Changes

Line 720: Line 720:  
In the context of ''atisthula'' and ''atikrisha'', Charaka has explored these conditions from the standpoint of their diathesis, clinical presentation, and management, which is comparable to approaches taken today to the study of obesity and leanness. Suśruta has considered ''rasa dhatu'' as the main culprit for both obesity and emaciation (''rasa nimittameva sthaulyam karshyam ca'')<ref>Acharya, J.T. (translator) (1915).  Sushrut Sanhita of Sushrut, Nirnay Sagar Press, Mumbai, India, p. 65, Su.Su-15/39. </ref>.  
 
In the context of ''atisthula'' and ''atikrisha'', Charaka has explored these conditions from the standpoint of their diathesis, clinical presentation, and management, which is comparable to approaches taken today to the study of obesity and leanness. Suśruta has considered ''rasa dhatu'' as the main culprit for both obesity and emaciation (''rasa nimittameva sthaulyam karshyam ca'')<ref>Acharya, J.T. (translator) (1915).  Sushrut Sanhita of Sushrut, Nirnay Sagar Press, Mumbai, India, p. 65, Su.Su-15/39. </ref>.  
   −
Lipid precursors are acted upon by fat-specific energy (''medhodhatvagni'') for their conversion into adipose tissue (''medodhatu'')<ref>Mishra, L.C. (2003). Scientific Basis of Ayurvedic therapy, Chapter 9 Obesity (Medoroga) in Ayurveda; eBook, published by CRC press, Taylor & Francis Group.  </ref>. Vitiation of ''kapha dosha'' and excessive accumulation of fat-specific energy and waste products of adipose tissues (''kleda'') lead to dysfunction of adipose tissues. Adipose channels have two origins - kidney, adrenal and fat around them and other are visceral and omental fat (''vapavahana'')<ref>Shastri, P.K (1983), (translater), Caraka samhita, Part I, 2nd ed., Chaukhambha Sanskrit Sansthan, Varanasi, India, p. 595. </ref>. These channels draw nutrition, including lipid from the antecedent flesh and transient lipid and then convert them into a stored form of lipid. As per biomedical science, obesity is associated with increased adipose stores in the subcutaneous tissues, skeletal muscles and internal organs such as kidney, heart, liver and omentum. Adipose tissues (''medodhatu'') form a crucial link to the concept of tissue metabolism. Low levels of fat-specific energy (''medodhatvagni''), despite a normal food intake, can lead to a steady accumulation of fat and the outcome is obesity<ref>Bleich S, Cutler D, Murray C, Adams A (2008). "Why is the developed world obese?". Annu Rev Public Health29: 273–95. doi:10.1146/annurev.publhealth.29.020907.090954. PMID 18173389. </ref>  <ref>Drewnowski A, Specter SE (January 2004). "Poverty and obesity: the role of energy density and energy costs". Am. J. Clin. Nutr.79 (1): 6–16.  </ref>. The conventional system of medicine has given due consideration to certain factors such as insufficient sleep, genetic predisposition, later age pregnancy, certain medications and other epigenetic factors in the etiopathogenesis of obesity and its related disorders.
+
Lipid precursors are acted upon by fat-specific energy (''medhodhatvagni'') for their conversion into adipose tissue (''medodhatu'')<ref>Mishra, L.C. (2003). Scientific Basis of Ayurvedic therapy, Chapter 9 Obesity (Medoroga) in Ayurveda; eBook, published by CRC press, Taylor & Francis Group.  </ref>. Vitiation of ''kapha dosha'' and excessive accumulation of fat-specific energy and waste products of adipose tissues (''kleda'') lead to dysfunction of adipose tissues. Adipose channels have two origins - kidney, adrenal and fat around them and other are visceral and omental fat (''vapavahana'')<ref>Shastri, P.K (1983), (translater), Caraka samhita, Part I, 2nd ed., Chaukhambha Sanskrit Sansthan, Varanasi, India, p. 595. </ref>. These channels draw nutrition, including lipid from the antecedent flesh and transient lipid and then convert them into a stored form of lipid. As per biomedical science, obesity is associated with increased adipose stores in the subcutaneous tissues, skeletal muscles and internal organs such as kidney, heart, liver and omentum. Adipose tissues (''medodhatu'') form a crucial link to the concept of tissue metabolism. Low levels of fat-specific energy (''medodhatvagni''), despite a normal food intake, can lead to a steady accumulation of fat and the outcome is obesity<ref>Bleich S, Cutler D, Murray C, Adams A (2008). "Why is the developed world obese?". Annu Rev Public Health29: 273–95. doi:10.1146/annurev.publhealth.29.020907.090954. PMID 18173389. </ref>  <ref>Drewnowski A, Specter SE (January 2004). "Poverty and obesity: the role of energy density and energy costs". Am. J. Clin. Nutr.79 (1): 6–16.  </ref>. The conventional system of medicine has given due consideration to certain factors such as insufficient sleep, genetic predisposition, later age pregnancy, certain medications and other epigenetic factors in the etiopathogenesis of obesity and its related disorders<ref>Keith SW, Redden DT, Katzmarzyk PT et al. (2006). "Putative contributors to the secular increase in obesity: Exploring the roads less traveled". Int J Obes (Lond)30 (11): 1585–94. doi:10.1038/sj.ijo.0803326. PMID 16801930. </ref>.
    
==== Increased desire to eat among the obese (verse 4) ====
 
==== Increased desire to eat among the obese (verse 4) ====