Changes

==== Clinical features ====

==== Clinical features ====

Ārōcaka (aversion to food), vairasya (distaste), prasēka (excessive salivation) are general gastro intestinal manifestations of indigestion. Tamaka or blackout occurs due to nutritional deficiency. Mal-absorption causes diarrhea which leads to decrease in circulating liquid, a cause of hypotension a reason for blackout. Impaired absorption of iron, folate, vit. B12 leads to anemia which may be the cause for blackout (tamakānvitaḥ). Resulting anemia and electrolyte depletion (particularly K+) leads to weakness.   

''Arochaka'' (aversion to food), ''vairasya'' (distaste), ''praseka'' (excessive salivation) are general gastrointestinal manifestations of indigestion. ''Tamaka'' or blackout occurs due to nutritional deficiency. Mal-absorption causes diarrhea which leads to decrease in circulating liquid, a cause of hypo-tension a reason for blackout. Impaired absorption of iron, folate, vit. B12 leads to anemia which may be the cause for blackout (''tamakanvitah''). Resulting anemia and electrolyte depletion (particularly K+) leads to weakness.   

1) Peripheral neuropathy due to Vit B12 and thiamine deficiency  

#Peripheral neuropathy due to Vit. B12 and thiamine deficiency  

2) Dermatitis due to deficiency of Vit. A, Zinc and essential fatty acid  

#Dermatitis due to deficiency of Vit. A, Zinc and essential fatty acid  

3) Night Blindness/Xeropthalmia due to Vit A mal-absorption.

#Night Blindness/Xeropthalmia due to Vit A mal-absorption.

4) Bleeding due to Vit K malabsorption and hypo prothrombinemia

#Bleeding due to Vit K malabsorption and hypo prothrombinemia

5) Anemia impaired absorption of iron, folate, and vitamin B12

#Anemia impaired absorption of iron, folate, and vitamin B12

6) Amenorrhea, decreased libido due to protein depletion decreased calories and secondary hypopituitarism.   

#Amenorrhea, decreased libido due to protein depletion decreased calories and secondary hypo-pituitarism.   

7) Tetany, paresthesia due to calcium and magnesium mal-absorption   

#Tetany, paresthesia due to calcium and magnesium mal-absorption   

8) Glossitis, cheilosis, stomatitis due to deficiency of iron, Vit B12, folate and Vit A (Verse 52-54).

#Glossitis, cheilosis, stomatitis due to deficiency of iron, Vit B12, folate and Vit A (Verse 52-54).

Spices are basically a combination of acids. When too much of these acids are introduced in gastrointestinal tract which has its own acidic contents it starts damaging the mucosal lining of walls of gastrointestinal tract. It also reduces the pH thus activation of enzyme is hampered leading to indigestion.

Spices are basically a combination of acids. When too much of these acids are introduced in gastrointestinal tract which has its own acidic contents it starts damaging the mucosal lining of walls of gastrointestinal tract. It also reduces the pH thus activation of enzyme is hampered leading to indigestion.

Etiological factors as mentioned in the text have impact mainly on the neural stimulation of digestive secretions affecting the flow of gastrointestinal secretions into the gastrointestinal tract thereby hampering the digestion. Hence it is explained that aggravated vāta encompasses the agni. Altered canalicular functions hampers digestion, easily understood in primary biliary cirrhosis wherein biliary secretion is restricted. Atrophy of gastric mucosa reduces HCl secretion causing indigestion. The gastric gland contains three types of exocrine gland cells that secrete their products into stomach lumen. ‘srotasām kharatvam’ (hardness in channels) quality of tikta rasa destroys the exocrine gland cell reducing their secretions. Gastric glands include a type of enteroendocrine cell, the G cell which is located mainly in the pyloric antrum and secretes the hormone gastrin into the blood stream which stimulates parietal cells to secrete HCl and chief cells to secrete pepsinogen, it also contracts the lower esophageal sphincter, increases motility of the stomach and relaxes pyloric sphincter.  G cells when get destroyed the above action of kapha inturn agni is hampered so also contraction and relaxation karma of vāta is vitiated.

Etiological factors as mentioned in the text have impact mainly on the neural stimulation of digestive secretions affecting the flow of gastrointestinal secretions into the gastrointestinal tract thereby hampering the digestion.

Further kaṣāya rasa reduces peristaltic movements called as mixing waves which reduces the maceration and mixing of food with secretions of gastric glands, thus improper chyme is formed. Deficiency of gastrointestinal secretions due to damage to the glands or canaliculi or intestine may be mostly considered as having vātaja origin. Loss of pravartan karma is to be understood where the transport of secretions is hampered (except in obstructive pathology where kapha to be considered). Hartnup’s syndrome a defect in neutral amino acid transport and cystinuria a defect in dibasic amino acid transport explain the rare genetic disorders (Bija Dusti) involved in protein digestion absorption.

Hence it is explained that aggravated ''vata'' encompasses the ''agni''. Altered canalicular functions hampers digestion, easily understood in primary biliary cirrhosis wherein biliary secretion is restricted. Atrophy of gastric mucosa reduces HCl secretion causing indigestion. The gastric gland contains three types of exocrine gland cells that secrete their products into stomach lumen.''Srotasam kharatvam'' (hardness in channels) quality of ''tikta rasa'' destroys the exocrine gland cell reducing their secretions. Gastric glands include a type of enteroendocrine cell, the G cell which is located mainly in the pyloric antrum and secretes the hormone gastrin into the blood stream which stimulates parietal cells to secrete HCl and chief cells to secrete pepsinogen, it also contracts the lower esophageal sphincter, increases motility of the stomach and relaxes pyloric sphincter.

Further due to vāta prakopa, intestinal activity is increased which is manifested as mal-absorption. For e.g. lactose intolerance is related to rate of gastric emptying. Symptoms are more likely when gastric emptying is rapid than when gastric emptying is slower. Therefore it is more likely that skim milk will be associated with symptoms of lactose intolerance than with whole milk as rate of gastric emptying is more rapid in skim milk. Milk proteins, particularly caseins have appropriate amino acids composition for growth and development of young. Caseins are highly digestible in intestine and high quality source of amino acids. Most of whey proteins are relatively less digestible in intestine, although all of them are digested to some degree. When substantial whey proteins are not digested fully, some of intact protein may stimulate a localized intestinal or systemic immune response this is due to beta lactoglobullin referred to milk protein allergy. Similarly, diarrhea observed following subtotal gastrectomy is often a result of lactose intolerance as gastric emptying is accelerated in patients with gastrojejunostomy, rapid small intestinal transit time develops symptoms of lactose intolerancy. 

G cells when get destroyed the above action of ''kapha'', in turn, ''agni'' is hampered so also contraction and relaxation karma of ''vata'' is vitiated.

Kaṇṭhāsya-Śōṣaḥ (dryness of mouth also known as xerostomia) occurs due to diminish salivary gland secretion. Primary cause being fluid loss through diarrhea secondarily it may be association of Sjogrens syndrome with autoimmune disease like primary biliary cirrhosis ~ a secondary Sjogrens syndrome. In this syndrome involvement of other exocrine glands occur leading to diminished secretion of exocrine glands of the gastrointestinal tract, leading to esophageal mucosal atrophy, atrophic gastritis and subclinical pancreatitis.

Increased appetite (Kṣudhā) is seen because of a negative feedback due to mal-absorption or it may be understood under rasasheshājīrṇa.  

Further ''kashaya rasa'' reduces peristaltic movements called as mixing waves which reduces the maceration and mixing of food with secretions of gastric glands, thus improper chyme is formed. Deficiency of gastrointestinal secretions due to damage to the glands or canaliculi or intestine may be mostly considered as having vātaja origin. Loss of ''pravartana karma'' is to be understood where the transport of secretions is hampered (except in obstructive pathology where ''kapha'' to be considered). Hartnup’s syndrome a defect in neutral amino acid transport and cystinuria a defect in dibasic amino acid transport explain the rare genetic disorders (''Bija Dusti'') involved in protein digestion absorption.

Tṛṣṇā is manifested due to increased Rukṣa Guna of vāta and decreased Jalādi Ansha due to diarrheas and low fluid intake.  

Further due to ''vata prakopa'', intestinal activity is increased which is manifested as malabsorption. For e.g. lactose intolerance is related to rate of gastric emptying. Symptoms are more likely when gastric emptying is rapid than when gastric emptying is slower. Therefore it is more likely that skim milk will be associated with symptoms of lactose intolerance than with whole milk as rate of gastric emptying is more rapid in skim milk. Milk proteins, particularly caseins have appropriate amino acids composition for growth and development of young.  

Timira (blurred vision) results from vitamin A mal-absorption and anemia.

Caseins are highly digestible in intestine and high quality source of amino acids. Most of whey proteins are relatively less digestible in intestine, although all of them are digested to some degree. When substantial whey proteins are not digested fully, some of intact protein may stimulate a localized intestinal or systemic immune response this is due to beta lactoglobullin referred to milk protein allergy. Similarly, diarrhea observed following subtotal gastrectomy is often a result of lactose intolerance as gastric emptying is accelerated in patients with gastrojejunostomy, rapid small intestinal transit time develops symptoms of lactose intolerance. 

Tinnitus is a symptom also found in Pāndu (anemia)(Ca. Ci. 15/61),  which is observed due to mal-absorption of essential elements like vitamin B12.

''Kanthasya-shosah'' (dryness of mouth also known as xerostomia) occurs due to diminish salivary gland secretion.  

Pain in flanks, thigh, pelvis, cervical area occurs due to calcium and Vitamin D mal-absorption. Pain is also contributed by protein deficiency due to low nutritional diet, osteoporosis, anemia and decrease lactic acid neutralization due to reduce peripheral circulation.  

 

 

 

 

 

Pain in flanks, thigh, pelvis, cervical area occurs due to calcium and Vitamin D malabsorption. Pain is also contributed by protein deficiency due to low nutritional diet, osteoporosis, anemia and decrease lactic acid neutralization due to reduce peripheral circulation.  

Whipple’s disease is chronic multisystem disease associated with diarrhea, steatorrhea, weight loss, arthralgia and CNS and cardiac problems caused due to tropheryma whipple.  

Whipple’s disease is chronic multisystem disease associated with diarrhea, steatorrhea, weight loss, arthralgia and CNS and cardiac problems caused due to tropheryma whipple.  

   

   

Hr̥tpīḍā is chest discomfort or chest pain which may be resultant of anemia but most probably due to gastro esophageal reflux disease.  

''Hritpeedha'' is chest discomfort or chest pain which may be resultant of anemia but most probably due to gastro-esophageal reflux disease.

 

 

''Vairasyam'' (distaste) is probably because of taste projections to the hypothalamus and limbic system, there is a strong link between the taste and pleasant and unpleasant emotions. ''Parikartika'' (cutting pain) is due to ''shushka-mala pravritti'' (pellet stools) which causes pressure and rupture of anal-mucosal lining that may lead to cutting pain.

Mal-absorption may be for single entity or for various minerals and vitamins and may lead to emaciation and weakness.  

Craving for all types of food (''griddhih sarvarasanam'') is seen due to malabsorption of various elements, mineral and vitamins causing deficiency of the essential requirements of elements. The negative feedback system creates the craving for essential elements which is presented in the form of craving for all six ''rasa''. ''Rasa'' should be understood for food which will fulfill the requirements.

Vairasyaṁ (distaste) is probably because of taste projections to the hypothalamus and limbic system, there is a strong link between the taste and pleasant and unpleasant emotions. Parikartikā (cutting pain) is due to Śuṣkā-mala Pravṛtti (pellet stools) which causes pressure and rupture of anal mucosal lining that may lead to cutting pain.

Mood disorders are observed due to depletion of essential vitamins, mineral and other elements. Electrolyte difference creates confusion which may be the cause for ''mano avasada''.

Craving for all types of food (Gr̥ddhiḥ Sarvarasānāṁ) is seen due to mal-absorption of various elements, mineral and vitamins causing deficiency of the essential requirements of elements. The negative feedback system creates the craving for essential elements which is presented in the form of craving for all six rasa. rasa should be understood for food which will fulfill the requirements.

Bloating of abdomen is manifested while digestion is in process or after digestion is completed because of indigestion that causes abnormal growth of gut microbiome. Bacterial fermentation of unabsorbed carbohydrates leads to flatus. Carbohydrates metabolism occurs in small and large intestine therefore the symptom occurs during ''Jeerne jeeryati chadhmanam'' i.e. during and after the process of digestion. Once the patient takes food, circulation towards stomach is increased and digestive activity in the colon is reduced thus carbohydrate metabolism is depressed reducing the formation of flatus in rectum thereby reducing the bloating of abdomen.

Mood disorders are observed due to depletion of essential vitamins, mineral and other elements. Electrolyte difference creates confusion which may be the cause for Mano Avasāda.

Patient doubts as if he may be suffering from following of the disorders like ''vatavikara, gulma, hridroga'' and ''pleeha''. Due to formation of flatus and later on bloating of abdomen makes the patient feel he is suffering from ''vatika'' disorders related to gastrointestinal tract. Especially ''gulma'' since the patient feels the movement of flatus, so doubts about ''gulma''.  

Bloating of abdomen is manifested while digestion is in process or after digestion is completed because of indigestion that causes abnormal growth of gut microbiome. Bacterial fermentation of unabsorbed carbohydrates leads to flatus. Carbohydrates metabolism occurs in small and large intestine  therefore the symptom occurs during Jīrṇē Jīryati Cādhmānaṁ i.e. during and after the process of digestion. Once the patient takes food, circulation towards stomach is increased and digestive activity in the colon is reduced thus carbohydrate metabolism is depressed reducing the formation of flatus in rectum thereby reducing the bloating of abdomen.

''Ushna'' and ''teekshna guna'' of ''pitta'' trigger inflammatory response by irritating the intestinal mucosa.  

Patient doubts as if he may be suffering from following of the disorders like vātavikār, gulma, hridroga and pleeha. Due to formation of flatus and later on bloating of abdomen makes the patient feel he is suffering from vātika disorders related to gastrointestinal tract. Especially gulma since the patient feels the movement of flatus, so doubts about gulma.  

Indigestion causes depletion of beneficial gut bacteria thus breakdown in the balance between the putative protective and harmful intestinal bacteria leads to chronic inflammation.  

Ūṣnā and Tīkṣṇa Guna of pitta trigger inflammatory response by irritating the intestinal mucosa. Indigestion causes depletion of beneficial gut bacteria thus breakdown in the balance between the putative protective and harmful intestinal bacteria leads to chronic inflammation.  

Antigenic nature of endogenous factors can be understood when helpful bacteria and ''ushna, teekshna guna'' of ''kapha'' trigger inflammatory response leading to autoimmune pathogenesis.

Antigenic nature of endogenous factors can be understood when helpful bacteria and ūṣnā, tīkṣṇa Guna of kapha trigger inflammatory response leading to autoimmune pathogenesis.

In case of hypersecretion of gastrin in gastrinoma [Zollingers – Ellison Syndrome] stimulate the parietal cells of the stomach to secrete acid to their maximal capacity and increase the parietal cell mass three to six fold. The acid output may be so great that it reaches the upper small intestine reducing the luminal pH to 2 or less.

In case of hypersecretion of gastrin in gastrinoma [Zollingers – Ellison Syndrome] stimulate the parietal cells of the stomach to secrete acid to their maximal capacity and increase the parietal cell mass three to six fold. The acid output may be so great that it reaches the upper small intestine reducing the luminal pH to 2 or less. Pancreatic lipase is inactivated and bile acids are precipitated. It results in diarrhea and steatorrhea. Subtotal villous atrophy occurs due to hyper-secretion which may cause mal-absorption. Excessive gastrointestinal secretions cause derangements in fluid and electrolyte transport across the entero-colonic mucosa leading to diarrhea. They are characterized clinically by watery, large volume fecal outputs that are typically painless and persist with fasting because there is no mal-absorbed solute; stool osmolalirity is accounted for normal endogenous electrolytes with no fecal osmotic gap.

Pancreatic lipase is inactivated and bile acids are precipitated. It results in diarrhea and steatorrhea. Subtotal villous atrophy occurs due to hyper-secretion which may cause malabsorption. Excessive gastrointestinal secretions cause derangement in fluid and electrolyte transport across the entero-colonic mucosa leading to diarrhea. They are characterized clinically by watery, large volume fecal outputs that are typically painless and persist with fasting because there is no malabsorbed solute; stool osmolalirity is accounted for normal endogenous electrolytes with no fecal osmotic gap.

Other than excessive secretion, condition like ileal dysfunction caused by either Crohn’s disease or surgical resection results in a decrease in bile acid re absorption in the ileum and an increase in the delivery of bile acids to the large intestine. The resultant is a diarrhea with or without steatorrhea. It becomes a cause for mal-absorption syndrome.  

Other than excessive secretion, condition like ileal dysfunction caused by either Crohn’s disease or surgical resection results in a decrease in bile acid re absorption in the ileum and an increase in the delivery of bile acids to the large intestine. The resultant is a diarrhea with or without steatorrhea. It becomes a cause for mal-absorption syndrome.  

Inflammatory Bowel Disease needs consideration in pittaja grahaṇī. Exogenous factors trigger inflammatory response that the mucosal immune system may fail to control. With mild inflammation the mucosa is erythematous and in severe condition the mucosa becomes hemorrhagic, edematous and ulcerated  (Verse 65).

Inflammatory Bowel Disease needs consideration in ''pittaja grahani''. Exogenous factors trigger inflammatory response that the mucosal immune system may fail to control. With mild inflammation the mucosa is erythematous and in severe condition the mucosa becomes hemorrhagic, edematous and ulcerated  (Verse 65).

Loose motions (Drava Mala Pravṛtti) are mainly due to excessive secretion of bile juice (Drava guna of pitta). Excessive secretion may be due excessive formation in liver or decrease absorption in the intestine.

Loose motions (''Drava Mala Pravritti'') are mainly due to excessive secretion of bile juice (''Drava guna'' of ''pitta''). Excessive secretion may be due excessive formation in liver or decrease absorption in the intestine.

Bile acids are not present in the diet but are synthesized in the liver by a series of enzymatic steps that also include cholesterol catabolism. Bile acids are either primary or secondary. Primary bile acids are synthesized in the liver from cholesterol and secondary bile acids are synthesized from primary bile acids in the intestine by colonic bacterial enzymes. Bile acids are primarily absorbed by active, sodium dependent process that is located exclusively in the ileum; secondly bile acids can also be absorbed to a lesser extent by non carrier mediated transport processes in the jejunum, ileum and colon. Conjugated bile acids that enter the colon are deconjugated by colonic bacterial enzyme to unconjugated bile acids and are rapidly absorbed. Colonic bacterial enzymes also dehydroxylate bile acids to secondary bile acids, thus if exogenous factors like diet as discussed above disturb the colonic bacterial growth than bile acids are not absorbed. A decrease in the amount of bile acids returning to the liver from the intestine is associated with an increase in bile acids synthesis/cholesterol catabolism, which helps keep bile acid pool size relatively constant. Defects in any of the steps of the enterohepatic circulation of bile acids can result in decrease in duodenal concentration of conjugated bile acids as a result steatorrhea. Thus steatorrhea can be caused by abnormalities in bile acid synthesis and excretion, their physical state in the intestinal lumen and reabsorption. The bile gives the yellowish nature to the stools  (Verse 66).

Bile acids are not present in the diet but are synthesized in the liver by a series of enzymatic steps that also include cholesterol catabolism. Bile acids are either primary or secondary. Primary bile acids are synthesized in the liver from cholesterol and secondary bile acids are synthesized from primary bile acids in the intestine by colonic bacterial enzymes. Bile acids are primarily absorbed by active, sodium dependent process that is located exclusively in the ileum; secondly bile acids can also be absorbed to a lesser extent by non carrier mediated transport processes in the jejunum, ileum and colon. Conjugated bile acids that enter the colon are de-conjugated by colonic bacterial enzyme to unconjugated bile acids and are rapidly absorbed. Colonic bacterial enzymes also dehydroxylate bile acids to secondary bile acids, thus if exogenous factors like diet as discussed above disturb the colonic bacterial growth than bile acids are not absorbed. A decrease in the amount of bile acids returning to the liver from the intestine is associated with an increase in bile acids synthesis/cholesterol catabolism, which helps keep bile acid pool size relatively constant. Defects in any of the steps of the enterohepatic circulation of bile acids can result in decrease in duodenal concentration of conjugated bile acids as a result steatorrhea. Thus steatorrhea can be caused by abnormalities in bile acid synthesis and excretion, their physical state in the intestinal lumen and reabsorption. The bile gives the yellowish nature to the stools  (Verse 66).

Guru, snigdha and sītā  ahara is dominated by prithvi and jala mahābhuta, these qualities help in reducing the impact of agni mahābhuta thus causing jatharāgni māndyatā resulting in indigestion leading to formation ama. Such ama is responsible for doṣha prakopa.(Madhukoshatika Ma. Ni. Jwara adhyaya/2)  

Guru, snigdha and sītā  ahara is dominated by prithvi and jala mahābhuta, these qualities help in reducing the impact of agni mahābhuta thus causing jatharāgni māndyatā resulting in indigestion leading to formation ama. Such ama is responsible for doṣha prakopa.(Madhukoshatika Ma. Ni. Jwara adhyaya/2)