Changes

*''Eka rasa satmyata'' (literally, one ''rasa'' suitability) provides minimal nutrition to the ''dhatus'' of body, whereas ''sarva rasa satmyata'' provides the most nutrition. ''Sarva rasa abhyasa'' (or, all ''rasa'' exercise/habit) is a practice that helps meet all the nutrient requirement of the body. Consumption of one ''rasa dravyas'' for prolonged periods of time can create imbalances in the body. For example, ''madhura rasa'' is rich in carbohydrates and its habitual consumption may lead to excess carbohydrate and lack of other nutrients.

*''Eka rasa satmyata'' (literally, one ''rasa'' suitability) provides minimal nutrition to the ''dhatus'' of body, whereas ''sarva rasa satmyata'' provides the most nutrition. ''Sarva rasa abhyasa'' (or, all ''rasa'' exercise/habit) is a practice that helps meet all the nutrient requirement of the body. Consumption of one ''rasa dravyas'' for prolonged periods of time can create imbalances in the body. For example, ''madhura rasa'' is rich in carbohydrates and its habitual consumption may lead to excess carbohydrate and lack of other nutrients.

Some researchers in Finland reported that significant reduction of salt from their diets played a critical role in adding 5 to 6 years to the life expectancies of the Finnish population . They also reported that hypertension is the leading cause of death in developed countries. Reduction of salt intake is recommended as a key measure in the prevention and basic treatment of hypertension both in the United States and worldwide. The Renin-Angiotensin Aldosterone (RAA) system is maximally activated when an individual is subjected to prolonged very low sodium intakes of less than 5 mmol a day. Half-maximal stimulation (or inhibition) of plasma rennin activity takes place at sodium intake levels of approximately 30 mmol a day. Sodium intake at the level of 50 mmol a day suppresses secretion of the sodium-retaining hormone, aldosterone, almost completely. The control range of the RAA mechanism is therefore in excellent agreement with the sodium amounts, which can be derived from diets comprising only of natural articles without any artificial addition of salts or other sodium compounds. These findings strongly support the view that human beings are genetically programmed to eat foods that contain sodium in amounts that are naturally present but do not contain added salt.

*Some researchers in Finland reported that significant reduction of salt from their diets played a critical role in adding 5 to 6 years to the life expectancies of the Finnish population . They also reported that hypertension is the leading cause of death in developed countries. Reduction of salt intake is recommended as a key measure in the prevention and basic treatment of hypertension both in the United States and worldwide. The Renin-Angiotensin Aldosterone (RAA) system is maximally activated when an individual is subjected to prolonged very low sodium intakes of less than 5 mmol a day. Half-maximal stimulation (or inhibition) of plasma rennin activity takes place at sodium intake levels of approximately 30 mmol a day. Sodium intake at the level of 50 mmol a day suppresses secretion of the sodium-retaining hormone, aldosterone, almost completely. The control range of the RAA mechanism is therefore in excellent agreement with the sodium amounts, which can be derived from diets comprising only of natural articles without any artificial addition of salts or other sodium compounds. These findings strongly support the view that human beings are genetically programmed to eat foods that contain sodium in amounts that are naturally present but do not contain added salt.

 

*Blood pressure may continue to build as water is consumed hours after salt is ingested. As excess sodium is excreted by the kidneys, blood pressure drops accordingly.  Diets that consistently contain high salt content will increase blood pressure over time. Fortunately, as many studies have shown, limiting salt intake in the diet can reverse these effects . Since most cases of hypertension are essential hypertension, it is unlikely that a single factor can be attributed to the cause of hypertension in most hypertensive patients . Excessive dietary salt consumption over an extended period of time has been associated with hypertension and cardiovascular diseases, in addition to other adverse health effects.

*Blood pressure may continue to build as water is consumed hours after salt is ingested. As excess sodium is excreted by the kidneys, blood pressure drops accordingly.  Diets that consistently contain high salt content will increase blood pressure over time. Fortunately, as many studies have shown, limiting salt intake in the diet can reverse these effects . Since most cases of hypertension are essential hypertension, it is unlikely that a single factor can be attributed to the cause of hypertension in most hypertensive patients . Excessive dietary salt consumption over an extended period of time has been associated with hypertension and cardiovascular diseases, in addition to other adverse health effects.

A phytochemical study revealed that pipeline’s major active principle is closely related in structure to those of known natural carcinogens – safrole, estragle, and methyleugenol which are also widely distributed in spices and plant oils (Ames, 1983). Piperine might interfere with enzymatic drug biotrasformations resulting in the inhibition of hepatic aryl hydrocarbon hydroxylase (AHH) and UDP-glucuronyltransferase and altered the pharmacokinetic parameters of barbiturates and phenytonin. The immuno-toxicological effects of piperine were investigated in Swiss mice, at a dose of 1.12, 2.15, or 4.5 mg/kg body weight for five consecutive days . All these dose levels had no overt toxic effect, while the lowest dose had no immunotoxic effect.

*Piperine, a major active constituent found in ''pippali'' (Piper longum) has been reported to enhance drug bioavailability . Some researchers studied the interaction of piperine with drug biotransforming reactions in hepatic tissues in vitro and in vivo . Piperine inhibited aryl hydrocarbon hydroxylation, ethylmorphine-N-demethylation, 7-ethoxy-coumarin-O-deethylation, and 3-hydroxybenzo () pyrene (3-OH-BP) glucuronidation in rat liver post-mitochondrial supernatant in vitro in a dose-dependent manner. Piperine’s inhibition of these reactions in liver post-mitochondrial supernatant from 3-methylcholanthrene- and phenodarbital-treated rats was similar to the controls. Inhibition by piperine of aryl hydrocarbon hydroxylase (AHH) from 3-methyleholanthrene-treated rats was comparable to that observed with 7.8-benzoflavone. Piperine caused noncompetitive inhibition of hepatic microsomal AHH from the untreated and 3-methylcholanthrene-treated rats with a Ki of 30 M which was close to the apparent Km of AHH observed in the controls. Similarly, the kinetics of inhibition of ethylmorphine-N-demethylase from control rats liver microsomes exhibited noncompetitive inhibition with aKm of 0.8 mM and Ki or 35 M. These studies demonstrated that piperine is a nonspecific inhibitor of drug metabolism which shows little discrimination between different eytochrome P450 forms.

Excess of intake of ''kshaara'': Oral administration of kshaara (alkali) is recommended for maintaining blood pH level. Reduction in the pH level of the blood- acidic blood is stated to be the prime cause of many inflammatory and degenerative disorders. However excessive alkalinity is again a trouble shooter with regard to tissue functioning.

 

*Excess of intake of ''kshaara'': Oral administration of kshaara (alkali) is recommended for maintaining blood pH level. Reduction in the pH level of the blood- acidic blood is stated to be the prime cause of many inflammatory and degenerative disorders. However excessive alkalinity is again a trouble shooter with regard to tissue functioning.

Metabolic alkalosis is an elevated arterial pH an increase in the serum [HCO3-] and an increase in the Pco2 as a result of compensatory alveolar hypoventilation. Major exogenous causes can be detected as

Metabolic alkalosis is an elevated arterial pH an increase in the serum [HCO3-] and an increase in the Pco2 as a result of compensatory alveolar hypoventilation. Major exogenous causes can be detected as

The University of Maryland Medical Centre reports nausea and vomiting as another typical alkalosis symptom, but again, these symptoms by themselves cannot lead one to the conclusion that elevated alkalinity is the root cause. Interestingly, prolonged vomiting can also cause alkalosis, according to the National Institutes of Health. Such instances are specified as hypochloremic alkalosis (achlorhydria), brought on by extremely low levels of chloride due to the loss of stomach liquids and other contents.

The University of Maryland Medical Centre reports nausea and vomiting as another typical alkalosis symptom, but again, these symptoms by themselves cannot lead one to the conclusion that elevated alkalinity is the root cause. Interestingly, prolonged vomiting can also cause alkalosis, according to the National Institutes of Health. Such instances are specified as hypochloremic alkalosis (achlorhydria), brought on by extremely low levels of chloride due to the loss of stomach liquids and other contents.

However it is noteworthy that the alkali consumed orally may not induce the acute effects of metabolic alkalosis. There seems a vivid variation in the features of acute alkalosis and the effects of long term alkali consumption as explained in [[Charak Samhita]].

However it is noteworthy that the alkali consumed orally may not induce the acute effects of metabolic alkalosis. There seems a vivid variation in the features of acute alkalosis and the effects of long term alkali consumption as explained in [[Charak Samhita]].

== Further reading ==

== Further reading ==