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Line 777: − − === Contemporary views and research updates === − − ==== Understanding proper quantity of food (sauhitya matra) and physiological mechanism of satiation==== − <div style="text-align:justify;"> − − 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 .<ref>Benelam B. Satiation, Satiety and their effects on eating behavior. Nutrition Bulletin. London UK. British Nutrition Foundation. May 2009;34(2):126–173. − https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1467-3010.2009.01753.x </ref>Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.<ref>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</ref> − − 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. <ref>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 </ref> <ref>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 </ref> − − The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food.<ref>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</ref> <ref>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</ref>. 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.<ref>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 https://journals.plos.org/plosone/articleid=10.1371/journal.pone.0090872</ref> − − ===== 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.<ref>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</ref>,<ref>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</ref> 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.<ref>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 </ref>In other works also this is used as a tool to assess the gastric capacity.<ref>Tate CM, Geliebter A. Intragastric Balloon Treatment for Obesity: Review of Recent Studies. Adv Ther 34, 1859–1875 (2017). https://doi.org/10.1007/s12325-017-0562-3</ref> − − '''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.<ref>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. − https://journals.physiology.org/doi/full/10.1152/ajpendo.00457.2011?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org</ref> − − 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.<ref>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</ref><ref>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</ref> Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.<ref>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</ref> − − 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.<ref>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.https://academic.oup.com/ajcn/article/72/2/421/4729460</ref> − − Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake.<ref>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</ref><ref>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</ref> 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.<ref>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. https://doi.org/10.1038/sj.npp.1300670</ref> Peptide YY has a suppressive effect on food intake.<ref>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.</ref>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.<ref>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.</ref> − − ===== 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.<ref>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</ref> <ref>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.</ref> <ref>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.</ref> − − 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.<ref>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. https://www.sciencedirect.com/science/book/9780857095435</ref> 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 intake regulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.<ref>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.</ref> − − 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.<ref>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.</ref> − − '''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.<ref>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.</ref> <ref>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.</ref> − − '''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.<ref>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. https://doi.org/https://doi.org/10.1006/appe.1997.0096</ref> − − '''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.<ref>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. https://doi.org/10.1533/9780857098719.5.273</ref> − − =====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 [[agni]] 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 strenght of [[agni]]. 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]]. <ref>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.</ref>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.<ref>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.</ref> Patil VC, Baghel MS et. al. have developed formulae for assessment of the digestive function ([[agni]]) in during administration of [[snehana]] (internal oleation). <ref>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</ref> − − [[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]] (anemia and blood deficiency disorders) 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 Hypochlorhydria (found in 72.8% of the patients) indicates hypofunction of [[agni]].<ref>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.</ref> − − ==== 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.<ref>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.</ref> − − 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 .<ref>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. </ref> <ref>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.</ref>Gut microbiome has a regulatory role in behavior and cognition and it is exercised through gut-brain axis.<ref>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.https://link.springer.com/article/10.1007/s00394-018-1703-4</ref> − − 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 .<ref>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.</ref>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.<ref>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.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/#:~:text=The%20gut%2Dbrain%20axis%20(GBA,microbiota%20in%20influencing%20these%20interactions.</ref> − − 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.<ref>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.</ref> − − 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.<ref>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.</ref> <ref>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. https://doi.org/https://doi.org/10.1016/B978-1-4160-3661-6.00041-9 − https://www.sciencedirect.com/topics/immunology-and-microbiology/gut-brain-axis</ref> Probiotic consumption also has been reported to reduce self-reported feelings of sadness and aggressive thoughts.<ref>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.</ref> Study of Sudo et al supports that the hyypothalamic–pituitary–adrenal (HPA) reaction to stress is influenced greatly by gut microbiota.<ref>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.</ref> <ref>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.</ref> <ref>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.</ref>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.<ref>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.</ref> − − ==== 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. − − [[File:VM_Pic.PNG|400px|'''Fig.3: Deficiency of food'''|thumb]] − − 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.<ref>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. www.who.int/nutgrowthdb/estimates</ref> <ref>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. www.who.int/nutgrowthdb/estimates</ref> − − '''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.<ref>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</ref> − − '''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.<ref>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.</ref> 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.<ref>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.</ref> <ref>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.</ref> − − '''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.<ref>Hickson M. Malnutrition and ageing. Postgrad Med J. 2006;82(963):2-8. doi: 10.1136/ pgmj .2005.037564</ref> − − 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.<ref>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.</ref> − − 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.<ref>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.</ref> − − 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.<ref>Shetty, P. (2006). Malnutrition and undernutrition. Medicine, 34(12), 524–529. https://doi.org/10.1053/j.mpmed.2006.09.014</ref>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.<ref>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. https://doi.org/10.1016/j.clnu.2013.12.001</ref> 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.<ref>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</ref> − − '''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.<ref>Santilli V, Bernetti A, Mangone M, Paoloni M. Clinical definition of sarcopenia. Clin Cases Miner Bone Metab. 2014;11(3):177-180</ref>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.<ref>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</ref>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.<ref>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</ref> − − =====Treatment strategies===== − − Provide dietary solutions considering Guts changes of the elderly.<ref>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</ref> − − Manipulation in energy / nutritive density of food.<ref>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.</ref> − − * Changes in hedonic pattern (taste, flavor, appearance) of foods. − * Provide healthy environment to support emotional quotient. − * Provide feeding assistance. − * Give motivation for physical activities.<ref>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.</ref> − * Adopt interdisciplinary approach like inclusion of Yoga techniques to improve mental health.<ref>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.</ref>
Trividhakukshiya Vimana (view source)
Revision as of 07:21, 27 October 2020
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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.
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.
=== Contemporary views and research updates ===
==== Understanding proper quantity of food (sauhitya matra) and physiological mechanism of satiation====
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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 .<ref>Benelam B. Satiation, Satiety and their effects on eating behavior. Nutrition Bulletin. London UK. British Nutrition Foundation. May 2009;34(2):126–173.
https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1467-3010.2009.01753.x </ref>Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.<ref>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</ref>
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. <ref>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 </ref> <ref>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 </ref>
The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food.<ref>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</ref> <ref>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</ref>. 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.<ref>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 https://journals.plos.org/plosone/articleid=10.1371/journal.pone.0090872</ref>
===== 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.<ref>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</ref>,<ref>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</ref> 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.<ref>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 </ref>In other works also this is used as a tool to assess the gastric capacity.<ref>Tate CM, Geliebter A. Intragastric Balloon Treatment for Obesity: Review of Recent Studies. Adv Ther 34, 1859–1875 (2017). https://doi.org/10.1007/s12325-017-0562-3</ref>
'''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.<ref>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.
https://journals.physiology.org/doi/full/10.1152/ajpendo.00457.2011?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org</ref>
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.<ref>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</ref><ref>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</ref> Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.<ref>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</ref>
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.<ref>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.https://academic.oup.com/ajcn/article/72/2/421/4729460</ref>
Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake.<ref>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</ref><ref>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</ref> 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.<ref>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. https://doi.org/10.1038/sj.npp.1300670</ref> Peptide YY has a suppressive effect on food intake.<ref>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.</ref>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.<ref>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.</ref>
===== 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.<ref>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</ref> <ref>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.</ref> <ref>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.</ref>
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.<ref>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. https://www.sciencedirect.com/science/book/9780857095435</ref> 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 intake regulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.<ref>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.</ref>
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.<ref>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.</ref>
'''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.<ref>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.</ref> <ref>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.</ref>
'''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.<ref>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. https://doi.org/https://doi.org/10.1006/appe.1997.0096</ref>
'''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.<ref>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. https://doi.org/10.1533/9780857098719.5.273</ref>
==== 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.
[[File:VM_Pic.PNG|400px|'''Fig.3: Deficiency of food'''|thumb]]
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.<ref>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. www.who.int/nutgrowthdb/estimates</ref> <ref>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. www.who.int/nutgrowthdb/estimates</ref>
'''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.<ref>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</ref>
'''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.<ref>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.</ref> 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.<ref>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.</ref> <ref>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.</ref>
'''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.<ref>Hickson M. Malnutrition and ageing. Postgrad Med J. 2006;82(963):2-8. doi: 10.1136/ pgmj .2005.037564</ref>
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.<ref>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.</ref>
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.<ref>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.</ref>
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.<ref>Shetty, P. (2006). Malnutrition and undernutrition. Medicine, 34(12), 524–529. https://doi.org/10.1053/j.mpmed.2006.09.014</ref>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.<ref>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. https://doi.org/10.1016/j.clnu.2013.12.001</ref> 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.<ref>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</ref>
'''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.<ref>Santilli V, Bernetti A, Mangone M, Paoloni M. Clinical definition of sarcopenia. Clin Cases Miner Bone Metab. 2014;11(3):177-180</ref>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.<ref>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</ref>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.<ref>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</ref>
=====Treatment strategies=====
Provide dietary solutions considering Guts changes of the elderly.<ref>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</ref>
Manipulation in energy / nutritive density of food.<ref>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.</ref>
* Changes in hedonic pattern (taste, flavor, appearance) of foods.
* Provide healthy environment to support emotional quotient.
* Provide feeding assistance.
* Give motivation for physical activities.<ref>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.</ref>
* Adopt interdisciplinary approach like inclusion of Yoga techniques to improve mental health.<ref>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.</ref>
=====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 [[agni]] 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 strenght of [[agni]]. 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]]. <ref>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.</ref>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.<ref>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.</ref> Patil VC, Baghel MS et. al. have developed formulae for assessment of the digestive function ([[agni]]) in during administration of [[snehana]] (internal oleation). <ref>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</ref>
[[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]] (anemia and blood deficiency disorders) 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 Hypochlorhydria (found in 72.8% of the patients) indicates hypofunction of [[agni]].<ref>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.</ref>
==== 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.<ref>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.</ref>
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 .<ref>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. </ref> <ref>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.</ref>Gut microbiome has a regulatory role in behavior and cognition and it is exercised through gut-brain axis.<ref>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.https://link.springer.com/article/10.1007/s00394-018-1703-4</ref>
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 .<ref>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.</ref>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.<ref>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.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/#:~:text=The%20gut%2Dbrain%20axis%20(GBA,microbiota%20in%20influencing%20these%20interactions.</ref>
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.<ref>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.</ref>
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.<ref>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.</ref> <ref>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. https://doi.org/https://doi.org/10.1016/B978-1-4160-3661-6.00041-9
https://www.sciencedirect.com/topics/immunology-and-microbiology/gut-brain-axis</ref> Probiotic consumption also has been reported to reduce self-reported feelings of sadness and aggressive thoughts.<ref>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.</ref> Study of Sudo et al supports that the hyypothalamic–pituitary–adrenal (HPA) reaction to stress is influenced greatly by gut microbiota.<ref>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.</ref> <ref>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.</ref> <ref>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.</ref>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.<ref>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.</ref>
=== Concept of [[ama]] ===
=== Concept of [[ama]] ===
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]
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]
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==== Contemporary views and research updates on [[ama]] ====
==== Contemporary views and research updates on [[ama]] ====