Changes

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>.(Verse 3-4)

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>.(Verse 3-4)

==== Increased desire to eat among the obese (verse 4) ====

==== Increased desire to eat among the obese ====

Charaka correlated an increased desire to eat with increased ''agni'' in the morbidly obese. Recent evidence suggests that leptin and ghrelin had shown their influence on appetite. In this context, ghrelin is produced from the stomach, and leptin is produced by the adipose tissue of fat storage reserves in the body, which is responsible for short-term and long-term appetite control respectively in the body<ref>Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes104 (4): 293–300. doi:10.1055/s-0029-1211457. PMID 8886745. </ref>.  In the brain melanocortin pathway has drawn the attention of research scholars that this pathway has a specific role in stimulating appetite, which is located in the area of the lateral and ventromedial hypothalamus and arcuate nucleus. These areas are directly related to the feeding and satiety centers<ref name=ref30>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref> .  

Charaka correlated an increased desire to eat with increased ''agni'' in the morbidly obese. Recent evidence suggests that leptin and ghrelin had shown their influence on appetite. In this context, ghrelin is produced from the stomach, and leptin is produced by the adipose tissue of fat storage reserves in the body, which is responsible for short-term and long-term appetite control respectively in the body<ref>Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes104 (4): 293–300. doi:10.1055/s-0029-1211457. PMID 8886745. </ref>.  In the brain melanocortin pathway has drawn the attention of research scholars that this pathway has a specific role in stimulating appetite, which is located in the area of the lateral and ventromedial hypothalamus and arcuate nucleus. These areas are directly related to the feeding and satiety centers<ref name=ref30>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref> .  

There are two distinct groups of neurons in the arcuate nucleus viz- The first group contains neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the second group contains Pro-opiomelanocortin (POMC) and cocaine and amphetamine regulated transcript (CART). The first group of neuron i.e. NPY/AgRP exerts stimulatory inputs to the LH while inhibitory inputs to the VMH, which stimulate feeding and inhibit satiety respectively. Both groups of arcuate nucleus neurons are the under the regulation of leptin, which inhibits the NPY/AgRP group of neurons and stimulating the POMC/CART group of neurons. Hence, the leptin deficiency or leptin resistance leads to develop overfeeding tendency, which is caused by some genetic and acquired forms of obesity<ref name=ref30/>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref>  <ref>Raina GS (2011). Obesity being the major health burden needed to be chased: A systemic review. J Appl Pharm Sci. 2011;1:238–45.  </ref>. These findings suggest the genetic inputs in overweight and obesity, which is quite comparable to the Ayurvedic lexicons.

There are two distinct groups of neurons in the arcuate nucleus viz- The first group contains neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the second group contains Pro-opiomelanocortin (POMC) and cocaine and amphetamine regulated transcript (CART). The first group of neuron i.e. NPY/AgRP exerts stimulatory inputs to the LH while inhibitory inputs to the VMH, which stimulate feeding and inhibit satiety respectively. Both groups of arcuate nucleus neurons are the under the regulation of leptin, which inhibits the NPY/AgRP group of neurons and stimulating the POMC/CART group of neurons. Hence, the leptin deficiency or leptin resistance leads to develop overfeeding tendency, which is caused by some genetic and acquired forms of obesity<ref name=ref30/>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref>  <ref>Raina GS (2011). Obesity being the major health burden needed to be chased: A systemic review. J Appl Pharm Sci. 2011;1:238–45.  </ref>. These findings suggest the genetic inputs in overweight and obesity, which is quite comparable to the Ayurvedic lexicons.(verse 4)

==== Consequences of obesity (verse 5-8) ====

==== Consequences of obesity (verse 5-8) ====