. After the completion of 80 obesity patients treatment, result came statistically highly significant minimum 3 kg weight reduce in one month.

Weight and Height Chart : (LinkName) Appendix-I The following table are the average value for Indians derived from the exhaustive data prepared by Dr. J. J. Cursetii of oriental life Insurance Company. Table - A HEIGHT (CENTIMETREWS ) AND WEIGHT (KILOGRAMS ) FOR INDIAN MALES Age : 35 Kg. 47.6 48.5 49.0 50.4 53.5 54.7 56.3 58.5 60.1 62.

Height In C. M. S. 148 150 153 155 158 160 163 165 168 170

20 Kg. 42.7 43.6 45.4 46.3 48.6 49.7 51.1 53.1 54.0 56.5

25 Kg. 44.2 44.9 47.0 48.1 50.0 51.1 52.7 54.7 56.3 57.9

30 Kg. 46.2 46.9 49.0 49.0 52.0 53.1 54.9 56.9 58.1 60.3

40 Kg. 48.8 49.7 51.7 52,7 54.5 55.6 57.6 59.7 61.5 63.7

45 Kg. 50.0 50.8 52.3 53.5 55.7 56.7 58.8 60.6 62.4 64.7

50 Kg. 50.9 51.5 53.5 54.2 56.3 57.4 59.4 62.0 63.7 65.8

173 175 178 180 183

58.1 60.1 61.9 64.0 66.0

60.1 62.2 64.0 66.2 68.5

62.2 64.2 66.3 68.5 71.0

64.0 66.0 68.5 71.0 73.3

65.8 68.1 70.6 73.3 75.6

67.0 69.7 71.9 74.4 71.1

68.3 71.0 72.4 75.1 77.8

Table - B HEIGHT (CEMTIMETRE) AND WEIGHT (KILOGRAMS ) FOR INDIAN FEM ALES Age : 35 Kg. 44.0 44.8 46.6 47.7 49.5 50.6 52.1 54.1 55.6

Height In C.M.S 148 150 153 155 158 160 163 165 168

20 Kg. 38.6 40.3 41.9 42.8 44.9 46.0 47.3 49.1 50.0

25 Kg. 41.0 41.6 43.5 44.3 46.3 47.3 48.8 50.6 52.1

30 Kg. 42.6 43.5 45.3 46.2 48.1 49.1 50.8 52.6 53.8

40 Kg. 45.1 46.0 47.9 48.8 50.4 51.5 52. 55.3 56.8 Table - c

45 Kg. 46.3 47.0 48.4 49.5 51.6 52.4 54.1 56.0 57.7

50 Kg. 47.1 47.7 49.5 50.1 52.1 53.0 54.8 57.3 59.0

BODY MASS INCEX FOR GIVEN AGES Sr. no. 1. 2. 3. 4. 5. 6. Age group years 19 - 24 Yrs. 25 - 34 Yrs. 35 - 44 Yrs. 45 - 54 Yrs. 55 - 64 Yrs. 65 B.M.I (kg/m2) 19 - 24 20 - 25 21 - 26 22 - 27 23 - 28 24 - 29

Bray G. A. -The obese patients major problems in internal medica. Philadelphia.

Bibliography : (Link Name)