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Chapters for further reading –
 
Chapters for further reading –
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[[. Matrashiteeya Adhyaya]]
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1. Charak Samhita sutrasthan Chapter 5- Matrashiteeya Adhyaya
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[[ Yajjah Purushiya Adhyaya]]
2. Charak Samhita sutrasthan Chapter 25- Yajjah Purushiya Adhyaya
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3. Charak Samhita Vimansthan Chapter 1- Rasa Vimana
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[[Rasa Vimana]]
4. Charak Samhita Sharirsthan Chapter 6- Sharira Vichaya Sharira
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5. Charak Samhita Chikitsasthan Chapter 15- Grahani Chikitsa.
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[[Sharira Vichaya Sharira]]
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[[Grahani Chikitsa]]
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'''CONTEMPORARY VIEWS AND RESEARCH UPDATES-'''
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Understanding proper quantity of food (Sauhitya Matra): physiological mechanism of satiation-
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The process that leads to the termination of eating, which may be accompanied by a feeling of satisfaction.
 +
 
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Two times of meal is appreciated by ancient scientists: at the start of the day and before sunset. 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.
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Proper quantity of food is considered as 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 .Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.  
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Abbreviations-
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1. Cha.Sa.Su. – Charak Samhita Sutrasthan
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2. Cha.Sa.Ni.- Charak Samhita Nidansthan
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3. Cha.Sa.Vi.- Charak Samhita Vimansthan
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4. Cha.Sa.Sha.- Charak Samhita Sharirsthan
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5. Cha.Sa.Chi.- Charak Samhita Chikitsasthan
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6. A.H.Su.- Ashtang Hriday Sutrasthan
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7. A.H.Chi.- Ashtang Hriday Chikitsasthan
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8. A.S.Sha.- Ashtang Hriday Sharirsthan
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9. A.S.Su. – Ashtang Sangrah Sutrasthan
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10. Bh.Pr.Pra.Kh.- Bhava Prakash Pratham Khand
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CONTEMPORARY VIEWS AND RESEARCH UPDATES-
  −
Understanding proper quantity of food (Sauhitya Matra): physiological mechanism of satiation-
  −
The process that leads to the termination
  −
of eating, which may be accompanied by
  −
a feeling of satisfactio
  −
The process that leads to the termination
  −
of eating, which may be accompanied by
  −
a feeling of satisfactio
  −
Two times of meal is appreciated by ancient scientist: at the start of the day and before sunset. 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.
  −
Proper quantity of food is considered as 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 . Sørensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode .
   
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) –
 
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. Sørensen 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.  
 
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. Sørensen 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  . The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food  . 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 .
+
 
 +
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  . The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food  . 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.
 +
 
 
2. Gastric mechanism of satiation-
 
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  . 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 .In other works also this is used as a tool to assess the gastric capacity .
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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 .
  −
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  . Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake .
  −
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 .
  −
Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake  . 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 .  Peptide YY has a suppressive effect on food intake . 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 .
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Signaling pathways involved in the mechanism of satiation-
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Food is considered the basic necessity for sustenance of life and attain physical stoutness [Cha.Sa.Su.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    .
     −
D Chapelot has described subjective and objective tools for measuring meal size, microstructure of the meal, meal request and intermeal intervals. A multidimensional approach for assessing satiety is proposed with intensity, duration and intake as main variables . Commings DE et.al 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 intakeregulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature .  
+
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.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 .In other works also this is used as a tool to assess the gastric capacity.
   −
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 .
+
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.
   −
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  .
+
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  . Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.  
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 .
  −
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 .  
      +
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.
    +
Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake. 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.Peptide YY has a suppressive effect on food intake.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.
 +
 +
'''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.
 +
 +
D Chapelot has described subjective and objective tools for measuring meal size, microstructure of the meal, meal request and intermeal intervals. A multidimensional approach for assessing satiety is proposed with intensity, duration and intake as main variables . Commings DE et.al 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 intakeregulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.
 +
 +
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.
 +
 +
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.
 +
 +
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.
 +
 +
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.
 +
 +
'''Research tools to assess digestive fire (Jathragni)-'''
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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 . 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 . Patil VC, Baghel MS et al have developed formulae for assessment of the digestive function (agni) in during administration of internal oleation . 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]].
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'''Understanding links between mental health and gastrointestinal track mediated through gut microbiota-'''
   −
Research tools to assess digestive fire (Jathragni)-
  −
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 . 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 . Patil VC, Baghel MS et al have developed formulae for assessment of the digestive function (agni) in during administration of internal oleation . 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 .
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Understanding links between mental health and gastrointestinal track 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 .
 
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 .
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  . Gut microbiome has a regulatory role in behavior and cognition and it is exercised through gut-brain axis .
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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  .Gut microbiome has a regulatory role in behavior and cognition and it is exercised through gut-brain axis .
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 . 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 .
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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 .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 .
    
   
 
   
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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.
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World health organization explains the malnutrition phenomenon of childhood age under four categories: Stunting, Wasting and overweight and underweight 
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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.
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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.
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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.
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4.Underweight- (refers weight-for-age below –2SD)
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Determinants of undernutrition-  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.
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'''Consequences of undernutrition:'''  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 . Malnutrition in children’s by impacting cognitive functions, further impend individuals’ ability to lead productive lives and thus contribute to poverty.
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'''Undernutrition in adults-'''
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Undernutrition 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.
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Determinants- Hickson M has Categorized the causes of malnutrition under three category as medical factos (like poor appetite, physical disability, endocrine disorders etc), lifestyle and social factors (lack of knowledge of nutrition, loneliness, povery etc.) and psychological factors .  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.
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Old age persons are at high risk of developing protein-energy malnutrition. It affects health, congnitive 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.
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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.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 . 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.
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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 . 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 . 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.
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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.
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'''Treatment strategies-'''
World health organization explains the malnutrition phenomenon of childhood age under four categories: Stunting, Wasting and overweight and underweight   
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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.
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Provide dietary solutions considering Guts changes of the elderly.  
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.
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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.
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Manipulation in energy / nutritive density of food .
4. Underweight- (refers weight-for-age below –2SD)
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Determinants of undernutrition-  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 .
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Consequences of undernutrition:  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 . Malnutrition in children’s by impacting cognitive functions, further impend individuals’ ability to lead productive lives and thus contribute to poverty.
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Undernutrition in adults-
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Undernutrition 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  .
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Determinants- Hickson M has Categorized the causes of malnutrition under three category as medical factos (like poor appetite, physical disability, endocrine disorders etc), lifestyle and social factors (lack of knowledge of nutrition, loneliness, povery etc.) and psychological factors .  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 .
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Old age persons are at high risk of developing protein-energy malnutrition. It affects health, congnitive 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 .
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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 .  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 . 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 .
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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 . 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 . 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 .
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Treatment strategies-  
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Provide dietary solutions considering Guts changes of the elderly .  
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Manipulation in energy / nutritive density of food .
   
Changes in hedonic pattern (taste, flavor, appearance) of foods.
 
Changes in hedonic pattern (taste, flavor, appearance) of foods.
 
Provide healthy environment to support emotional quotient.
 
Provide healthy environment to support emotional quotient.
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Adopt interdisciplinary approach like inclusion of Yoga techniques to improve mental health .
 
Adopt interdisciplinary approach like inclusion of Yoga techniques to improve mental health .
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Ama-  
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'''Ama-'''
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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 track (grahani-seat of jathragni) and at the level of tissues (dhatvagni-abodes of dhatus). 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 doshas with metabolic waste results in ama formation, which is considered the initial stage of disease formation. Origin of ama is mainly considered from gastrointestinal track (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.
 
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 track (grahani-seat of jathragni) and at the level of tissues (dhatvagni-abodes of dhatus). 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 doshas with metabolic waste results in ama formation, which is considered the initial stage of disease formation. Origin of ama is mainly considered from gastrointestinal track (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 . 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 .
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                    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 .  
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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 . 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.
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 .
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                    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 .
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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 .  
                    Ama formation occurs due to the accumulation of toxic or intermediatory product of metabolism in the body termed as mala. These intermediatory 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 intermediatory products in the body. This intermediatory products act as ama and leads to many disease conditions.
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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.
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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 .
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Ama formation occurs due to the accumulation of toxic or intermediatory product of metabolism in the body termed as mala. These intermediatory 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 intermediatory products in the body. This intermediatory products act as ama and leads to many disease conditions.
 
Metabolic waste functions as ama: Tissue nutrients after action of metabolic fire (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.  
 
Metabolic waste functions as ama: Tissue nutrients after action of metabolic fire (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.  
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===Abbreviations==
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*Cha.Sa. – Charak Samhita
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*A.Hr.-Ashtanga Hridaya
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*A.S.-Ashtanga Sngraha
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*B.P.-Bhava Prakasha
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==References ==
 
==References ==
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