clinical study rush i med ho har

8/2/2019 Clinical Study Rush i Med Ho Har

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Clinical Study

Rushi Medohar :

Introduction :

Ayurveda the Ancient Indian Medicine , Based on terminology established after minute observation and onscientific goruns and medical experience. These knowledge led to a high level of differentiation and awide spectrum of differentiation and a wide spectrum of therapeutical experience. Ayurveda medicinetreat the patient rather the disease. These are not enough but it is towards the goal of happiness that theentire activity of every creature is held to be directed. On account, however, of the divergent conditions ofknowledge and ignorance there is seen divergence of the right and the wrong approaches to the goal ofhappiness.

It is also said that, the whole of suffering which cleaves to mind and body has ignorance for its basis andconversely all happiness is founded in clear scientific knowledge.

It suggests that to overcome the Dukha, clear knowledge of Ayurveda and ultimately knowledge ofDravyaguna 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 mentionedin 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 todefine. Aesthetic considerations a side, obesity is best defined as any degree of excessadiposity that imparts a health risk.Visual inspection of a patient can give a subjective but fairly accurate estimate of thedegree of obesity.

Obesity can be assessed in several ways. The direct methods of measuring body fatinclude underwater weighing (Densitometry) estimation of total body water, estimation oftotal body potassium and estimation of fat cell mass by isotope dilution method. Bothcomputed topography and nuclear magnetic resonance imaging can be used to distinguishbetween 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 fieldpractice, and they have the advantage of use of less sophisticated equipment's.

Most Commonly Used Parameters Are:

BMI= Weight (Ib) X 703.1Height (Inches)This simple measurement correlates quite highly with other estimates of obesity and thuspore 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 = 40Health risks increases as BMI increases above 25.The national institute of healthconsensus panel on obesity agreed with the definitional and concluded that a 20 percentincrease in relative weight or a BMI above the 85th for young adults constitutes a healthrisk; by the use of these criteria, 20 to 30 percent of adult men and 30 to 40 percent of adultwomen 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 thebody just below the ribs between the thumb and index finger if the thickness of the fold


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exceeds one inch, a person is obese. Assessment of skin fold thickness over various areasof body together with height, weight and age can be used to assess the degree ofadiposity.More precise assessment of obesity can be made with measurements of body density orwith 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) for150 cm (5Ht) individual and adding 2 kg. (5 Lb) for each 2.5 cm. (1 INCH) over 150cm. Plus2kg. 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. ormore 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 givenpatient over weight dose not take into account the distribution of body fat, which as will beexplained below, influences the morbidity from excess weight, as well as other importantfactors 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 heightand weight standard tables; A prevalence rate of 10-12 % in the adult population of USAhas been reported. Racial and socioeconomic conditions influence the developm entobesity.

ETIOLOGY:

Hyperphagia is a striking cause of obesity. When caloric intake exceeds expenditure, theexcess calories are stored in adipose tissue, and if this net positive caloric balance isprolonged obesity results. I.e. there are two c omponents of weight balance, and anabnormality on either side (intake or expenditure) Can lead to obesity. An individualgradually increases his caloric intake, and the pounds accumulate. The effect is cumulativesecond one due to some endocrine disorder or pathological condition. In first type manyhave a physiological imbalance which accounts foe their overeating. Thus,'' Obesity is an outcome of race between energy input and energy output where energyinput always WINS''

Energy intake : the regulation of eating behaviour is incompletely understood. To someextent, 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 bysending 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 bypsychology 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 isanother p ossible inhibitory factor. The cerebral cortex receives positive signals from thefeeding center that stimulates eating and the satiety center modulates this process bysending inhibitory impulses to the feeding centre. In animals destruction of the feedingcentre results in decreased food intake, and destruction of the satiety centre leads toovereating and obesity.

Ultimately, the cerebral cortex controls eating behaviour, and impulses from the feedingcentre to the cerebral cortex are only one input.

2. EXTERNAL SIGNALS: Psychological, social, and genetic factors also influence food intake. In many obese


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subjects these influences are overriding ; indeed, obese subjects usually responds toexternal signals such as time of day, social setting, and smell o r taste of food to a greaterextent than do persons of normal weight. The sight of desirable food leads to a rise in thelevel of insulin in the blood the ''anticipatory insulin response''. It is of interest in thisconnection that external responders have a large anticipatory insulin response, but this isusually 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. Dailycaloric needs range between 31 and 35 Kcl per kilogram of body weight; this is higher inactive and lower in sedentary individuals.

4. EMOTIONAL STATE:

It is generally held that emotional perturbation can affect our desire to eat, some people aremore affected in this way than others. In 1965, Silverstone proved when the appetitive response to emotional distress is in thedirection 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 totalfat stores are unknown.

Glycerol release from far cells and ascending neural impulse may be signals of adiposetissue size. Additionally, the hypothalamic centres are sensitive to catecholamines, andbeta-adrenergic stimulation inhibits eating behaviour. This provides at least one relationalfor the anorexiant effects of amphetamines.

ENERGY OUTPUT (EXPENDITURE) :

Expenditure of energy is by 3 ways :


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A1 - Resting metabolic rateB - Thermo genesisC - Physical exertion

A. RESTING METABOLICRATE:

Even whi le resting , the body needs at least that many calories for its various functions. Themetabolic rate is the energy required to maintain the normal processes of the body likebreathing and heart beat.

The basal metabolic rate, measured at a time of complete rest in thermo neutral, variesfrom 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 theirfriends, but still tend to weight gain. This can only mean that their metabolic rate issluggish-slower than that of their lean friends. But exercise can help such patients. Themetabolic rate continues to increase for a while after the exercise. So that even while thebody is resting, calories are being burned.

The rate of metabolism at basal conditions has been found to vary in different individualsand therefore the B. M. R. var ies with different factor .

FACTORS AFFECTING BASALMETABOLIC RATE:

1) AGE2) SEX3) SURFACE AREA4) CLIMATE5) HABIT6) DIET7) HORMONES8) BEROMETRIC PRESSURE9) PREGNANCY10) BODY11) DRUGS12) RACIAL VARIATION

PATHOGENESIS:

Obesity may result from primary defects in adipose tissue in a way, whereby lipolysis isdiminished and/or lipogenesis is enhanced. But no convincing evidence is there to blameon dimished lipolysis. Bray (1969) reported decreased oxidation of glycerophosphate in themitochondria of fat cells in fatty tissue, so more of glycerophosphate is spared for furthersynthesis of triglyceride and this may favour lipogenesis. Glycerophosphate oxidationefficiently regulates the mechanism to couple the oxidation and phosphorylation reactions.On the other hand, increased oxidation of glycerophosphate in mitochondria occurs innormal persons on high calorie diet, whereby more heat and energy is produced, andenergy expenditure become more. Therefore this system favors prevention of weight gaineven with excess caloric intake. Conversely, a deficiency in the related oxidative enzymesystem at the mitochondria level cannot oxidise glycerophosphate in obese people causingimpairment 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, andabove 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 typeof obesity is aneroid; i.e. man pattern obesity and when W.H.R. is below this it suggestgynoid type i.e. female pattern obesity.Waist circumferenceHip circumference.


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SYMPTOMS:

1) General lassitude2) Day time hypersomnalism3) Dyspnoea on exertion.

TYPE OF OBESITY AND DIFFERENT DIAGNOSIS:

1) According to severity:

(a) mild (b) moderate (c) Severe

2) According to distribution of fata) Generalizedb) Central - involving only the trunk and neckc) 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 tocorrelate 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 possible cause of weight gain havebeen investigated and ruled out.c) Water Salt retention - Characterized by sudden increases of body weight which respondspromptly to diuretic therapy.

d) Derumis disease- obesity associated with symmetrical tender and painful lumps over thebody.e) Hyper insulinism -obesity observed in cases of pancreatic tumor associated with attacksof 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 somewhatexcessive under the and over the abdomen.b) Endogenous -

(1) Cushing 's syndrome - Rounded pelthoric appearance central obesity, buffalo lumpaccumulation 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 decreasein the secretion of gonadotropin hormones by the anterior pituatary. If this occurs p rior topuberty, it causes typical eunuchism.

(3) Hypothyroidism: these include fatigue and extreme sleep (14 to 16 hrs. / day) extrememuscular sluggishness; slowed heart rate, decreased cardias output, decreased bloodvolumes, constipation, mental slugishness, development of an edematous appearancethroughout 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.


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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 mostlyin association with fatty acids. Depending on their source and composition, lipids areclassified as simple,compound and derived. Five categories of lipid viz. Triglycerides (TG),free fatty acid (FFA) phospholipids (PL) glycolipids and cholesterol occurs as physiologiallyimportant constituents of the body.Triglycerides, fatty acid esters of glycerol, constitute the bulk of simple lipids (Fat) stored inthe adipose tissue. In the postabsorptive and fasted states,50-90% of the energy demandis met by FFA released from the adipose tissue on hydrolysis of triglycerides. The sourcesof 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 aremetabolically most active, hence plasma level at any given time remains l ow (8-20mg/di)although around 25 g is transported per hour.Choledterol, an exclusive product of animals metabolism is very widely distributed in thehuman system. All nucleated cells, except in the CNS, can synthesis cholesterol whiledietary sources contributes 200 to 500 mg per day.An essential component component of plasma membranes in all cells, cholesterol is ingreat demand by rapidly proliferating tissues. Assessment of cholesterol status hasassumed great clinical significance as cholesterol is the major constituent of atheromatousplaques and biliary calculi.

TRANSPORT OF LIPID:

The active involvement of lipids in cellular metabolism necessitates and efficientmechanism for their transport in plasma. Two thirds of FFA circulates as reversiblecomplexes 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 formspecialised i.e. PL and FC, are placed on the surface while nonpolar ones (TG and CE) thebibding of the same to specific receptors present on surfaces of approriate cells and thusfacilitate the metabolism of the macromolecules. Some of the apoproteins also act asenzyme 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 densitylipoproteins are also present in circulation.


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These are known as chylomicron remnants. Or VLDL remnants (IDL) Intermediate densitylipoprotein) A new group has been identified, referred to as lipoprotein a (LP- a) or mediumdensity lipoprotein (M.DL).

The sources, transport and metabolism of lipids and lipoproteins may be considered undertwo 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 withcholesterol are processed in the intestinal mucosal cell to from triglycerides and CE. Thesecombine mostly with ApoB48 and some amounts of ApoC ApoE synthesised in th emucosal cell to from "chylomicrons'' the largest of all lipoproteins chylomicrons passthrough the lacteals, lymphatics and the thorasic duct to reach venous blood. Duringcirculation, these arehydrolysed by the enzyme lipoprotein lipase (LPL) at the capillaryendothelial interface of tissues such as muscles and fat. APoCII Catalyses the process ofhydrolusis 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 intakewhile their remnants are taken up by the liver (hepatocytes), through specific receptorshaving affinity for ApoE, for final disposal.

2. Endogenous : triglycerides synthesised by the liver combine with ApoB100 as well asAP0C, APoE, and cholesterol to from VLDL. The VLDL molecules accept further APoCform HDL in circulation and follow a similar path as ehylomicrons except that the process isless efficient and much slower. On losing part of the TG by the action of LPL, VLDL getsreduced to remnant particles or IDL. A portion of these remnants are further processedduring circulation and during passage through the liver to loss nearly all TG and allapoproteins except. B100 and become cholesterol rich, Thus forming LDL.The restaretaken up by hepatocytes and catabolised through hepatic endothelial lipase (HEL).

The FFA librated from hydrolysis of TG in chylomisrons and VLDL are utilised by musclesfor geberation of energy, taken up by adipose tissue to be converted into storage fat, orpass on to the liver for beta-oxidation or resunthesis of VLDL.

Minor:Absorption, synthesis, transport, utilisation and excretion of cholesterol and its eslersconstitute the minor lipid circuit.

1. Sources of cholesterol : Cholesterol in cricul ation is mostly derived from diet and fromdenova synthesis by hepatocytes and mucosal cells of the small gut. carried from theintestine in chylomicrons,cholesterol is rapidly removed from the circulatio and does notproduce immediate hypercholesterolaemis. Cholesterol synthesised by the liver isincorporated 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


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apoprotein, it is taken up by those cells that possess the corresponding receptors. ThusLDL delivers cholesterol to the liver and to a variety of peripheral tissues includingfibroblasts and cells in the vascular wall. However if the amount of cholesterol in these cellsis adequate from prior acquisition or denova synthesis, there occurs a reduction in thenumber of specific receptors (down regulation ) As a result, there is a reduction in thedelivery of cholesterol from circulation to the intracellular compartment. Choles trol rich LDLis mostly catabolised, after receptor binding and internalization, by intracellular lysome. Asmall proportion is phagocytosed and broken down by macrophages (scavengers).

3. Reverse Cholesterol Transport : Normally the cholesterol content of cells is in a state ofdynamic equilibrium where influx from circulating lipoproteins denovo synthesis and effluxinto the circulation are maintained by a sensitive receptors for Apo-B-E, the efflux isencouraged by ApoA, contained in H DL. Further HDL provides the carrier for centripetaltransport of cholesterol released from the tissues.

HDL originates as a nascent disc shaped molecule (HDLn) formed mostly in the liver andpartly in the intestinal endothelium. In the circulation, HDLn recives ApoA, Lecithin and Fe,while it tranxfers Apoe to triglyceride - rioch lipoproteins. Esterification of the cholesterolcontent of HDL occurs by the action of an enzyme lecithin; Cholesterol acyltransferase(LCAT) Thus, HDLn gets converted to a spherical molecule termed HDL3 furtheracceptance of cholesterol from the peripheral tissues and ApoE from circulation convertsHDL3 into a larger molecule (HDL2)this transfers part of its CE content to VLDL and toremnant particles in the course of their conversion to LDL and is finally taken up by tissuepossessing APoE receptors. In the liver, HDL regulates the hydrolysis of cholesterol, HDL2gets reconverted to HDL3 and reenters the circulation. Cholesterol thus released frominternalized HDL2as well as from remnant perticles and LDL is utilised for the synthesis ofbile acids which is excreted into the gut along with FC.

Anprmalities in synthesis, transport, deposition, metabolism, dissimilation and excretion oflipids are associated with disoeders charact erised by obesity, premature atherosclerosis ,xanthome, pancreatitis, cholelithiasis and hepatosplenomegaly, for prematureathersoclerosis, excess of certain types of lipoproteins(hyperlipidaemia/hyperlipoproteinaemia) as well as improper distribution of cholesterol andTG among the lipoproteins (dyslipoproteinaemia) constitute the most important risk factors.

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Auyrvedic aspect of obesity : (Link Name)

(1) VYITPATI & NIRUKTI: Sthula: It is derived from the root ''sthul brimhane '' with an addition of ac pratyaya. Which stand probablybe 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


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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, whichresults into pendulous appearance of sphika, udara, and Stana and whose increased bulk is not matchedby a corresponding increase in energy.

CLASSIFICATION:

In Ayurvedic literature, systematic classification of the disease Sthauly is not availabl e. Vagbhatta hasmentioned 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 diseaseprocess 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 whiledescribing thetypes of Nidanas as the Bahya Nidana and Abhyantra Nidana are included separately they are just likethe exogenous and endogenous causes.

The exogenous causes are those which affect the body from outside like unwholesome diets andregiments 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 exogenouscauses to produce the disease which is the nearest cause of the disease and also called as Samavayikarana.

All the Nidanas, mentioned by various Acaryas can be classified under four groups as follows:

1. Aharatmaka Hetus2. Viharatmake Hetus3. Manas Vyaparatmaka Hetus4. Other Hetus.For better understanding these causes are being tabulated as follows:

1.

2.

3.

4.

NIDANA

Atibhojana

Overeating)

Guru Aharasevana

(excessive consumption of heavyfood )

Madhura Ahrarsevana (sweetfood)

Sita Aharasevana (Excessiveconsumption of cold diet)

CA.

+

+

+

Su.

+

-

-

Ah.

+

-

-

MNi.

-

-

-

BH.

-

-

+

Yr.

-

-

-


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5.

6.

7.

8.

9.

Snigdha Aharasevana

(Excessive consumption ofunctuous food)

Navanna Sevana

(Usage of fresh alcoholic

preparation)

Nava Madhyasevana

(Usage of fresh alcoholicpreparetion)

Gramya Rasasevana

(Usage of domestic animal'smeat & Soups)

Paya Vikara Sevana

(Excessive Usage of milk and itspreparations)

Dadhi Sevana

(Excessive usages of milk and itsPreparation)

+

+

+

+

+

+

-

-

-

-

-

-

-

+

-

-

-

+

-

-

-

-

-

-

-

+

-

-

-

-

-

-

-

-

-

-

NIDANA CA. SU. Ah. Mni. BH. YR.

1.

2.

Preparations)

Dadhi Sevana (Excessive use ofcurd)

Sarpi Sevana (Excessive use ofghee)

+

+

- + - - -


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3.

4. 5.

6. 7.

8. 9.

10.

Slesmala Ahrasevana

(Kapha increasing food)

Iksu Ssevana (Usage ofSugarcane)

Guda Vikara Sevana

(Usage of Jaggery's preparations)

Mamsa Sevana

(Excessive use of meat)

Salisevana(excessive use ofbasmati rise)

Masa Sevana (Excessive use ofphasilous munga)

Godhuma Sevana (excessivewheat)

Audak Rasasevana (Usages ofaquatic animal's meat & soups)

+

+

+

+

+

+

+

+

-

+

-

-

-

-

-

-

-

_+

-

+

-

-

-

-

-

-

-

+

-

-

-

-

-

-

-

-

+

-

-

-

-

-

-

-

-

+

-

-

-

-

-

-

-

VOHARATMAKA NIDANA:

NIDANA CA. AH. SU. Mni. Bh. Yr.1

2

3

4

5

Avayayama

Avyvaya

Divasvapa

Sukha Saiya

Gandhamalyanu Sevana

+

+

+

+

+

+

-

+

-

-

-

-

-

-

-

+

-

+

-

-

+

-

+

-

-

+

-

+

-

-


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6 Svapna Prasangat + - - - - -

MANASAVYAPARATMAKA NIDANA

NIDANA CA. SU. AH. Mni. BH. YR.

Harsantiyatavat

Acintan

Mansonivrti

Priyadarsana

Saukhyena

+

+

+

+

-

-

-

-

-

-

+

+

-

-

+

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

ANYA NIDANA

NIDANA Ca . Su. Ah. Mni. BH. YR. 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 KarmaSamanya 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 excessMedovardhaka PosakaSubstances. The Hetus like Madhur, Guru etc. and Divasvapa etc. increase thekapha 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 isalso 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 Medaincreasing aetiological factors, heavy food does not undergo perfect digestion and undigested foodmaterial Ama is produced.

THIRD & FOURTH KRIYAKALA:

Alongwith Kapha the Maduratara Anna rasa is absorbed in the membrane of gastrointestinal track andcirculates by Vyanavayu. While circulating in Medovahasrotas Mdadhuratara Ama combines with MedoDhatu and Dosa-dusya samurshana takes place.This leads to the impairment of Medodhatvagni which causes formation of Apakva ama meda. Further theVyana Vayu is obstructed by Amameda and this obstructed by Amameda and this obstructed Vayu goesto the kostha.Thus, Jatharagnisandhuksana results in Ksudhadhikya and Sighrajarana of the ingested food thus theperson ingests more food which is rapidly digested, and crave for more food. So the person becomesvoracious eater now due to the constant incoming of the Medaposakansa the capacity to digest theMedamsa by the Medadhatvagni is hampered and again formation of Apakvameda takes place.


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FIFTH KRIYAKALA:

In this stage eight undesirable manifestation of sthaulya takes place. There is the fat alone that keepsincreasing and not the other body elements (Uttar Dhatu). Consequently, there is shortening of the life-span (Ayusohrasa). Saithilya, Saukumarya and Guruta of Meda results in Javoparodha. Sukra-Abahutvaand Avruta Marga of its cause Krucchravyavaya.

Owing to imbalance of Sapta Dhatu, debility results. Due to excessive sweating, due to vitiation of Medaand 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. 28/19and Ca.Ci. 11/12 where ever Purvarupas are not mentioned weak manifestation of Rupa should beconsidered as Purvarupas, So in the 1st stage of Sthaulya a some Laksanas are observed due to KaphaVrddhi which should be considered as Purvarupas of Sthaulya. They are as follows:

Alasya,Angasaithily, Madurasya, Atinidra Atipipasa Etc.

RUPA OF STHAULYA:

No. Rupa Ca . Su. As Ah MNI. BH. YR. 1 Cala Shika + - + + + + - 2 Cala Udara + - + + + + - 3 Cala Stana + - + + + + - 4 Ayatha Upacaya + - + - + + - 5 Anutsaha + - + - + + - 6 Ayusohrasa + - - - - + - 7 Javoparodha + - - - - + - 8 Kricch Vyavaya + - - - - - + 9 Daurbalya + - + - - - - 10 Daurgandhya + + + - + + + 11 Svedabadha + - - - - - + 12 Ksudhatimatra + + + - + + + 13 Pipasatiyoga + + + - + + + 14 Ksudra Svasa - + + - + + + 15 Nindradhikya - + + - + + + 16 Gatrasada - + - - + + + 17 Gadgadvani - + + - - - -

18 Krathana - + - - + + + 19 Alpaprana - + + - + + + 20 Survakriyasu Asamarthata + - - + + -

21 Alpaprana - + - - + + - 22 Kasa - + - + - - - 23 Svasa - + + - - - -

24 Snigdhangata - + - + - - - 25 Udaraparsva Vriddhi - + - + + + - 26 Alasya - - + - - - - 27 Ama - - - + - - - 28 Moha - - - - + + + 29 Saukumarata + + - - - - - 30 Anga Satihilya + + - - + + - 31 Alpabala - - + - - - - 32 Aplavega - - + - - - -


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(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 enlistedBy 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 Updrava Su. As. Ah. YR. BH. Mni. 1 Prameha - + + + + - 2 Pramehapidika + + - - - + 3 Jvara + + + + + + 4 Bhagandara + + + + + + 5 Vidradhi + - - - - + 6 Vatavikara - - - - - + 7 Udar - Roga - + + - - - 8 Urustambha - + - - - - 9 Svasa - + - - + - 10 Apaci - - + + + - 11 Kasa - - + + - -

12 Sanyasa - - + - + - 13 Kustha - - + + + - 14 Visarpa - - - + + - 15 Atisara - - - + + - 16 Arsa - - - + + - 17 Slipada - - - + + - 18 Kamala - - - + + - 19 Mutrakriccha - - + - - - 20 Ajirna - - + - - -

(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 thatthe 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 orinherited sthaulya is incurable.Acarya Caraka has clearly mentioned the drastic nature of the disease. He described that the gastric fireand the vata are the special workers of havos. They burn up the corpulent man, as the forest fire burs upthe forest. The fat element in the body having increased inordinately, the vata and other humors, breakingout 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 Acaryacaraka. The treatment of sthaulya should aim at reducing Vata, Agni, Meda, neither Santarpana; norApatarpana, mode of treatment is efficacious for combating Sthaulya, because santarpana cliktsa pacifiesvayu 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 andsuch 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 increasedMedodhatu disturbs other balabced Dhatus of body and cause imbalance of other Dhatus also. Thisimbalabced state is the main factor for the pathogenesis of sthaulya, other factors involved are Meda,Kapha, Agni and Ama.


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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 thepathogenesis 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 two1. Bahya Sodhana2. Abhyantara Sodhana

Ruksa Udvartana is one type of Bahya Sodhana,Vaman, Virecana, Asthapana basti are abhyantaraSodhana. These all are useful measures for sthaulya also.Acarya Caraka has mentioned that Atisthula person possessing stamina and strength; should be treatedwith Vamana and Virecana Karma.Non-unctuous, warm and strong enemata also suggested byAcaryaCaraka (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 includedunder the Langhana (Apatarpana)Dipan - Pacan Dravya Stimulates Jatharagni, Bhutagni and Dhatvagni, thus it will be effective in digestingthe Ama and Meda. Fasting (Ksudhanigraha) means administration of Laghu and Ruksa. Ahara in smallquantity. This stimulates Agni and digests Ama. Control of thirst (trusa Nigraha) also helps in thedigestion. Vata sevan causes Kleda sosana of kapha and Meda. whiLe Atapa Sevan enhances Usma inthe body Vyayama builts the stamina, lightens the body,stimulates Agni. According to modern scienceexercise 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 principallyperform the Lekahana Karma of excess and abnormal Meda, causing weight reduction as well as relief inother signs and symptoms. These revu;sives drugs are given below-

1. Mustaka2. Kustha3. Haridra4. Vaca5. Atievisa6. Katu rohini7. Citraka8. Citrabilva9. Daruharidra10. 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 itprevents the further formation of fat.Regarding these properties following diet can be used. The ancient Acaryas have listed numberousPathys and Apathyas for Sthula person. These are as follows

PATHYA - APATHYA AHARA:

Aharavargag pathya Apathya


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Suka Dhanya Yava, Veuyava,Kodrava

Nivar, Jurna,

Godhum, Navanna

Sali,Sami Dhanya Mudga, Rajmasa,Kulattha

Canak,Masur, Adhaki,

Masa, Tila

Saka Varga Vruntak, Partrasaka, Patol Madhursaka

Kanda. Phala Kapitha, Jamun, Amalak MadhurphalaDravya Takra, Madhu, Usnodaka

Till tail, Sarasap tail,

Aristha Asava,Jirnamadya

Dugdha, Iksu

Navni, Ghrt,

Mamsa Rohit Matsya Anupa, Audaka

PATHYA-APATHYA VIHARA:

PATHYA APATHYA

Srama Sitala Jalasnana Jagarana Diva Svapa Vyavaya AvyayamNitya Bhramana Avyavaya, Svapna Prasanga Cintana Sukha Saiya Soka NityaharsaKrodha 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 avictim of innumerable maladies and ailments. In order to get rid of suffering from diseases, he resorts tovarious therapies the chief being the drug therapy. The treatment without drug would be same as cipherswithout 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 hasasserted that each substance on this earth is useful in combating illness when applied with planning andfor a specific purpose.

Ayurveda describes four basic factors which are most essential for avocation of proper treatment. Amongthese, 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 fornames which could serve as vehicles of communication. Modern Botany originated in Europe in the 1 6thcentury A. D, Since the various languages of different countries could not furnish precise names for all


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plants. Botanists all over the world were compelled to invent a vocabulary of their own for consistency anduniformity in scientific names because the use of scientific names rather than of common or vernacularnames, 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 meaningwhich is particularly pertinent to the needs of descriptive phrases of the biological sciences Latin names ofDrugs are-

DETAILS OF DRUGS

1) Haritaki

2) Trifla Gugglgu Combination ofA. HardeB. AmlakiC. Lindi PipperD. Gugglu

3) Trikatu Combination ofA. SunthB. MariC. Pipper

4) Panurnava

HARITAKI:

1 Latin Names : Terminalia chebula retz.2 Family: Combretaceae3 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. GUNA: Ladhu, RukhhsuB. VIPAK: MAdhurC. RASA: Madhur, Amla, Katu, Atikta, KashayaD. VIRYA: UshanaE. 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 TRIFLA GUGGLU CONTAIN :

HARDE (Haritaki) Mentioned Above


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BAHEDA

1. Latin name : Terminali bellirica Roxb.2. Family : Combretaceae3. 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, Laghu2 RASA : Kashhay3 VIPAK: Madhu4 VIRYA: Ushana

This drugs mainly used on kapha and meda(Fat) diseas.Introduction: Anti - Obji ty

Anti - ImflamataryAnti - DipretionAnti - HElmentic

AMLAKI

1 Latin Names : Emblic myrobalan Gaertn.2 Family: Euphorbiaceae3 English Name : Emblic myrobalan4 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, Shit2 RASA : Kashhay,Madhur, AMla, Katu, Tikta3 VIPAK: Madhur4 VIRYA: Shit

5 PRABHAV: Tri-dosh. HarIntroduction: Anti - ObjityAnti - OxidantAnti - DiabeterAnti - RejuvenatorGood for eyes, liver, and dijestive

It is work as dieuratic, thus it elimanate dosha through urinary systems.

LINDI PIPER

1 Latin Names : Piper longum Linn2 Family: Piperaceae3 English Name : Long Pepper4 Chemical compound :Volentine oil-0.7%, Piperine - 4 to 5 % and sa lt material of

piplartine.There are also Piperloguminin, and steroid, glycocide.

According to ayurvedic science property of long Pepper

1 GUNA : Laghu, Snigdha, Tikshana2 RASA : Katu3 VIPAK: Anushnshit5 PRABHAV: Pita samak, vat samuk

Introduction: AppitiserImprove metabolic systemAnti - Obej ity


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Anti - HelmenticBlood PurifierDieureticRejuvenator

GUGGULU

1 Latin Names : Commiphora mukul (hook ex stocks ) engl2 Family: Burseraeae3 English Name : Gum - guggul, Indian bedellium4 Chemical compound : Diterpenes

EstersFatty alcoholsKetone fraction composed of steroids e - and z- guggulsterone(chdesterol lowering components)StredsVolatile oil containing cembrene a

TOXICITY "No know Toxicity"

According to ayurvedic science property of guggulu

1 GUNA : Laghu, Ruksha, Sar Snigah- Pichchhil, Tikshana, Sushma,2 RASA : Katu, Tikta3 VIPAK: Katu4 VIRYA: Ushna5 PRABHAV: Tridosh - Har

Therapeutic Actions:Activates the thyroid glandAnti - ObejityAnti - FangalAnti - Inflummatory in acute models, comparable to 1/5 hydrocortisone and

equal to Phenylbutazone and ibuprofen, in chronic models, it ismore effective than all three.

AntioxidantAntisepticIncrease cateeholamine biosysthesis and activityInhibits Platelet aggregationLower VLDL, and LDTS while elevating HDLSStimulates liver metabolism of LDL cholesterl.

TRIKATU is three drugs compound

1 Shunthi Ginger root2 Mari Black PePPer3 PiPPli Pippl i berry

The traditional uses of trikatu Rasayana are:

Anti- ObjityTo stimulate digestionPromote the flow of gastric juicesStimulate the bodies own enzyme productionImprove the metabolismIncrease circulationImprove appetiteStimulate the taste budsImprove the immune systemIncrease absorption of nutrientsUsed as a chutney to flavor food


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It has beenused traditionally to coounteract:

ItchingCandidaIntestinal toxinsWormsMcus congestionBlood impuritiesConstipationIndigestionGasBloatingMucus formationUndigested meals

Trkatu Rasayana strengthens digestion. Help to remove stagnated food from the digestivetract and to restore normal functioning of the spleen and stomach in digesesting, transporting anddistention, belching, acid regurgitation, stuffiness, anorexia, abdominal pain, nausea, vomiting andirregular bowel movements.

Shunthi

1 Latin Names :Zingiber officinale Rose.2 Family: Zingiberaceue3 English Name : Ginger4 Chemical compound : Moisture - 80 .6% Protein - 2.3% Fat -0.6% Carbohydrates - 12.3% Minerals -

1.2% Calcium 20mg /100gm Phosphorus 60mg/100mg Iron -60m g/100/mg Iodine,clorine Vitamin A-B orC Oil of Ginger Oleo - res in Giggerol, Shogaol, Zingerone.

According to ayurvedic science Property of ginger

1 GUNA : Laghu, Shnigdha2 RASA : Katu3 VIPAK: Katu,Madhur4 VIRYA: Ushna5 PRABHAV: Kapha - vat shamak

Therapeutic Actions:Anti- obejityStimulates liver metabolism of LDL cholesterolLowers ULDLS and LDLS while elevation HDLSAnti-inflammatoryImprove metabolic systemAnti- Pyritis

used in rinits, asthma,cough,expectorant

Marich

1 Latin Names :Piper nigrum Linn2 Family: Piperaceea3 English Name : Black Pepper4 Chemical compound : Piperine 5-10% Piperdine 5% Piprettine Chavicine Volatile

oil containing 1-2.6% Fat -7% Moisture 13.2% Proteine -11.5% Carbohydrattes41.2% Phosphorus 168mg/100mg Iron -16.8mg/100/m g Vitamin B ,E


1 GUNA : Laghu,Tikshana2 RASA : Katu3 VIPAK: Katu4 VIRYA: Ushna5 PRABHAV: Kaoha nashak i.e. it works as anti- obejity


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Therapeutic Actions:Anti- obejityLowering VLDLS and LDLS while elevation HDLSused in asthma,Skin DiseaseImprove metabolic systemRejuvenatorBlood Purifier

PIPPLI : Indian Long Pepper(Mentipned above)

PUNARNAVA

1 Latin Names :Boerhavia diffuse linn2 Family: Nyctaginuseae3 English Name : Spreading hogweed4 Chemical compound : Punarnavien-0.04% Potesium Nitrate -0.52% Sulphet Nitrate

Clorate.


1 GUNA : Laghu,Auksha2 RASA : Madhur, Tikta, Kashqya

3 VIPAK: Madhur4 VIRYA: Ushna5 PRABHAV:Tri -dhose-har

Therapeutic Actions:Punarnava is Tri-dhoshar drugs i.e. it work as anti-obejityAnti-inflamatoryHeart stimulatarAnti- poisioningGood 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 possibledimensions because if a know drug is not properly administered, will cause disaster and Vaidya won'tsucceed in his profession. (Ca.Su. 1/126). Every body will agree with the fac t that to evaluate theparticular action of the drug in the particular symptoms, a clinical study is most essential and keenobservation dur ing the clinical study is the final aspect to prove the effec t. Tab - Har itaki (TDS), Tab -Trifla guglu, Tab - Trikatu (TDS), Tab- Punarnava (TDS) as a Medphara Dravya has been described invarious Nighantus but a scientific base of this aspect is still needed. So, the present study has beenframed to assess its results on multifold parameters and in this chapter, to get conclusive opinion


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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, fromRushu Herbal pvt. Ltd. (Ashirvad Building ) and also Relief Road (Elora Building ), AhmedabadIrrespective of age, sex, etc.

Patients were subjected to thorough clinical examinations and the relevantdata recorded in a speciallyprepared Performa.Clinical diagnosis was done according Laksana (Symptoms) samuccaya of the Vyadhi laid down in theclassical 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 ona) 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 excess sweets was sugested. Patients were also advised to avoid daytime 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. Age in yrs. No. of patients Perecentage 1 15-25 22 27.50 2 26-35 28 32.50 3 36-45 28 32.50 4 46-55 02 02.50

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


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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 2GENDER WISE DISTRIBUTION OF 80 PATIENTS

Sr.No. Gender No.of patients Percentage 1 Female 56 70.00

2

Male

24

30.00

Maximum incidence of Sthaulya i.e. 70.00%found in female w hile 30.00% in male.

Table 3RELICION WISE DISTRIBUTION OF 80 PATIENTS

Sr. no. Religion No.of patients Percentage1 Hindu 72 90.00 2 Muslim 00 00.00 3 Shikh 00 00.00 4 Jain 08 10.00

Maximum patients i.e. 36 (90.00%) were Hindu and 4 (10%) patients wer e Jai n.

Table 4OCCUPATION WISE DISTRIBUTION OF 80 PATIENTS

Sr. No. Occupation No.of patients Perecentage1 Labour 04 05.00 2 House wife 38 47.50 3 Student 12 15.00 4 Service 20 25.00 5 Business 09 07.00

Table 5

DISTRIBUTION OF 80 PATIENTS ACCORDINGS TO NATURE OF OCCUPATION

Sr. no. Nature of occupation No.of patients Percentage1 Very light physical

work 38 47.50%

2 Light physical work 18 22.50% 3 Mental work 24 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 6SOCIO-ECONOMIC STATUS WISE DISTRIBUTION OF 80 PATIENTS

Sr. No. Socio -Economicstatus

No. of patients Percentage

1 Rich 10 12.50 2 Upper middle class 24 30.00 3 Middle class 32 40.00 4 Lower middle class 14 17.50

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


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Table 7MARITAL STATUS WISE DISTRIBUTION OF 80 PATIENTS

Sr. No. Matital Status No.of patients Percentage 1 Married 60 75.00 2 Unmarried 20 25.00

The above data reveals that the maximum patients were married i.e. 75.00%

while 25.00% were unmarried.

Table 8FAMILY HISTORY WISE DISTRIBUTION OF 80 PATIENTS

Sr. No. Family History No. of patients Percentage 1 Present 32 40.00 2 Absent 48 60.00

Family history of Sthaulya was presented in 40% while 60% had no fam ily history.

Table 9MASTICATION WISE DISTRIBUTION OF 80 PATIENTS

Sr. No. Mastication No. of paints Percentage1 Proper 32 40.00 2 Improper 48 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 10DISTRBUTION OF 80 PATIENTS ACCORDING TO THE RASA DOMINANCE IN THE DIET

SR. No. Dominant Rasa indiet

No. of patients Percentage

1 Madhura 36 75.00% 2 Amla 30 62.50 3 Lavana 30 62.50 4 Katu 14 17.50 5 Tikta 00 00.00 6 Kasaya 00 00.00

Maximum patients (75.00%) reported Madura Rasa dominance followed byAmla and Lavana (62.50%) and Katu Rasa (17.50%)

Table 11DISTRIBUTION OF 80 PATIENTS ACCORDING SARA

Sr. No. Sara No.of patien ts Percentage1 Pravara 18 22.50 2 Madhyama 56 70.00 3 Avara 06 07.50

Madhyama sara was noted in maximum i.e. 70.00% of patients while pravara and Avara Sara was notedin 22.50% and 7.50% patients respectively.

Table 12DISTRIBUTION OF 80 PATIENTS ACCORDING TO VYAYAMA SAKTI


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SR.No. Vyayama sakti No.of patients Percentage1 Pravara 02 02.50 2 Madhyama 36 45.00 3 Avara 42 52.50

Avara vyayamsakti was found in maximum patients i.e. 52.50% followed byMadhyama vyayamsakti in 45.00% of patients and pravara Vyayama Sakti wasfound in minimum patients i.e. 02.50%

Table 13DISTRIBUTION OF 80 PATIENTS ACCORDING TO JATHARAGNI

SR.NO. Jatharagni No. of patients Percentage1 Manda 04 05.00 2 Tiksna 34 42.50 3 Visama 24 30.00 4 Sama 18 22.50

In maximum patients i.e. 42.50% Tiksna Agni was noted followed by Visama Agniin 30.00% of patients. While Sama Agni was found in 22.50% andManda Agni in 50.00% of patients.

Table 14DISTRIBUTION OF 80 PATIENTS ACCORDING TO VAYATAH

Sr. no. Vayatah No. of patients Percentage1 Bala 04 05.00 2 Yuva 28 35.00 3 Madhya 48 60.00

The above table shows that maximum patients belongs to Madhyama Vaya i.e. 60.00% followed by Yuvaand Bala Vaya 35.00% and 05.00% respectively.

Table 15DISTRBUTION OF 80 PATIENTS ACCORDING TO NIDANA SEVANA

Sr.no. Nidana No.of patients Percentage 1 Acintana 22 27.50 2 Adhyasana 36 45.00 3 Atibhojana 56 70.00 4 Atigurudravya sevana 32 40.00 5 Ati Snigdha Sevana 44 55.00 6 Ati Nidra 44 55.00 7 Avyayama 64 80.00 8 Asanasukha 42 52.50 9 Bijadosa Svabava 28 35.50 10 Chestadvesa 42 52.50 11 Dadhisevana 18 22.50 12 Madhura Ahara Sevana 36 45.00 13 Mamsa Sevana 14 17.50 14 Paya vikara Sevana 22 27.50 15 Sarpisevana 12 15.00

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


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The other nidanas like payavikara sevana, mamsa sevana, sarpisevana were found in 27.50%,22.50%, 17.50% respectively.

Table 17DISTRIBUTION OF 80 PATIENTS ACCORDING TO CHRONICITY

SR.NO. Chronicity No.of patients Percentage1 3 months to 1 yrs. 14 17.50

2

4 yrs. to 5yrs.

36

45.00

3 6 yrs.to 10 yrs. 30 37.50

The above data reveals that maximum number of patients i.e. 45.00% were suffering from the diseasesince 2 to 5 years. Followed by 37.50% of patients suffering since6 to 10 years. While in 17.50% of patients the chronically was between 3 months to1 years.

Table 18DISTRIBUTION OD 80 PATIETNS ACCORDING TO WEIGHT RANGE

SR. NO. Weight In kg. No.of patients Percentage 1 60 to 70 28 35.00

2

71 to 80 28

35.00

3 81 to 90 16 20.00 4 91 to 100 04 05.00 5 100 to 110 04 05.00

The table shows that maximum 35.00% of patients belonged to the weight range 60 to70 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 19DISTRIBUTION OF 80 PATIENTS ACCORDING TO BODY MASS INDEX

SR. No. BMI range kg/m No. of patients Percentage 1 25-30 46 57.50 2 >30-34 20 25.00 3 >34-38 10 12.50 4 >38-42 00 00.00 5 >42-46 02 02.50 6 >46-50 02 02.50

Maximum i.e . 57.50% of patients have B. M.I between 25 - 30 kg/m whileminimum i.e. 02.50% of patients had BMI. In the range >42- 46, and 46-50 kg/m.

Table 20DISTRIBUTION OF 80 PATIENTS ACCORDING TO TIME OF ONSET

SR. NO. Time of onset No. of patients Percentage1 Childhood 12 15.00 2 Adulthood 68 85.00

Table shows that maximum i.e. 85.00% patients have adulthood onset of the disease.

Table 21DISTRIBUTION OF 80 PATIENTS ACCORDING TO

AGGRAVATING FACTORS


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Sr. No. Aggrivating No.of patients percentage 1 Over eat 26 37.50 2 Sedentary life style 20 25.00 3 Delivery 12 15.00 4 Oral contra Ceptive 09 07.50 5 IUCD 09 07.50 6 Leproscopy 04 05.00 7 Menopause 02 02.50

In maximum patients i.e. 37.50 % over eat was noted as aggravating factor followedby sedentary life style (25.00%), delivery (15.00%), oral contraceptive (07.50%),IUCD (07.50%), leproscopy (05.00%) and menopose(02.50%).

Table 22DISTRIBUTION OF 80 PATIENTS ACCORDING TO UPADRAVA

SR. NO. Upadrava No.of patients Percentage1 Knee joint pain 28 35.00 2 Depression 14 17.50 3 Backache 09 07.50 4 Hypertation 09 07.50

5 Flat foot 09 07.50 6 Piles and fissure 04 05.00 7 Exertional dyspnoea 04 05.00 8 Sterility 02 02.50

Table shows that 35.0% of patients had complaint of knee joint pain. While depression had been seen in17.50 % of patients, backache, hypertention and flat foot was noted similar in 07.50 % of patientsminimum patients was complaining for sterility i.e. 02.50%

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Effects of Therapy : (Link Name)


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Table - 23 EFFECT OF MEDICINE ON SIGNS AND SYMPTOMS

mean Sr Signs &

Symptoms B.T. A.T.

Diff. s.d. s.e. t P

1 Anga Gaurava 1.08 0.00 1.08 0.28 0.08 13


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Statistically highly significant (P 0.05 2 Diastolic 86.78 80.53 5.92 4.38


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Screening of the history reveals that maximum patients were housewives (47.5%). Adhyasana andVisamasana 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 highlysignificant.

In the present study on screening of overall effect of test drug showed that maximum patients hadmoderate 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 patientstreatment, 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 - AHEIGHT (CENTIMETREWS ) AND WEIGHT (KILOGRAMS ) FOR INDIAN MALES

Age :

Height InC. M. S.

20 25 30 35 40 45 50

Kg. Kg. Kg. Kg. Kg. Kg. Kg. 148 42.7 44.2 46.2 47.6 48.8 50.0 50.9 150 43.6 44.9 46.9 48.5 49.7 50.8 51.5 153 45.4 47.0 49.0 49.0 51.7 52.3 53.5 155 46.3 48.1 49.0 50.4 52,7 53.5 54.2 158 48.6 50.0 52.0 53.5 54.5 55.7 56.3 160 49.7 51.1 53.1 54.7 55.6 56.7 57.4 163 51.1 52.7 54.9 56.3 57.6 58.8 59.4 165 53.1 54.7 56.9 58.5 59.7 60.6 62.0 168 54.0 56.3 58.1 60.1 61.5 62.4 63.7 170 56.5 57.9 60.3 62. 63.7 64.7 65.8


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173 58.1 60.1 62.2 64.0 65.8 67.0 68.3 175 60.1 62.2 64.2 66.0 68.1 69.7 71.0 178 61.9 64.0 66.3 68.5 70.6 71.9 72.4 180 64.0 66.2 68.5 71.0 73.3 74.4 75.1 183 66.0 68.5 71.0 73.3 75.6 71.1 77.8

Table - BHEIGHT (CEMTIMETRE) AND WEIGHT (KILOGRAMS ) FOR INDIAN FEMALES

Age :

Height InC.M.S

20 25 30 35 40 45 50

Kg. Kg. Kg. Kg. Kg. Kg. Kg.

148 38.6 41.0 42.6 44.0 45.1 46.3 47.1 150 40.3 41.6 43.5 44.8 46.0 47.0 47.7 153 41.9 43.5 45.3 46.6 47.9 48.4 49.5 155 42.8 44.3 46.2 47.7 48.8 49.5 50.1 158 44.9 46.3 48.1 49.5 50.4 51.6 52.1 160 46.0 47.3 49.1 50.6 51.5 52.4 53.0 163 47.3 48.8 50.8 52.1 52. 54.1 54.8 165 49.1 50.6 52.6 54.1 55.3 56.0 57.3

168 50.0 52.1 53.8 55.6 56.8 57.7 59.0

Table - c

BODY MASS INCEX FOR GIVEN AGES

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

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


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Bibliography : (Link Name)

clinical study rush i med ho har

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