Changes

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.

*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 micro-somes 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 froms.

*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 micro-somes 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 froms.

 

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.

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.

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

-Acute alkali administration

*Acute alkali administration

-Milk alkali syndrome

*Milk alkali syndrome

-Vomiting

*Vomiting

-Gastric aspiration

*Gastric aspiration

-Diuretics

*Diuretics

-Tobacco chewing

*Tobacco chewing

The National Institutes of Health reports light-headedness as a common alkalosis symptom, as well as confusion. In extreme cases, such symptoms can worsen to the level of catatonic stupor and even coma. Arthur Greenberg and Alfred K. Cheung's "Primer on Kidney Diseases" states that alkalosis may also cause a predisposition to seizures, and Cichoke's book adds that severe cases can also put victims in a state of shock and could cause death. These symptoms, taken together, are very similar to the range of symptoms caused by hypocalcemia, and in isolated cases the milder symptoms could suggest dozens of different health issues. To be sure that the cause of one or more of these symptoms is an elevated level of alkalinity, blood tests administered by a physician are required.

The National Institutes of Health reports light-headedness as a common alkalosis symptom, as well as confusion. In extreme cases, such symptoms can worsen to the level of catatonic stupor and even coma. Arthur Greenberg and Alfred K. Cheung's "Primer on Kidney Diseases" states that alkalosis may also cause a predisposition to seizures, and Cichoke's book adds that severe cases can also put victims in a state of shock and could cause death. These symptoms, taken together, are very similar to the range of symptoms caused by hypocalcemia, and in isolated cases the milder symptoms could suggest dozens of different health issues. To be sure that the cause of one or more of these symptoms is an elevated level of alkalinity, blood tests administered by a physician are required.