Talk:Trividhakukshiya Vimana

From Charak Samhita
Jump to navigation Jump to search


Importance of quantity of diet in preservation of health

A wholesome diet reserves the highest place for proper growth, development, and health maintenance in human life [Cha.Sa.Sutra Sthana25/31], [Chakrapani on Cha.Sa.Sutra Sthana 5/2]. The effect of food articles on body tissues primarily depends on eight factors (ashta aahara vidhi vishesha aayatana), including the quantity of food (rashi). The tetrad of chapters on health (Swastha chatushka) in sutra sthana aims preservation of health and prevention of diseases. It commences with a discussion on food (ahara) and importance of its proper quantity (matra). This indicates the utmost importance of the quantity of food for the maintenance of health [Cha.Sa.Sutra Sthana 5/3]. This chapter discusses the effect of food articles on body physiology concerning amount explicitly. It further explains dosha specific disorders with predominant involvement of dosha in manifestation of the disease; and negligible involvement of dushya (dhatu and mala).

Assessment of food ingestion capacity (ahara shakti)

Fig.1: Extrinsic factors
Fig.2: Intrinsic factors

The food ingestion capacity (aahara shakti) of a person is assessed on two parameters:

  1. Food ingestion capacity (abhyavaharana shakti) and
  2. Digestion capacity (jarana shakti) [Cha.Sa.Vimana Sthana 8/120]

The proper quantity of food depends on the strength of agni ( factors responsible for digestion and metabolism). The strength of agni varies according to season, age and other factors. Thus the amount of food will also vary as per the power of agni. The suitable variation in quantity of food helps maintaining proper digestion and metabolism. The quantity further subjects to heavy to digest (gurutva) and light to digest (laghutva) nature of food.

Proper quantity of food

If a person has taken excellent quality food as per the eight specific dietary factors (ashta aahara vidhi vishesha ayatana) and followed all the rules while taking food (aahara vidhi vidhana), then the food is digested in due time without disturbing the equilibrium of dosha (prakriti), and that amount of food is termed as the "proper quantity of food for that person".

The extrinsic and intrinsic factors influencing quantity of food are shown in fig.1 and fig.2 respectively.

Role of satiety and three parts of ingestion capacity

Satiety is one of the subjective parameters to assess the ingestion capacity of a person. The maximum ingestion capacity of a person should be divided into three parts. One-third part of food intake should be consumed in solid form and one third part as liquid diet, remaining one third part of total capacity should be kept empty for movement of vata, pitta and kapha. This is the indicator of satiety. This means once the two third part of stomach will be filled, a person will have the feeling of satisfaction [Cha.Sa.Sutra Sthana25/40]. At this point the person should stop eating. If this limit is crossed, the excess food stuff will occupy the third part of stomach which interrupts the process of digestion, causing extra burden on agni (digestive power) and may result indigestion. The divisions of stomach (amashaya) are not in equal proportion, but it is in accordance with user’s suitability and the adaptive pattern of food consumption [Chakrapani on Cha.Sa.Vimana Sthana2/3]. Power of ingestion (abhyavaharana shakti) is different for every individual and it depends upon the strength of digestive capacity (jatharagni). The proper quantity of food (aahara matra) to be consumed is subjected to power of ingestion and consistency of food articles i.e. solid and liquid.

Some Ayurveda scholars have divided ingestion capacity of amashaya in four parts and advised to take two parts with solid food, one part with liquids and rest one fourth part to be left empty for dosha (as a normal physiology of digestion). [A.Hr.Sutra Sthana8/46-47][1] Arundatta, commentator of Vagbhata has considered this capacity of amashaya as the measurement of satiety.

Understanding of Amashaya

Amashaya is described in physiological consideration as a site of digestion of food. Surface anatomy describes amashaya as the organ situated between the umbilicus and the breast. All that is eaten, masticated, drunk and licked up is digested here. Once the digestion is completed, the digested essence of food reaches all the body organs by means of vessels. Amashaya is also considered as seat of pitta dosha and kapha dosha. [Cha. Sa.Sutra Sthana 20/8] There observes predominance of kapha and vata dosha in manifestation of respiratory disorders like hikka (hiccups) and shwasa (dysnoea). These disorders originate at the site of pitta. [Cha.Sa.Chikitsa Sthana17/8] In this context, Chakrapani mentioned the two segments of amashaya as upper segment (urdhva amashaya) and the lower segment (adho amashaya). Seat of pitta refers lower segment (adho amashaya) which clearly differentiates from the upper segment of kapha dosha. Anatomically Stomach can be considered as upper segment of amashaya. Small intestine along with liver and pancreas can be considered as the lower segment of amashaya. Amashaya rooted disorders are specifically grouped as the disorders having a predominance of kapha and pitta dosha.[Cha.Sa.Vimana Sthana 6/3]

Classification of food

Depending on the consistency, the food articles are classified into four categories: drinkable, likable, eatable, and chewable. These four types are further abbreviated under two classes as liquid foods and solid foods respectively. Thus both type of food shall be consumed till half of it satiety or till feeling of satiety. This quantity will definitely be digested in due time, without disturbing dosha physiology (prakriti), thus indicates proper qunatity (aahara matra). Subjective parameters shall be observed carefully to decide the proper quantity of food. [Cha. Sa.Vimana Sthana 2/6] Food consumed in the appropriate quantity enhances strength, complexion, and nourishment of tissues.

There are other six types of food patterns described depending upon the consistency of food viz.

  1. Suckables(chushya) e.g. sugercane
  2. Drinkable(peya) e.g. water, milk etc.
  3. Lickables (lehya) e.g. rasala (curd mixed with sugar and spices) and kadhi (a traditional Indian dish consisting mainly of yogurt and gram floor)
  4. Bhojya (soft eatables) e.g. Dal Rice
  5. Bhakshya (hard eatables) e.g. Laddu, Modak (kind of sweet meal),
  6. Charvya (chewables) e.g. poha, roasted horse gram.

These food articles are heavy for digestion in ascending order. [B.P. Prathama Khanda 4/142-143][2]

Effects of deficient quantity of food

A deficient and excessive quantity of food both are detrimental to human health. The deficient quantity of food reduces strength, complexion, and nourishment of body tissues and makes the person a home for various disorders of vata dosha. The quantity of food is one of the major factors which decide the wholesome and unwholesome effect of food on body tissues. [Cha.Sa.Sutra Sthana 25/32]

Under eating or intake of food in reduced quantity (pramitashanam) is mentioned as the principal cause of emaciation (karshaniyanam) [Cha.Sa.Sutra Sthana25/40]. Fasting or over eating does not kindle digestive fire, as like fire in environment is extinguished if there is no fuel supply or if excessive fuel covers the fire. [Cha.Sa.Chikitsa Sthana 15/211] Taking wholesome food in appropriate quantity after complete digestion of previously eaten food helps to continue good health for long duration.[Cha.Sa.Chikitsa Sthana 15/214] It is observed that deficient quantity of food deteriorate the digestive capacity of agni and in absence of sufficient nutrients leads to malnourishment disorders and poor health status.

There are two ways to measure the quantity of food:

  1. Total quantity of food to be consumed in a meal (sarvagraha)
  2. Quantity of each food article in a meal (parigraha).

The inclusion of different food articles in a meal is to ascertain all the six rasas (tastes) in the required proportion. The nutritional requirement of everybody tissue is different. Proportionate quantity of six rasa will ensure the tissue requirement. The balanced diet concept of Ayurveda is essentially based of this principle. Imbalanced diet concerning six rasa leads to improper nourishment of body tissues, which further leads to depletion of body tissues (dhatu) [Cha. Sa.Sutra Sthana 5/4-Chakrapani]. Long-term exposure of imbalanced diet triggers wear and tear mechanism of tissues and may result in early senility.

Effects of excessive quantity of food

Excessive food triggers all three dosha vitiation as there is no space left for dosha functioning. Dosha are the main functional unit of human physiology. Dosha also govern the physiology of digestion. Samana vayu functions nearby the abode of digestive fire (jatharagni), kindles agni. Prana vayu and apana vayu supports the functions of agni. Pachaka pitta when devoid of its liquid property, functions as digestive fire.[A. Hr. Sutra Sthana 12/10-11][1] Kledaka kapha is responsible to moisten the ingested food. Thus the process of digestion is driven by dosha. Factors responsible for complete transformation and absorption of food(ahara parinamakara bhava) explain this phenomenon in-depth. [Cha.Sa.Sharira Sthana6/14],[Cha.Sa.Chikitsa Sthana 15/6-8]. The vitiated dosha leads to the formation of ama.

Excessive eating is one of the etiological factors for non-communicable diseases like obesity and diabetes mellitus which are more prevalent in society. Excess intake of calorie food which is not processed properly by digestive power (jatharagni) and further utilized by dhatvagni (type of agni present at tissue level) leads to obesity and related disorders.

Concept of ama

Causes of ama formation

This chapter provides details regarding causative factors of ama formation. Ama is unique concept of Ayurveda. It is the undigested and non-metabolized food material which remains inside the body and produces toxic effects. Quantity of food is considered as an important causative factor in formation of ama. Excessive as well as deficient quantity of food leads to ama formation. Along with quantity, if dietetic code and conduct are not followed it may leads to ama formation. Quality of food like heavy to digest and food with properties like dry, cold, dehydrated, disliked by the consumer, constipation-causing, causing a burning sensation, unclean, incompatible, and/or consumed untimely leads to ama formation.

Mental factors like food intake while the mind being afflicted with passion/desires, anger, greed, infatuation, envy, bashfulness, grief, conceit, excitement, and fear are also the cause of formation of ama. Any unwholesome food, even if taken in right quantity also leads to ama formation. An individual who regularly consumes an incompatible diet, multiple heavy meals (in short intervals) and eats even before the previous meal is digested, results in a clinical state of indigestion characterized by the manifestation of toxic symptoms termed as "ama visha". Some scholars opine that ama originate from highly vitiated dosha itself by their conjugation; as visha (aflatoxins) develops in (stored up, edible) kodo millet (kodrava). [A.Hr. Sutra Sthana 13/26][1] In recent years many non-communicable and metabolic disorders like obesity, diabetes, and thyroid dysfunction are prevalent in society due to indulgence of above factors leading to ama formation which triggers enormous pathological conditions. Various causal factors should be avoided by an individual to maintain the status agni and preserve health.

Nature of ama

The ama is termed as "ama visha" (clinical state of indigestion characterized by manifestation of toxic symptoms) because of resemblance of manifested symptoms to that of poisoning. It is considered incurable because of its acute presentation and contradictory line of management. Physicians describe two types of diseases caused by ama namely visuchika (cholera like symptoms) and alasaka (sluggish bowels). The ama which is formed due to weak digestive fire is heavy, liquid, different colored, unctuous, slimy, sticky, undigested, have fetid smell, continuous pain and considered as root cause of many diseases [Arundatta on A.Hr.Sutra Sthana 13/27].[1] This form of food will not be absorbed, gets associated with dosha leading to "saama dosha" (undigested food with vitiated dosha) condition.

Food if it is properly digested and metabolized by agni leads to proper tissue formation otherwise leads to poisonous state like ama formation. Due to various etiological factors deteriorated state of agni is unable to digest even the light food. [Cha.Sa.Chikitsa Sthana 15/43]. This vitiated digestive fire forms an intermediate substance called ama, which turns sour (shukta) during fermentation and finally turns in poisonous substance. (ama visha) [Cha.Sa.Chikitsa Sthana 15/44]

Symptoms produced due to ama

Following are symptoms produced by ama in various body systems and comprise symptoms of dosha associated with ama. [A.H. Sutra Sthana 13/23-24][1]

  • Obstruction of body channels (srotorodha)
  • loss of strength (balabramsha)
  • heaviness of body (gaurava)
  • laziness (alasya)
  • impaired activity of vata dosha (anila mudhata)
  • indigestion (apakti)
  • excessive salivation (nishthivana)
  • constipation and accumulation of wastes (mala sanga)
  • lack of taste (aruchi)
  • lethargy (klama).

The dosha and dushya (dhatu and mala) which are in liaison with ama are designated as "saama" i.e. mixed with ama. The diseases originating from these are termed as "saama diseases".

Disorders of ama

Two types of diseases caused by ama namely cholera-like symptoms (visuchika) and sluggish bowels (alasaka). A frail person having weak digestive power and aggravated kapha condition, even exerting pressure does not push the undigested food out of the passage since it is obstructed by kapha. This condition is called "alasaka". Taking food either in excess quantity or very little quantity is a type of "vishamashana" (a type of unhealthy dietary pattern). This leads to various ama disorders [Cha.Sa.Chikitsa Sthana 15/236].

Assessment of ama

The assessment of ama state is primarily done on the basis of clinical features of ama described above.

Stool mixed with ama (saama mala) sinks into the water due to heaviness property of ama; whereas stool without ama (pakva or niraama mala) floats over the water; provided the stools consistency is not watery or not very compact and if not vitiated by cold (sheeta) property of kapha. [Cha.Sa.Chikitsa Sthana 15/94] Patient should first be evaluated for presence or absence of ama and then appropriately be treated with pachana etc. treatment. [Cha.Sa.Chikitsa Sthana 15/94-95]

Management principles of ama

Ama is the preliminary cause for many disorders; hence the term ‘aamaya’ (means indigestion) is enlisted as the synonym of disease. [Chakrapani on Cha.Sa.Nidana Sthana 1/15] Physician should assess the status of agni and severity of ama before starting any treatment or therapeutic procedure. Treatment in 'saama' (presence of ama in pathogenesis of disease) and 'niraama' (absence of ama in pathogenesis) conditions are totally different.

Contraindication of shodhana in ama associated state

Saama dosha, which are spread all over the body, which remain latent/dissolved in tissues (dhatu) and are not dislodged from their sites, should not be expelled out by eliminative (shodhana) therapy. It can lead to destruction of the substratum, similar to the extraction of juice from an unripe fruit. [Cha.Sa.Chikitsa Sthana 3/147-149] Therapeutic elimination procedures should commence once person is free from ama state.

Primary treatment measures

Langhana (measures of fasting and lightness by removing wastes) and pachana (digestive therapy) is the foremost treatment used to treat ama disorders. [Cha.Sa.Chikitsa Sthana 15/95] Fasting helps to digest ama and kindles digestive fire. Absolute fasting or liquid light food is advised considering state of ama. Agni is responsible for digestion of food; kindled digestive fire in absence of food will digest increased dosha or remainant of ama in the body. [A. Hr. Chikitsa Sthana 10/91][1]

When the digestion of food is completed, but yet the patient experiences fullness and heaviness of the stomach, medicines are to be given which bring about the breakdown of the remaining dosha and increase digestive process. After langhana and pachana therapies, patient should be advised to follow special dictum of dietary regimen starting from thin gruel (peyadi sansarjana krama) to ignite digestive fire. Fasting reduces the aggravated dosha, kindles digestive power, restores appetite, and renders lightness to the body. Fasting should be performed to that extent which will not hamper the vitality or strength of an individual. The aim of all these measures is to regain the health which also depends on the physical, mental and spiritual well being. [Cha.Sa.Chikitsa Sthana 3/140-142]

Secondary treatment (in niraama state)

When patient is relieved from excessive morbidity of ama; the dosha are free from ama state (pakava avastha) and once digestive fire is kindled; oil embrocation (abhyanga), internal unction (snehapana), corrective and unctuous enema (asthapana and anuvasana types of basti) should be administered.

Emesis treatment

Due to impairment of agni, the ingested food will not be digested properly and this undigested food material is termed as ama anna. This ama, which is inert (alasaka), is to be expelled out by means of emesis with use of lukewarm saline water. If it is not achieved properly, use of strong emetics like Madanphala (randia dumetorum)), Pippali (Piper longum), Nagadanti (Croton oblongifolius Roxb) and paste of Siddharthaka (Brassica campestris Linn.) is advised. [A.S. Sutra Sthana 11/17]

Anal suppositories

After emesis, anal suppository play significant role to expel the feces and flatus and to restore the downward movement of apana vayu. Swedana (sudation therapy) is effective to remove obstruction and to pacify vata dosha.

Stimulation of digestion

After complete elimination of food toxins, to breakdown the remaining dosha and to ignite the digestive power, Hingvadi powder (compound formulation of herbs) and Mustadi decoction is effective. [A.S.Sutra Sthana 11/20-21]

Treatment of abdominal pain due to ama

A paste prepared from barley powder and yavakshar (alkali prepared from the ashes of burnt green barley-corns) mixed with butter milk is very effective to cure abdominal pain caused due to indigestion.

Cauterization (Agni karma)

Cauterization treatment on heels in case of visuchika : In severe cases of visuchika (indigestion with vomiting and diarrhea), cauterization on the heels is recommended. [A.S. Sutra Sthana 11/26]

Clinical assessment of complete digestion

The following features are observed after complete digestion and are applied for assessment for complete digestion.

  • Clear belching (udgar shuddhi)
  • Enthusiasm (utsaha)
  • Timely evacuation of feces and urine (vegotsarga)
  • Lightness of body (laghuta)
  • Natural feeling of hunger and thirst (kshut pipaasa)

This assessment is essential to know while treating indigestion.[A.S.Sutra Sthana 11/58]

Prevention of ama formation

The dietary guidelines (ahara vidhi) shall be strictly followed to prevent formation of ama. Taking food twice only in day is important measure to prevent formation of ama. Ayurveda prohibits the ingestion of food during night time. Hence, during day two meal times are suggested for health preservation. The ideal times are when the person feels hungry in the morning and evening before sunset. [Indu on A.S.Sutra Sthana 11/54] Bhavamishra advises to take food after three hours of sunrise for proper digestion suggest avoiding food past afternoon. The second meal can be taken before sunset. [B.P.Pradhama Khanda 4/115-116] It is advisable to consume that quantity of food which will be digested within twelve hours, without disturbing daily physical activities. Many efforts have been taken in biomedical science to unlock the complex mechanism underling this appetite science.

Depending on the predominance of afflicted dosha, four types of digestive patterns (jatharagni) are described:

  1. Samagni (Normal state of digestion and metabolism)
  2. Vishamagni (irregular state of digestion and metabolism)
  3. Tikshagni (rapid or intense state of digestion and metabolism)
  4. Mandagni (slow or weak state of digestion and metabolism).

The first type of normal digestion (samagni) needs 12 hours (4 yama) for complete digestion of food, and 6 hours (2 yama) for proper digestion of medicine. [A.S. Sutra Sthana 11/53]

Contemporary views and research updates

Understanding proper quantity of food (sauhitya matra) and physiological mechanism of satiation

Satiation is a process that leads to the termination of eating, which may be accompanied by a feeling of satisfaction. Proper quantity of food (sauhitya matra) means eat till the filling of satiety. This satiety term is further differentiated into two functionally different terminologies namely satiation and satiety. Benelam B defines Satiation as the process that leads to termination of eating, accompanied by feeling of satisfaction. This is also called as within meal satiety. Further he defines Satiety as the feeling of fullness that persists after eating, potentially suppressing further energy intake until hunger returns .[3]Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.[4]

Complex network of signals has been involved in development of satiation and satiety. Satiation and satiety involves mechanism which exert their effect through physiological and/or psychological processes. Satiation can modulate the size of meals consumed, controls how much to consume. The physiological mechanism, as outlined by Benelam B. has been referred along with current knowledge which will help to explicit the concept and support to develop objective parameters to asses proper quantity of food (Ahara Matra) –

1. Sensory and cognitive factors

Sensory and cognitive factors affect intake of food predominantly. Foods sensory properties like taste, smell, texture, appearance, and food type to be consumed affect satiation in the initial period. These sensory specific properties of food are linked with the sensory specific satiety. Sorensen LB et al have reviewed the multiple aspects related to sensory perception of food and their role in appetite regulation. Sensory-specific satiety has an important influence on the amount of food eaten. Palatability of food greatly influences appetite and food intake. Increase in food variety observed rise in quantity of food and energy intake. This study also reviewed standard procedure to test sensory-specific satiety and identified flavor, texture and appearance-specific satieties.

Variety in food and pleasantness of food to sensory organs increase the intake of food. De Graaf C et al concluded that pleasantness of food affect satiation but do not have significant effect on satiety. [5] [6]

The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food.[7] [8]. Study of Spetter M S et al shows that oral food ingestion evokes greater neural activation of brain signaling pathways specifically in the midbrain, amygdala, hypothalamus, and hippocampus area neural activity related to sensory-specific satiety.[9]

2. Gastric mechanism of satiation

a)Gastric distention: Stomach functions as key component in digestion. It acts as a reservoir of food. The reservoir capacity of the stomach allows it to increase its volume significantly. Its capacity limits the amount of food to be ingested. Stomach distention significantly controls the food intake and satiety.[10],[11] Geliebter A and team while assessing the changes in gastric capacity of obese patients determined the gastric capacity by oral insertion of a latex gastric balloon method.[12]In other works also this is used as a tool to assess the gastric capacity.[13]

b)Gastric and Intestinal Signals: In response to the food many gut peptides are secreted from enteroendocrine cells, which play essential role in regulating food. Steinert RE et al reveals that along with gastric distention, Gastric and intestinal signals (increased GLP-1 and PYY secretions and reduction in plasma ghrelin secretions) synergies to support satiation.[14]

Gut hormones such as cholecystokinin (CCK) and GLP-1, Oxyntomodulin (OXM), Peptide YY, Pancreatic polypeptide (PP) these are the important gut hormones involved in the mechanism of satiation, plays significant role in termination of meal. CCK is considered as potential biomarker for satiation.[15][16] Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.[17]

Leptin, insulin, and ghrelin act as long term regulators of appetite. These are long-acting adiposity hormones. While studying the role of leptin in prandial patterns, researchers observed that plasma leptin concentrations increase during a spontaneous intermeal interval and decline before the onset of a meal. Leptin works through regulation of hypothalamic feeding circuits. Through negative feedback mechanism leptin reduces food intake and regulates body weight homeostasis. Thus decreased leptin levels observed to stimulate appetite behavior. Leptin has an influential role in meal frequency and observed less responsible to control meal size.[18]

Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake.[19][20] Ghrelin secreted mainly from the gastric mucosa, its level are at their peak just before a meal, and decreased slowly when food nutrients are travelled into intestine. It acts on hippocampal neurons involved in spatial learning and memory, thus empty stomach passes signal to brain for asking to engage in appetite behavior, filling of hunger. Ghrelin as orexigenic factor promoted food intake and weight gain. Various cognitive components participate in the initiation of eating and in the selection of food. Schmid DA et al research findings suggest that along with stimulation of appetite, Ghrelin affects cognitive functions. They have noted vivid, plastic visualization of preferred meal by study subjects after administration of ghrelin.[21] Peptide YY has a suppressive effect on food intake.[22]PPY rise is observed in post prandial phase and are lowest in fasting state. Peripheral administration of PYY3e36 reduces food intake. PPY have shown effect on intestinal motility, delays gastric emptying.[23]

Signaling pathways involved in the mechanism of satiation

Food is considered the basic necessity for sustenance of life and attain physical stoutness [Cha.Sa.Sutra Sthana 25/40(1)]. Energy hemostasis depends on food we consume. Hypothalamus and brainstem are mainly involved to maintain the energy levels. The arcuate nucleus (ARC) of hypothalamus plays important role to control intake of food. ARC has orexigenic neurons (appetite stimulating) and anorexigenic neurons (appetite inhibiting). During digestion, food nutrients stimulate G-protein coupled receptor present on enteroendocrine cell, which stimulates release of gut hormone. Gut hormones influences the vagus nerve, hypothalamus and brainstem. Stimulating and inhibitory neurons present in hypothalamus interact with peripheral signals which results in alteration of eating drive. Vagal afferents stimulated by the gut hormone and sensitive to the stomach's mechanical stretch further connect with the nucleus of the brainstem. Brainstem passes neural signals to hypothalamus. Numerous hormonal and neural signals influence ARC nucleus, which projects to a number of regions including hypothalamic paraventricular nucleus where some essential energy regulating pathways arise.

Gastrointestinal track releases various peptide hormones. Stomach has its hormonal and neural control mechanism. Presence of food nutrients along with distention of stomach release gut hormones such as PPY, GLP-1, and oxyntomodulin (OXM).Theses are mainly responsible for phenomenon of satiation. These peptide, decreases hypothalamic orexigenic signaling and increases anorexigenic signaling. Negative feedback mechanism results due to these peptides also contribute to increase satiety between meals. Effect of these gut hormones in union with CNS effect results in satiation and satiety. The enteroendocrine cells released hormones interact at different brain levels through circulation and or through primary afferent neurons. Along with induction of satiation and meal termination, gut hormones also produce a positive feeling of reward and satisfaction.Nutrient sensors and their signaling to brain are vital to give feeling of satisfaction.[24] [25] [26]

D Chapelot has described subjective and objective tools for measuring meal size, microstructure of the meal, meal request and inter-meal intervals. A multidimensional approach for assessing satiety is proposed with intensity, duration and intake as main variables.[27] Commings DE have reviewed the interaction of gastric, intestinal, and pancreatic signals in food regulation. They have also discussed the important role of short acting GI factors and long-acting adiposity hormones in food intake regulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.[28]

Graaf CD et al have discussed various biomarkers of satiation and satiety and suggest there use as a tool to assess satiating efficiency of foods and energy balance. This study has also explained PET and fMRI techniques and referred many works that used these technologies to measure the brain responses to various stimuli in context of satiation.[29]

Satiety Cascade: Blundell JE and team developed a satiety cascade, referred as fundamental structure to examine the impact of food on satiation and satiety in future research.[30] [31]

The satiety quotient (SQ): GREEN SM et al developed a satiety quotient (SQ) to assess an eating episode's satiating effect. This is considered as a remarkable contribution in the field in quantifying satiating effects of foods. This quotient relates food intake with the rate of return of motivation to eat post ingestion, which is predictive of energy intake. Thus, for a person, the satiety quotient will vary based on weight, macronutrient composition, and energy density of food.[32]

Low satiety phenotype: ‘Low satiety phenotype’ is associated with specific behavioral and metabolic profiles that could explain their susceptibility to overeating. These individuals do not recognize their appetite sensation before and after meal. This is considered as an important step in individualized obesity treatment.[33]

Research tools to assess digestive processes (Jatharagni)

Wholesome diet is considered as the prime factor for nourishment and growth of a human being. Nourishing benefits of diet is subjected to the status of agni.Thus agni is an important facilitator between health and food. Assessment of the status of jatharagni is an essential component in maintenance of health as well as while treating diseased conditions. Singh A, Patwardhan K. et. al. have developed and validated a self-assessment tool to estimate Agnibala. The study also evaluates the practical utility of developed tool by recording serum lipid parameters. Lipid parameters vary significantly according to the status of [agni]]. [34]Eswaran H T et al have prepared an agni assessment scale with total 64 questions to evaluate the four types of nature of digestive fire (jatharagni). The study has validated the scale for internal consistency. Validation is essential for accuracy and reproducibility.[35] Patil VC, Baghel MS et. al. have developed formulae for assessment of the digestive function (agni) in during administration of snehana (internal oleation). [36] Agni performs various functions of digestion, metabolism and assimilation. Gastric secretions is a digestive fluid, formed in the stomach and contain numerous compounds including hydrochloric acid (HCL), pepsin, lipase, mucin. Kulatunga et al assessed the status of agni in the patients of pandu roga and find out its relationship with the acidity of gastric secretions by use of fractional test meal examination. Their study concluded that HCL reduction in patients of anemia seriously affects the protein and iron absorption; thus Hypochlohydria (found in 72.8% of the patients) indicates hypofunction of agni.[37]

Understanding links between mental health and gastrointestinal tract mediated through gut microbiota

The microbiome is the collective genome of all the microorganisms (bacteria, fungi, protozoa and viruses) living in a particular environment, especially living on and inside the human body. Microbiota is the community of microorganisms. Collective genome of various microorganisms of gastrointestinal (GI) tract, termed as gut microbiome.[38]

Gut microbiome plays a significant role in intestinal physiology and regulation. Gut microbiota produces microbial metabolites like short-chain fatty acids (SCFAs) mainly acetate, propionate, and butyrate; promotes local intestinal immunizations and systemic immunity .[39] [40]Gut microbiome has a regulatory role in behavior and cognition and it is exercised through gut-brain axis.[41]

Gut-Brain axis has bidirectional communication between central and enteric nervous system. It connects emotional and cognitive centers of brain to peripheral intestinal functions. By means of neural, endocrine, immune, and humoral links gut microbiota interact with GBA axis .[42]Marilia Carabotti et al in there review article have explored these interactions, as well as the possible pathophysiological mechanisms involved. Microbiota-gut-brain axis monitors and integrates gut functions and links emotional and cognitive centers of the brain with peripheral intestinal functions. This complex network includes central nervous system (CNS), the autonomic nervous system (ANS), the enteric nervous system (ENS) and the hypothalamic pituitary adrenal (HPA) axis. Central nervous system communicates with enteric nervous system (ENS), intestinal muscle layers and gut mucosa through various afferent and efferent autonomic pathways. Gastrointestinal wall connect with CNS through enteric, spinal and vagal efferent pathways. Limbic system which includes Amygdala (AMG), hippocampus (HIPP), and hypothalamus (HYP): predominantly responsible for memory and emotional responses. Hypothalamic pituitary adrenal (HPA) axis which is a part of limbic system activates in response to emotional stress and releases corticotropin-releasing factor (CRF) from the hypothalamus. CRF further stimulates adrenocorticotropic hormone (ACTH) secretion from the pituitary gland, causing the secretion of cortisol (main Stress hormone) from the adrenal glands. This hormone affects brain functions. Brain through neural communication influences various intestinal cell targets. The Gut microbiota also influences these same cells. Gut microbiota interact locally with intestinal cells and enteric nervous system (ENS), it also connect with central nervous system (CNS) through neuroendocrine and metabolic pathways.[43]

Review article of Clair R. Martin et al states that Gut microbes communicate to the central nervous system through at least 3 parallel and interacting channels involving nervous, endocrine, and immune signaling mechanisms. Based on preclinical and clinical evidence from various studies, scholars have concluded that brain by affecting community structure and functions of gut microbiota can modulate regional gut motility, intestinal transit and secretion, and gut permeability, and potentially through the luminal secretion of hormones that directly modulate microbial gene expression.[44]

Research validates the important role of brain and mental health in digestion and metabolism. Mental health is closely linked with gastrointestinal health. Emotions like stress, anxiety, mood swings may trigger stomach problems and gastrointestinal disturbances affect mental health.[45] [46] Probiotic consumption also has been reported to reduce self-reported feelings of sadness and aggressive thoughts.[47] Study of Sudo et al supports that the hyypothalamic–pituitary–adrenal (HPA) reaction to stress is influenced greatly by gut microbiota.[48] [49] [50]Based on extensive preclinical evidence and clinical observations showing bidirectional signaling pathways of BGM axis, Mayer et al proposed a systems biological model of bidirectional BGM interactions, which revalidate the impact of mental health on gastrointestinal health and vice versa.[51]

Insufficient/deficient quantity of food

Less quantity of food need be consider under two viewpoints: Total quantity of a meal (sarvagraha matra)) and quantity of each food item of a meal (parigraha matra). While serving different food articles in a meal (which is termed as parigraha matra) one must ascertain inclusion of all the six rasa (tastes) in required proportion.[Fig.3] Nutritional requirement of body tissues will be fulfilled by inclusion of all the six rasa (tastes) in desired proportion (Principle of shad rasa). Biomedical fundamentals of nutrition, macronutrients and micronutrients need to be studied in correlation with Six Rasa principle to offer better nutritional solutions to the society.

Fig.3: Deficiency of food

Malnutrition generally implies undernutrition but also includes other deviations like energy undernutrition and over-nutrition. Malnutrition starts due to deficiencies of specific nutrients or from diets based on inadequate and or inappropriate combinations or proportions of foods. Undernutrition is caused primarily due to an inadequate intake of dietary energy. The impact of a deficient diet on an individual is mainly depending on age factor. Age reflects the condition of body tissues. Body tissues (dhatu) attain different stages form immature growing state of childhood, to the attainment of all the qualities and strength of body tissues in young age, which further slowly enters the state of depletion in old age. Nutritional requirement of body tissues differs according to age. Considering the age of a person, consequences arise due to inadequate diet is discussed under two categories- a) Childhood age b) Adult age.

World health organization explains the malnutrition phenomenon of childhood age under four categories: Stunting, Wasting and overweight and underweight.[52] [53]

1.Stunting (height-for-age below –2 SD) refers to a child who is too short for his or her age. It is the devastating result of poor nutrition during early childhood. These children fell to attain complete possible height. It also hampers cognitive development.

2.Wasting (weight-for-height below –2SD) refers to a too thin child for his or her height. It results due to poor nutrient intake. Children suffering from wasting have weakened immunity, suffers long term developmental delay.

3.Childhood overweight (weight-for-height above +2SD )and obesity are considered an emerging face of malnutrition, resulting in unhealthy, processed food. In later life this increases the risk for diet related non communicable diseases.

4.Underweight (refers weight-for-age below –2SD)

Determinants of under nutrition

Faustin Habyarimana found key determinants of malnutrition of children below five years of age: age, gender, birth weights, mother’s knowledge of nutrition, birth order, incidence of recent fever, multiple pregnancies, education level of the mother, age of the mother at childbirth, body mass index, prevalence of anemia, province, source of drinking water and wealth quintiles. A positive correlation between stunting and underweight and wasting and underweight was also found.[54]

Consequences of under-nutrition: The consequences of poor nutrition include impaired growth, poor cognitive and social development, poor school performance, increased risk of morbidity and mortality and reduced productivity later in life.[55] Malnutrition in children’s by impacting cognitive functions, further impend individuals’ ability to lead productive lives and thus contribute to poverty.

Under-nutrition in adults: Under-nutrition in adults can be correlated with the etiopathogenesis of Karshya described in Ayurveda classics. Undernourishment may be caused by the lack of one or more nutrients (under‐nutrition), or an excess of nutrients (over‐nutrition). Physiological changes associated with the process of ageing may further support malnutrition.[56] [57]

Determinants: Hickson M has Categorized the causes of malnutrition under three category as medical factors (like poor appetite, physical disability, endocrine disorders etc), lifestyle and social factors (lack of knowledge of nutrition, loneliness, povery etc.) and psychological factors.[58]

Morley JE has enumerated the major causes of malnutrition as lack of food, paranoia, emotional factors (like depression), inappropriate dieting, anorexia, problem with feeding (tremors, dementia, functional impairment, and dysphagia), Enteral problems (e.g., gluten enteropathy), Wandering and other dementia related factors and malabsorption.[59]

Old age persons are at high risk of developing protein-energy malnutrition. It affects health, cognitive and physical functions as well as quality of life. Study concludes that increasing age, unmarried/separated/divorced status, difficulties walking 100 m, climbing stairs and hospitalization, cognitive impairment or receiving social support are the major predictors of malnutrition.[60]

Shetty P has validated scoring systems such as MUST, which indicates patients at risk of malnutrition. BMI less than 18.5 kg/m2 is a sign of undernutrition. Laboratory investigations like hemoglobin or packed cell volume (indicators of anemia, hydration), blood urea (indicating hydration and protein intake), C-reactive protein and ESR (inflammatory pathology), total lymphocyte count (for immune function) are also suggested to aid early diagnosis.[61]Donini LM et al developed and validated a screening tool for the easy detection and reporting of both undernutrition and over-nutrition, two types of malnutrition.[62] A systematic review to evaluate malnutrition biomarkers among older adults, concluded that BMI, hemoglobin, and total cholesterol are useful biomarkers of malnutrition in older adults.[63]

Consequences : Malnutrition in adults is greatly associated with risk of sarcopenia, frailty, falls, dependence in activities, respiratory muscle wasting, effects musculoskeletal system, experience metabolic changes in cellular electrolytes including calcium accumulation, reduced resistance to infection, poor functioning of excretory systems, longer hospital stay, poor response to other medical conditions. Sarcopenia is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength and it is strictly correlated with physical disability, poor quality of life and death.[64]Cachexia is a multifactorial syndrome with involuntary progressive weight loss as a result of reduction of skeletal muscle mass with or without depletion of adipose tissue.[65]Frailty is a common clinical syndrome in older adults and is associated with poor health outcomes including falls, disability, hospitalization, decline in functions of various physiological systems and mortality.[66]

Treatment strategies

Provide dietary solutions considering Guts changes of the elderly.[67]

Manipulation in energy / nutritive density of food.[68]

  • Changes in hedonic pattern (taste, flavor, appearance) of foods.
  • Provide healthy environment to support emotional quotient.
  • Provide feeding assistance.
  • Give motivation for physical activities.[69]
  • Adopt interdisciplinary approach like inclusion of Yoga techniques to improve mental health.[70]

Contemporary views and research updates on ama

Ama is an important principle to understand the etiopathogenesis of all disorders and to decide the treatment modalities. Agni is the digestive and metabolic fire which is responsible for any transformation in body. Transformation of food material predominantly takes place at the level of gastrointestinal tract (grahani-seat of jathragni) and at the level of tissues (dhatvagni-abodes of dhatu). Dysfunction of agni results into undigested or partly digested intermediator product called as ama. Ama act as toxic element and form the basis for many pathological conditions. It can be considered raw, uncooked, unripe, immature, undigested or incompletely oxidized / metabolized or similar to a poisonous substance that disrupts body physiology. Accumulation of metabolic waste (mala) may takes place at various levels in body physiology. The amalgamation of aggravated dosha with metabolic waste results in ama formation, which is considered the initial stage of disease formation. Origin of ama is mainly considered from gastrointestinal tract (amashaya). Agni functions at different levels; hence, ama can be formed at different levels at different body sites. Forms of agni - jatharagni, bhutagni and dhatvagni functions at different level hence any impairment at the corresponding level leads to ama formation.

Digestion process starts from mouth where mechanical and chemical digestion of food takes place. Thinking, smelling and seeing food secrets saliva, helps in digestion. Component of saliva like water, mucus, electrolytes and enzymes has a unique function. Starch breakdown starts here due to the enzyme in saliva called salivary amylase. Mucus lubricates the food and helps in the formation of bolus in mouth. Small food particles are dissolved by saliva and it makes dry food moist enough to swallow comfortably. If person is not following dietary codes, eating hurriedly without proper mastication, disturbed mental health while taking food will affect this cephalic phase of digestion. It will lead to ama formation due to improper digestion process in mouth. Mastication of food is subjected to condition of teeth. Studies have attempted to find a correlation between tooth loss and nutrition. Deteriorated dental health affects mechanical digestion process and leads to nutritional deficiency.[71] Another study observed that modifying the mastication rate alters the glycemic index of rice. Its glycemic index classification shows impact of digestion process on the final outcome of food.[72]

Health of a person is essentially dependents on healthy gut. Mucosal integrity is more important for proper absorption of nutrient from villi. The intestines also play an essential role in protecting the body from harmful bacteria and toxins. If mucosal integrity is hampered it results into leaky gut syndrome. It affects the lining of intestinal mucosa leading to bacteria and other toxins to pass into the bloodstream. It also leads to the imbalance of gut microbiome.[73]

This gut leakage and dysbiosis leads to gut inflammation, also disrupt an immune homeostasis. It causes systemic immune activation, neurological disturbances and auto immune diseases. All these predisposing conditions cause ama formation which triggers many complex pathological conditions, act as route cause for many diseases.[74]

Formation of ama occurs at the level of tissues or cellular level due to impaired metabolism or due to free radical activity. Free radicals are highly reactive atom or molecule which is having one or more unpaired electrons. It always tries to have stability by giving its electron or by acquiring extra electron form adjacent molecules. After providing the electron adjacent molecule becomes unstable and acts as a free radical, a chain reaction sets in to damage many molecules. A higher concentration of free radicals causes damage to the cellular structure like DNA, protein, lipid, and other cell parts. It causes disturbance in homeostasis of body leading to disease condition.[75]

Ama formation occurs due to the accumulation of toxic or intermediate product of metabolism in the body termed as mala. These intermediate products are formed due to defect in the metabolism of protein, carbohydrate or lipid. Excessive uric acid is formed due to improper metabolism of protein which is hazardous to body tissue and joint structure. Lactic acid, acetone and ketone bodies are formed due to improper metabolism of carbohydrate and fats. Lack of insulin activity defunct carbohydrate metabolism and leads to formation of intermediate products in the body. This intermediate products act as ama and leads to many disease conditions.

Metabolic waste functions as ama: Tissue nutrients after action of metabolism (dhatvagni) nourishes body tissues and part is formed as excretory product (mala). Accumulation of this metabolic waste beyond certain limits disrupts the dosha hemostasis, leads to formation of ama. Depending on the type of metabolic waste and predominance of doshas exhibits many diseases.

Research theses done (M.D./Ph.D. works)

  1. Badeka B.P.(1964 ) : Aam vivechan. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  2. Singh A. K. (1986) : Ama Vivecana. National Institute of Ayurveda,Jaipur.
  3. Ramesh Babu D (1989) : A critical study of Āma and its possible biological correlation with reference to the effect of Pancakola Kashaya in their management. Faculty of Ayurveda, I.M.S.,B.H.U., Varanasi.
  4. Smart Rachana (1996) : A .Concept of Dhatugata Āma and principles of management. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  5. Bishnupriya Mohanty( 2001): Concept of Manobhighatakara Bhavas on Āma Utpatti particular to Madhumeha (DM). Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  6. Gaurav sharma (2001) : Ama-Free radical-Amavaat. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  7. Smita Choradiya(2002) : Aharvidhi vidhaan-Annavah and purishvah srotas-Tanmana bhunjit. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  8. Anuradha Aggrawaal(2004) :Aharmatara atur bala. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  9. Mihir Vaja(2005) : Trividhakukshiya viman-Amotpatti. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  10. Manish Dhanani(2005) : Kale cha arabhate karma yat tat sadhyayati dhruvam in the context of Jatharagnimandya,Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  11. Rohit Dangayaych(2008) : Ahar in relation to Matra,desh,Kala and effect on health. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  12. Sangita More(2009) : Bhashaj Agnideepan. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar.
  13. Kishor G.satani.(2011) : An applied study of interrelationship of jatharagni and dhatvagni in context to dhatuvriddhi. Institute for Post Graduate Teaching & Research in Ayurveda, Gujarat Ayurved University, Jamnagar .


  • Cha. Sa.: Charak Samhita
  • A.Hr.: Ashtanga Hridaya
  • A.S.: Ashtanga Sngraha
  • B.P.: Bhava Prakasha

Related chapters


  1. 1.0 1.1 1.2 1.3 1.4 1.5 Vagbhata. Ashtanga Hridayam. Edited by Harishastri Paradkar Vaidya. 1st ed. Varanasi: Krishnadas Academy;2000.
  2. Bhavamishra. Bhavaprakasha -Volume I. Translated from Sanskrit by K.R. Srikantha Murthy. 1st ed. Varanasi: Krishnadas academy;2000.
  3. Benelam B. Satiation, Satiety and their effects on eating behavior. Nutrition Bulletin. London UK. British Nutrition Foundation. May 2009;34(2):126–173.
  4. Sørensen LB, Møller P, Flint A, Martens M, Raben A. Effect of sensory perception of foods on appetite and food intake: a review of studies on humans. Int J Obes Relat Metab Disord. 2003;27(10):1152-1166. doi:10.1038/sj.ijo.0802391
  5. De Graaf C, De Jong LS, Lambers AC. Palatability affects satiation but not satiety. Physiol Behav. 1999;66(4):681-688. doi:10.1016/s0031-9384(98)00335-7
  6. Raynor HA, Epstein LH. Dietary variety, energy regulation, and obesity. Psychol Bull. 2001;127(3):325-341. doi:10.1037/0033-2909.127.3.325
  7. Rolls ET, Rolls BJ, Rowe EA. Sensory-specific and motivation-specific satiety for the sight and taste of food and water in man. Physiol Behav. 1983;30(2):185-192. doi:10.1016/0031-9384(83)90003-3
  8. Rolls BJ, Van Duijvenvoorde PM, Rolls ET. Pleasantness changes and food intake in a varied four-course meal. Appetite. 1984;5(4):337-348. doi:10.1016/s0195-6663(84)80006-9
  9. Spetter M S, de Graaf C, Mars M, Viergever MA, Smeets PAM . The sum of its parts—effects of gastric distention, nutrient content and sensory stimulation on brain activation. PLoS ONE. 2014; 9(3): e90872: doi:10.1371/journal.pone.0090872
  10. Geliebter A, Hashim SA. Gastric capacity in normal, obese, and bulimic women [published correction appears in Physiol Behav 2002 Mar;75(3):433]. Physiol Behav. 2001;74(4-5):743-746. doi:10.1016/s0031-9384(01)00619-9
  11. Geliebter A. Gastric distension and gastric capacity in relation to food intake in humans. Physiol Behav. 1988;44(4-5):665-668. doi:10.1016/0031-9384(88)90333-2
  12. Geliebter A, Schachter S, Lohmann-Walter C, Feldman H, Hashim SA. Reduced stomach capacity in obese subjects after dieting. Am J Clin Nutr. 1996;63(2):170-173. doi:10.1093/ajcn/63.2.170
  13. Tate CM, Geliebter A. Intragastric Balloon Treatment for Obesity: Review of Recent Studies. Adv Ther 34, 1859–1875 (2017).
  14. Steinert RE, Meyer-Gerspach AC, Beglinger C. The role of the stomach in the control of appetite and the secretion of satiation peptides. Am J Physiol Endocrinol Metab. 2012 Mar 15;302(6):E666-73. doi: 10.1152/ajpendo.00457.2011. Epub 2012 Jan 3. PMID: 22215654.
  15. Melton PM, Kissileff HR, Pi-Sunyer FX. Cholecystokinin (CCK-8) affects gastric pressure and ratings of hunger and fullness in women. Am J Physiol. 1992;263(2 Pt 2):R452-R456. doi:10.1152/ajpregu.1992.263.2.R452
  16. Shah M, Vella A. Effects of GLP-1 on appetite and weight. Rev Endocr Metab Disord. 2014;15(3):181-187. doi:10.1007/s11154-014-9289-5
  17. Sam AH, Troke RC, Tan TM, Bewick GA. The role of the gut/brain axis in modulating food intake. Neuropharmacology. 2012;63(1):46-56.doi:10.1016/j.neuropharm.2011.10.008
  18. Chapelot D, Aubert R, Marmonier C, Chabert M, Louis-Sylvestre J. An endocrine and metabolic definition of the intermeal interval in humans: evidence for a role of leptin on the prandial pattern through fatty acid disposal. Am J Clin Nutr. 2000 Aug;72(2):421-31. doi: 10.1093/ajcn/72.2.421. PMID: 10919937.
  19. Wren AM, Seal LJ, Cohen MA, et al. Ghrelin enhances appetite and increases food intake in humans. J Clin Endocrinol Metab. 2001;86(12):5992. doi:10.1210/jcem.86.12.8111
  20. Kalra SP, Bagnasco M, Otukonyong EE, Dube MG, Kalra PS. Rhythmic, reciprocal ghrelin and leptin signaling: new insight in the development of obesity. Regul Pept. 2003;111(1-3):1-11. doi:10.1016/s0167-0115(02)00305-1
  21. Schmid DA, Held K, Ising M, Uhr M, Weikel JC, & Steiger A (2005). Ghrelin Stimulates Appetite, Imagination of Food, GH, ACTH, and Cortisol, but does not Affect Leptin in Normal Controls. Neuropsychopharmacology, 30(6), 1187–1192.
  22. Jones ES, Nunn N, Chambers AP, Østergaard S, Wulff BS, Luckman SM. Modified Peptide YY Molecule Attenuates the Activity of NPY/AgRP Neurons and Reduces Food Intake in Male Mice. Endocrinology. 2019 Nov 1;160(11):2737-2747. doi: 10.1210/en.2019-00100. PMID: 31074796; PMCID: PMC6806261.
  23. Asakawa A, Inui A, Yuzuriha H, Ueno N, Katsuura G, Fujimiya M, Fujino MA, Niijima A, Meguid MM, Kasuga M. Characterization of the effects of pancreatic polypeptide in the regulation of energy balance. Gastroenterology. 2003 May;124(5):1325-36. doi: 10.1016/s0016-5085(03)00216-6. PMID: 12730873.
  24. Sam AH, Troke RC, Tan TM, Bewick GA. The role of the gut/brain axis in modulating food intake. Neuropharmacology. 2012 Jul;63(1):46-56. doi: 10.1016/j.neuropharm.2011.10.008. Epub 2011 Oct 21. PMID: 22037149
  25. Murphy KG, Bloom SR. Gut hormones and the regulation of energy homeostasis. Nature. 2006 Dec 14;444(7121):854-9. doi: 10.1038/nature05484. PMID: 17167473.
  26. Berthoud HR. Vagal and hormonal gut-brain communication: from satiation to satisfaction. Neurogastroenterol Motil. 2008;20 Suppl 1(0 1):64-72. doi:10.1111/j.1365-2982.2008.01104.
  27. Chapelot D. Quantifying satiation and satiety. In: Blundell JE, Bellisle F, ed. Satiation, Satiety and the Control of Food Intake:Woodhead Publishing Series in Food Science, Technology and Nutrition; 2013:Pages12-39.
  28. Powley TL, Phillips RJ. Gastric satiation is volumetric, intestinal satiation is nutritive. Physiol Behav. 2004 Aug;82(1):69-74. doi: 10.1016/j.physbeh.2004.04.037. PMID: 15234593.
  29. de Graaf C, Blom WA, Smeets PA, Stafleu A, Hendriks HF. Biomarkers of satiation and satiety. Am J Clin Nutr. 2004 Jun;79(6):946-61. doi: 10.1093/ajcn/79.6.946. PMID: 15159223.
  30. Blundell JE, Rogers PJ, Hill AJ. Evaluating the satiating power of foods: Implications for acceptance and consumption. In: Solms J, Booth DA, Pangbourne RM, Raunhardt O, editors. Food Acceptance and Nutrition. Academic Press; London: 1987. pp. 205–219.
  31. Blundell J, de Graaf C, Hulshof T, et al. Appetite control: methodological aspects of the evaluation of foods. Obes Rev. 2010;11(3):251-270. doi:10.1111/j.1467-789X.2010.00714.
  32. Green SM, Delargy HJ, Joanes D, Blundell JE. A satiety quotient: a formulation to assess the satiating effect of food. Appetite. 1997 Dec;29(3):291-304. doi: 10.1006/appe.1997.0096. PMID: 9468762.
  33. DrapeauV, Gallant A.The low satiety phenotype. In: Blundell JE, Bellisle F, ed. Satiation, Satiety and the Control of Food Intake: Woodhead Publishing Series in Food Science, Technology and Nutrition; 2013:Pages 273–297.
  34. Singh A, Singh G, Patwardhan K, Gehlot S. Development, Validation and Verification of a Self-Assessment Tool to Estimate Agnibala (Digestive Strength). J Evid Based Complementary Altern Med. 2017 Jan;22(1):134-140. doi: 10.1177/2156587216656117. Epub 2016 Jul 4.
  35. Eswaran HT, Kavita MB, Tripaty TB, and Shivakumar. Formation and validation of questionnaire to assess Jāṭharāgni. Anc Sci Life.2015 Apr-Jun; 34(4): 203–209.
  36. Patil VC, Baghel MS, Thakar AB. Assessment of agni (digestive process) and koshtha (bowel movement with special reference to abhyantara snehana (internal oleation). Ancient Sci. Life. 2008; 28:26-28
  37. Kulatunga R D H, Rai N P, Ali Z. Status of Agni in Pandu Roga (anemia) and its association with the acidity of gastric secretions-A Clinical Study. IAMJ: Volume 7, Issue 1, January – 2019.
  38. Valdes AM, Walter J, Segal E, Spector TD. Role of the gut microbiota in nutrition and health. BMJ. 2018 Jun 13;361:k2179. doi: 10.1136/bmj.k2179. PMID: 29899036; PMCID: PMC6000740.
  39. Yoon MY, Lee K, Yoon SS. Erratum to: Protective role of gut commensal microbes against intestinal infections. J Microbiol. 2015 Jan;53(1):90. doi: 10.1007/s12275-015-0705-7. Erratum for: J Microbiol. 2014 Dec;52(12):983-9. Yoon, My Young [corrected to Yoon, Mi Young]. PMID: 25557484.
  40. Zhang H, Sparks JB, Karyala SV, Settlage R, Luo XM. Host adaptive immunity alters gut microbiota. ISME J. 2015 Mar;9(3):770-81. doi: 10.1038/ismej.2014.165. Epub 2014 Sep 12. PMID: 25216087; PMCID: PMC4331585.
  41. Mohajeri MH, Brummer RJM, Rastall RA, Weersma RK, Harmsen HJM, Faas M, Eggersdorfer M. The role of the microbiome for human health: from basic science to clinical applications. Eur J Nutr. 2018 May;57(Suppl 1):1-14. doi: 10.1007/s00394-018-1703-4. PMID: 29748817; PMCID:PMC5962619.
  42. Moloney RD, Desbonnet L, Clarke G, Dinan TG, Cryan JF. The microbiome: stress, health and disease. Mamm Genome. 2014 Feb; 25(1-2):49-74. doi: 10.1007/s00335-013-9488-5. Epub 2013 Nov 27.
  43. Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol. 2015 Apr-Jun;28(2):203-209. PMID: 25830558; PMCID:PMC4367209.,microbiota%20in%20influencing%20these%20interactions.
  44. Martin CR, Osadchiy V, Kalani A, Mayer EA. The Brain-Gut-Microbiome Axis. Cell Mol Gastroenterol Hepatol. 2018 Apr 12;6(2):133-148. doi: 10.1016/j.jcmgh.2018.04.003. PMID: 30023410; PMCID: PMC6047317.
  45. Park AJ, Collins J, Blennerhassett PA, Ghia JE, Verdu EF, Bercik P, Collins SM. Altered colonic function and microbiota profile in a mouse model of chronic depression. Neurogastroenterol Motil. 2013 Sep;25(9):733-e575. doi: 10.1111/nmo.12153. Epub 2013 Jun 17. PMID: 23773726; PMCID: PMC3912902.
  46. Washabau, R. J. (2013). Chapter 41 - Antispasmodic Agents (R. J. Washabau & M. J. B. T.-C. and F. G. Day (eds.); pp. 481–485). W.B. Saunders.
  47. Steenbergen L, Sellaro R, van Hemert S, Bosch JA, Colzato LS. A randomized controlled trial to test the effect of multispecies probiotics on cognitive reactivity to sad mood. Brain Behav Immun. 2015 Aug;48:258-64. doi: 10.1016/j.bbi.2015.04.003. Epub 2015 Apr 7. PMID: 25862297.
  48. Sudo N, Chida Y, Aiba Y, Sonoda J, Oyama N, Yu XN, Kubo C, Koga Y. Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. J Physiol. 2004 Jul 1;558(Pt 1):263-75. doi: 10.1113/jphysiol.2004.063388. Epub 2004 May 7. PMID: 15133062; PMCID: PMC1664925.
  49. Bowey E, Adlercreutz H, Rowland I. Metabolism of isoflavones and lignans by the gut microflora: a study in germ-free and human flora associated rats. Food Chem Toxicol. 2003 May;41(5):631-6. doi: 10.1016/s0278-6915(02)00324-1. PMID: 12659715.
  50. Pinto-Sanchez MI, Hall GB, Ghajar K, Nardelli A, Bolino C, Lau JT, Martin FP, Cominetti O, Welsh C, Rieder A, Traynor J, Gregory C, De Palma G, Pigrau M, Ford AC, Macri J, Berger B, Bergonzelli G, Surette MG, Collins SM, Moayyedi P, Bercik P. Probiotic Bifidobacterium longum NCC3001 Reduces Depression Scores and Alters Brain Activity: A Pilot Study in Patients With Irritable Bowel Syndrome. Gastroenterology. 2017 Aug;153(2):448-459.e8. doi: 10.1053/j.gastro.2017.05.003. Epub 2017 May 5. PMID: 28483500.
  51. Mayer EA, Labus JS, Tillisch K, Cole SW, Baldi P. Towards a systems view of IBS. Nat Rev Gastroenterol Hepatol. 2015 Oct;12(10):592-605. doi: 10.1038/nrgastro.2015.121. Epub 2015 Aug 25. PMID: 26303675; PMCID: PMC5001844.
  52. United Nations Children’s Fund, World Health Organization, World Bank Group. Levels and trends in child malnutrition: Key findings of the 2012 Edition of the Joint Child Malnutrition Estimates. United Nations Children’s Fund; 2012.
  53. United Nations Children’s Fund, World Health Organization, World Bank Group. Levels and trends in child malnutrition: Key findings of the 2018 Edition of the Joint Child Malnutrition Estimates. United Nations Children’s Fund; 2018.
  54. F. Habyarimana , T. Zewotir , S. Ramroop. Key determinants of malnutrition of children under five years of age in Rwanda: Simultaneous measurement of three anthropometric indices. African Population Studies. Vol. 30, No. 2, 2016
  55. Boah M, Azupogo F, Amporfro DA, Abada LA. The epidemiology of undernutrition and its determinants in children under five years in Ghana. PLoS One. 2019 Jul 31;14(7):e0219665. doi: 10.1371/journal.pone.0219665. PMID: 31365528; PMCID: PMC6668784.
  56. Guyonnet S, Rolland Y. Screening for Malnutrition in Older People. Clin Geriatr Med. 2015 Aug;31(3):429-37. doi: 10.1016/j.cger.2015.04.009. Epub 2015 May 13. PMID: 26195101.
  57. Elia M. Defining, Recognizing, and Reporting Malnutrition. Int J Low Extrem Wounds. 2017 Dec;16(4):230-237. doi: 10.1177/1534734617733902. Epub 2017 Nov 16. PMID: 29145755.
  58. Hickson M. Malnutrition and ageing. Postgrad Med J. 2006;82(963):2-8. doi: 10.1136/ pgmj .2005.037564
  59. Morley JE. Editorial: Defining Undernutrition (Malnutrition) in Older Persons. J Nutr Health Aging. 2018;22(3):308-310. doi: 10.1007/s12603-017-0991-3. PMID: 29484342.
  60. Corish CA, Bardon LA. Malnutrition in older adults: screening and determinants. Proc Nutr Soc. 2019 Aug;78(3):372-379. doi: 10.1017/S0029665118002628. Epub 2018 Dec 3. PMID: 30501651.
  61. Shetty, P. (2006). Malnutrition and undernutrition. Medicine, 34(12), 524–529.
  62. Donini LM, Ricciardi, L. M., Neri, B., Lenzi, A., & Marchesini, G. (2014). Risk of malnutrition (over and under-nutrition): Validation of the JaNuS screening tool. Clinical Nutrition, 33(6), 1087–1094.
  63. Zhang Z, Pereira SL, Luo M, Matheson EM. Evaluation of blood biomarkers associated with risk of malnutrition in older adults: A Systematic Review and Meta-Analysis. Nutrients. 2017 Aug 3;9(8):829. doi: 10.3390/nu9080829. PMID: 28771192; PMCID: PMC5579622
  64. Santilli V, Bernetti A, Mangone M, Paoloni M. Clinical definition of sarcopenia. Clin Cases Miner Bone Metab. 2014;11(3):177-180
  65. Vanhoutte G, van de Wiel M, Wouters K, et al. Cachexia in cancer: what is in the definition?. BMJ Open Gastroenterol. 2016;3(1):e000097. Published 2016 Oct 18. doi:10.1136/bmjgast-2016-000097
  66. Xue QL. The frailty syndrome: definition and natural history. Clin Geriatr Med. 2011;27(1):1-15. doi:10.1016/j.cger.2010.08.009
  67. Rémond D, Shahar DR, Gille D, et al. Understanding the gastrointestinal tract of the elderly to develop dietary solutions that prevent malnutrition. Oncotarget. 2015;6(16):13858-13898. doi:10.18632/oncotarget.4030
  68. Volkert D, Beck AM, Cederholm T, Cruz-Jentoft A, Goisser S, Hooper L, Kiesswetter E, Maggio M, Raynaud-Simon A, Sieber CC, Sobotka L, van Asselt D, Wirth R, Bischoff SC. ESPEN guideline on clinical nutrition and hydration in geriatrics. Clin Nutr. 2019 Feb;38(1):10-47. doi: 10.1016/j.clnu.2018.05.024. Epub 2018 Jun 18. PMID: 30005900.
  69. Hébuterne X, Bermon S, Schneider SM. Ageing and muscle: the effects of malnutrition, re-nutrition, and physical exercise. Curr Opin Clin Nutr Metab Care. 2001 Jul;4(4):295-300. doi: 10.1097/00075197-200107000-00009. PMID: 11458024.
  70. Baldwin C, Kimber KL, Gibbs M, Weekes CE. Supportive interventions for enhancing dietary intake in malnourished or nutritionally at-risk adults. Cochrane Database Syst Rev. 2016;12(12):CD009840. Published 2016 Dec 20. doi:10.1002/14651858.CD009840.pub2.
  71. Najeeb S, Zafar MS, Khurshid Z, Zohaib S, Almas K. The role of nutrition in periodontal health: An Update. Nutrients. 2016 Aug 30;8(9):530. doi: 10.3390/nu8090530. PMID: 27589794; PMCID: PMC5037517.
  72. Ranawana, V., Leow, M. K.-S., & Henry, C. J. K. (2014). Mastication effects on the glycemic index: impact on variability and practical implications. European Journal of Clinical Nutrition, 68(1), 137–139.
  73. Gerwyn Morris, Michael Berk, André F. Carvalho, Javier R. Caso, Yolanda Sanz and Michael Maes, “The Role of Microbiota and Intestinal Permeability in the Pathophysiology of Autoimmune and Neuroimmune Processes with an Emphasis on Inflammatory Bowel Disease Type 1 Diabetes and Chronic Fatigue Syndrome”, Current Pharmaceutical Design (2016) 22: 6058.
  74. Sharma H. Leaky Gut Syndrome, Dysbiosis, Ama, Free Radicals, and Natural Antioxidants. AYU. 2009; 30 (2): 88-105.
  75. Sharma GN, Gupta G, Sharma P. A Comprehensive Review of Free Radicals, Antioxidants, and Their Relationship with Human Ailments. Crit Rev Eukaryot Gene Expr. 2018;28(2):139-154. doi:10.1615/CritRevEukaryotGeneExpr.2018022258