Bob
16th August 2016, 23:02
This one affected me personally, so I can speak from experience..
Are you experiencing Shortness of Breath, or Leg Edema (swelling) ? Read on..
ARE you USING MUSTARD products (oil or condiment) and are you getting the symptoms below?
Normally one would use mustard, the condiment, the mustard oil as a seasoning, and of course to actually HELP with respiratory issues..
BUT, of all things, obtaining "bargain" grade mustard oil may not be the most sensible, or healthy. Here are some historical references to what happens when one uses a bargain grade, which contained a dangerous contamination.. I found myself getting unexpected edema in the legs after for a few years using a "bargain grade" mustard.
The moral to the story is, IF you find yourself not getting better from using Mustard for any issue, getting or increasing edema in the limbs, consider that just maybe it (your mustard) could be contaminated... The symptoms are the inability to fully use oxygen and to get rid of CO2 - one feels oxygen starved after the slightest work.. (It mimics as "heart failure" and in actuality can induce heart arrhythmias from the contaminant product..)
It is possible that fast food places or restaurants may be obtaining the mustard oil condiment at "bargain prices"... The article below describes how it happens, and why, the contamination.... and what it does to living organisms consuming the toxin..
I won't necessary speculate that such IS being used to contaminate food products, terroristically, but in these days, issues such as described below SHOULD NEVER BE DISCOUNTED when unusual body conditions happen, for no apparent (natural aging) reason.
Having stopped eating the "bargain priced mustard" I no longer have any of the symptoms below.
Check it out - do you use a mustard product?
====================
Epidemic dropsy is a form of edema of extremities due to poisoning by Argemone mexicana (Mexican prickly poppy).[1][2]
Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with Argemone mexicana seed oil.
Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.
Other major symptoms are bilateral pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.
Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys.
Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation.
Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.
Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.[1]
Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica juncea commonly known as Indian mustard ) as cooking medium is common.[2]
Besides India, widespread epidemics have been reported from Mauritius, Fiji Islands, Northwest Cape districts of South Africa, Madagascar and also from Nepal. Apart from a South African study, where the epidemic occurred through contamination in wheat flour, all the epidemics occurred through the consumption of mustard oil contaminated with argemone oil.[2]
In these populations mustard oil is the prime edible oil by culture.
The earliest reference to argemone oil poisoning was made by Lyon,[3] who reported four cases of poisoning in Calcutta in 1877 from the use of this oil in food.
Since then, epidemic dropsy has been reported from Bengal, Bihar, Orissa, Madhya Pradesh, Haryana, Assam, J&K, Uttar Pradesh, Gujarat, Delhi and Maharashtra, mainly due to consumption of food cooked in argemone oil mixed with mustard oil or occasionally by body massage with contaminated oil.[2]
The epidemic in 1998 at New Delhi, India is the largest so far, in which over 60 persons lost their lives and more than 3000 victims were hospitalized.[2]
Few studies reported the findings in patients affected with this condition.[4]
Even after that the epidemics occurred at alarming frequency in Gwalior (2000), Kannauj (2002) and Lucknow (2005) cities of India.[5]
Mortality is usually due to heart failure, pneumonia, respiratory distress syndrome or renal failure and is around 5%. Long-term follow-up studies are scanty so the long-term effects of argemone oil toxicity have not been documented.
It has been reported that 25% of cases will have oedema beyond 2 months and 10% beyond 5 months. Pigmentation of skin and excessive loss of hair, which lasted 4–5 months following the disease.
The majority of patients completely recover in about 3 months.[1]
ROS and Oxidative stress : Studies in the blood of dropsy patients has revealed that there is extensive ROS production (singlet oxygen and hydrogen peroxide) in the argemone oil intoxication leading to depletion of total antioxidants in the body and especially lipid-soluble antioxidants such as vitamin E and A (tocopherol and retinol).[5]
There is an extensive damage to the anti-oxidant defense system (anti-oxidant enzymes and anti-oxidants) of blood.
Prior, in vitro studies have shown that reactive oxygen species (ROS) are involved in AO induced toxicity causing peroxidative damage of lipids in various hepatic sub-cellular fractions including microsomes and mitochondria of rats.
The damage in hepatic microsomal membrane causes loss of activity of cytochrome P-450 and other membrane bound enzymes responsible for xenobiotic metabolism which leads to delayed bioelimination of sanguinarine and enhances its cumulative toxicity.[6]
Several lines of evidence have been shown to explain the mechanism of toxicity of argemone oil/alkaloid.[7]
The toxicity of sanguinarine has been shown to be dependent on the reactivity of its iminium bond with nucleophilic sites like thiol groups, present at the active sites of the enzymes and other vital proteins and thus suggesting the electrophilic nature of the alkaloid.
Pulmonary Toxicity: The decrease in glycogen levels following argemone oil intoxication could be due to enhanced glycogenolysis leading to the formation of glucose-1-phosphate, which enters the glycoltic pathway resulting in accumulation of pyruvate in the blood of experimental animals and dropsy patients. The enhancement of glycogenolysis can further be supported by the interference of sanguinarine in the uptake of glucose through blocking of sodium pump via Na+-K+-ATPase and thereby inhibiting the active transport of glucose across intestinal barrier.
It is well established that increased pyruvate concentration in blood uncouples oxidative phosphorylation, and this may be responsible for thickening of interalveolar septa and disorganized alveolar spaces in lungs of argemone oil-fed rats and the breathlessness as has been observed in human victims.[2]
Cardiac Failure:The inhibition of Na+-K+-ATPase activity of heart by sanguinarine is due to interaction with the cardiac glycoside receptor site of the enzyme, which may be responsible for producing degenerative changes in cardiac muscle fibers in the auricular wall of rats fed argemone oil and could be related to tachycardia and cardiac failure in Epidemic Dropsy patients.[8]
Delayed clearance:Destruction of hepatic cytochrome P450 significantly affects the metabolic clearance by liver,.[9][10] The retention of sanguinarine in the GI tract, liver, lung, kidney, heart, and serum even after 96 hrs of exposure indicates these as the likely target sites of argemone oil toxicity.[2]
Treatment
Withdrawal of the contaminated cooking oil is the most important initial step.
Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistaminics such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking.
Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as oedema is mainly due to increased capillary permeability.
Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.[1]
REFERENCES
1) a b c d e Sharma, B. D.; Malhotra, S.; Bhatia, V.; Rathee, M. (November 1999). "Epidemic dropsy in India". Postgraduate Medical Journal. 75 (889): 657–661. doi:10.1136/pgmj.75.889.657. PMC 1741391free to read. PMID 10621875.
2) a b c d e f g h Das, M.; Khanna, S. K. (1997). "Clinicoepidemiological, Toxicological, and Safety Evaluation Studies on Argemone Oil". Critical Reviews in Toxicology. 27 (3): 273–297. doi:10.3109/10408449709089896. PMID 9189656.
3) Lyon, I. B. (1889). Textbook of Medical Jurisprudence for India (1st ed.). p. 214.
4) Kar HK, Jain RK, Sharma PK, Gautam RK, Kumar P, Bhardwaj M (2001). "Epidemic dropsy: A study of cutaneous manifestations with histopathological correlation". Indian J Dermatol Venereol Leprol. 67 (4): 178–9. PMID 17664732.
5) a b Das, M.; Babu, K.; Reddy, N. P.; Srivastava, L. M. (2005). "Oxidative Damage of Plasma Proteins and Lipids in Epidemic Dropsy Patients: Alterations in Antioxidant Status". Biochimica et Biophysica Acta. 1722 (2): 209–217. doi:10.1016/j.bbagen.2004.12.014. PMID 15715957.
6) Reddy, N. P.; Das, M. (2008). "Interaction of Sanguinarine Alkaloid, Isolated from Argemone Oil, with Hepatic Cytochrome p450 in Rats". Toxicology Mechanisms and Methods. 18 (8): 635–643. doi:10.1080/15376510701738439. PMID 20020849.
7) Das, M.; Ansari, K. M.; Dhawan, A.; Shukla, Y.; Khanna, S. K. (2005). "Correlation of DNA Damage in Epidemic Dropsy Patients to Carcinogenic Potential of Argemone Oil and Isolated Sanguinarine Alkaloid in Mice" (pdf). International Journal of Cancer. 117 (5): 709–717. doi:10.1002/ijc.21234. PMID 15981203.
8) Seifen, E.; Adams, R. J.; Riemer, R. K. (1979). "Sanguinarine: A Positive Inotropic Alkaloid which Inhibits Cardiac Na+, K+ -ATPase". European Journal of Pharmacology. 60 (4): 373–377. doi:10.1016/0014-2999(79)90245-0. PMID 230984.
9) Upreti KK, Das M, Khanna SK (Jun 1991). "Biochemical toxicology of argemone oil. I. Effect on hepatic cytochrome P-450 and xenobiotic metabolizing enzymes.". J Appl Toxicol. 11 (3): 203–9. doi:10.1002/jat.2550110309. PMID 1918795.
10) Eruvaram, N. R.; Das, M. (2009). "Phenotype of Hepatic Xenobiotic Metabolizing Enzymes and CYP450 Isoforms of Sanguinarine Treated Rats: Effect of P450 Inducers on its Toxicity". Toxicology Mechanisms and Methods. 19 (8): 510–517. doi:10.1080/15376510903313825. PMID 19788401.
http://cc.amazingcounters.com/counter.php?i=3190880&c=9572953
https://upload.wikimedia.org/wikipedia/commons/thumb/1/1b/1-s2.0-S0304416504003162-gr1.jpg/488px-1-s2.0-S0304416504003162-gr1.jpg
The seeds of this pretty innocent looking flower are the cause, they often grow in mustard plant fields:
https://upload.wikimedia.org/wikipedia/commons/thumb/5/57/Argemone_mexicana_flower_2.jpg/330px-Argemone_mexicana_flower_2.jpg
Are you experiencing Shortness of Breath, or Leg Edema (swelling) ? Read on..
ARE you USING MUSTARD products (oil or condiment) and are you getting the symptoms below?
Normally one would use mustard, the condiment, the mustard oil as a seasoning, and of course to actually HELP with respiratory issues..
BUT, of all things, obtaining "bargain" grade mustard oil may not be the most sensible, or healthy. Here are some historical references to what happens when one uses a bargain grade, which contained a dangerous contamination.. I found myself getting unexpected edema in the legs after for a few years using a "bargain grade" mustard.
The moral to the story is, IF you find yourself not getting better from using Mustard for any issue, getting or increasing edema in the limbs, consider that just maybe it (your mustard) could be contaminated... The symptoms are the inability to fully use oxygen and to get rid of CO2 - one feels oxygen starved after the slightest work.. (It mimics as "heart failure" and in actuality can induce heart arrhythmias from the contaminant product..)
It is possible that fast food places or restaurants may be obtaining the mustard oil condiment at "bargain prices"... The article below describes how it happens, and why, the contamination.... and what it does to living organisms consuming the toxin..
I won't necessary speculate that such IS being used to contaminate food products, terroristically, but in these days, issues such as described below SHOULD NEVER BE DISCOUNTED when unusual body conditions happen, for no apparent (natural aging) reason.
Having stopped eating the "bargain priced mustard" I no longer have any of the symptoms below.
Check it out - do you use a mustard product?
====================
Epidemic dropsy is a form of edema of extremities due to poisoning by Argemone mexicana (Mexican prickly poppy).[1][2]
Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with Argemone mexicana seed oil.
Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.
Other major symptoms are bilateral pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.
Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys.
Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation.
Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.
Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.[1]
Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica juncea commonly known as Indian mustard ) as cooking medium is common.[2]
Besides India, widespread epidemics have been reported from Mauritius, Fiji Islands, Northwest Cape districts of South Africa, Madagascar and also from Nepal. Apart from a South African study, where the epidemic occurred through contamination in wheat flour, all the epidemics occurred through the consumption of mustard oil contaminated with argemone oil.[2]
In these populations mustard oil is the prime edible oil by culture.
The earliest reference to argemone oil poisoning was made by Lyon,[3] who reported four cases of poisoning in Calcutta in 1877 from the use of this oil in food.
Since then, epidemic dropsy has been reported from Bengal, Bihar, Orissa, Madhya Pradesh, Haryana, Assam, J&K, Uttar Pradesh, Gujarat, Delhi and Maharashtra, mainly due to consumption of food cooked in argemone oil mixed with mustard oil or occasionally by body massage with contaminated oil.[2]
The epidemic in 1998 at New Delhi, India is the largest so far, in which over 60 persons lost their lives and more than 3000 victims were hospitalized.[2]
Few studies reported the findings in patients affected with this condition.[4]
Even after that the epidemics occurred at alarming frequency in Gwalior (2000), Kannauj (2002) and Lucknow (2005) cities of India.[5]
Mortality is usually due to heart failure, pneumonia, respiratory distress syndrome or renal failure and is around 5%. Long-term follow-up studies are scanty so the long-term effects of argemone oil toxicity have not been documented.
It has been reported that 25% of cases will have oedema beyond 2 months and 10% beyond 5 months. Pigmentation of skin and excessive loss of hair, which lasted 4–5 months following the disease.
The majority of patients completely recover in about 3 months.[1]
ROS and Oxidative stress : Studies in the blood of dropsy patients has revealed that there is extensive ROS production (singlet oxygen and hydrogen peroxide) in the argemone oil intoxication leading to depletion of total antioxidants in the body and especially lipid-soluble antioxidants such as vitamin E and A (tocopherol and retinol).[5]
There is an extensive damage to the anti-oxidant defense system (anti-oxidant enzymes and anti-oxidants) of blood.
Prior, in vitro studies have shown that reactive oxygen species (ROS) are involved in AO induced toxicity causing peroxidative damage of lipids in various hepatic sub-cellular fractions including microsomes and mitochondria of rats.
The damage in hepatic microsomal membrane causes loss of activity of cytochrome P-450 and other membrane bound enzymes responsible for xenobiotic metabolism which leads to delayed bioelimination of sanguinarine and enhances its cumulative toxicity.[6]
Several lines of evidence have been shown to explain the mechanism of toxicity of argemone oil/alkaloid.[7]
The toxicity of sanguinarine has been shown to be dependent on the reactivity of its iminium bond with nucleophilic sites like thiol groups, present at the active sites of the enzymes and other vital proteins and thus suggesting the electrophilic nature of the alkaloid.
Pulmonary Toxicity: The decrease in glycogen levels following argemone oil intoxication could be due to enhanced glycogenolysis leading to the formation of glucose-1-phosphate, which enters the glycoltic pathway resulting in accumulation of pyruvate in the blood of experimental animals and dropsy patients. The enhancement of glycogenolysis can further be supported by the interference of sanguinarine in the uptake of glucose through blocking of sodium pump via Na+-K+-ATPase and thereby inhibiting the active transport of glucose across intestinal barrier.
It is well established that increased pyruvate concentration in blood uncouples oxidative phosphorylation, and this may be responsible for thickening of interalveolar septa and disorganized alveolar spaces in lungs of argemone oil-fed rats and the breathlessness as has been observed in human victims.[2]
Cardiac Failure:The inhibition of Na+-K+-ATPase activity of heart by sanguinarine is due to interaction with the cardiac glycoside receptor site of the enzyme, which may be responsible for producing degenerative changes in cardiac muscle fibers in the auricular wall of rats fed argemone oil and could be related to tachycardia and cardiac failure in Epidemic Dropsy patients.[8]
Delayed clearance:Destruction of hepatic cytochrome P450 significantly affects the metabolic clearance by liver,.[9][10] The retention of sanguinarine in the GI tract, liver, lung, kidney, heart, and serum even after 96 hrs of exposure indicates these as the likely target sites of argemone oil toxicity.[2]
Treatment
Withdrawal of the contaminated cooking oil is the most important initial step.
Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistaminics such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking.
Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as oedema is mainly due to increased capillary permeability.
Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.[1]
REFERENCES
1) a b c d e Sharma, B. D.; Malhotra, S.; Bhatia, V.; Rathee, M. (November 1999). "Epidemic dropsy in India". Postgraduate Medical Journal. 75 (889): 657–661. doi:10.1136/pgmj.75.889.657. PMC 1741391free to read. PMID 10621875.
2) a b c d e f g h Das, M.; Khanna, S. K. (1997). "Clinicoepidemiological, Toxicological, and Safety Evaluation Studies on Argemone Oil". Critical Reviews in Toxicology. 27 (3): 273–297. doi:10.3109/10408449709089896. PMID 9189656.
3) Lyon, I. B. (1889). Textbook of Medical Jurisprudence for India (1st ed.). p. 214.
4) Kar HK, Jain RK, Sharma PK, Gautam RK, Kumar P, Bhardwaj M (2001). "Epidemic dropsy: A study of cutaneous manifestations with histopathological correlation". Indian J Dermatol Venereol Leprol. 67 (4): 178–9. PMID 17664732.
5) a b Das, M.; Babu, K.; Reddy, N. P.; Srivastava, L. M. (2005). "Oxidative Damage of Plasma Proteins and Lipids in Epidemic Dropsy Patients: Alterations in Antioxidant Status". Biochimica et Biophysica Acta. 1722 (2): 209–217. doi:10.1016/j.bbagen.2004.12.014. PMID 15715957.
6) Reddy, N. P.; Das, M. (2008). "Interaction of Sanguinarine Alkaloid, Isolated from Argemone Oil, with Hepatic Cytochrome p450 in Rats". Toxicology Mechanisms and Methods. 18 (8): 635–643. doi:10.1080/15376510701738439. PMID 20020849.
7) Das, M.; Ansari, K. M.; Dhawan, A.; Shukla, Y.; Khanna, S. K. (2005). "Correlation of DNA Damage in Epidemic Dropsy Patients to Carcinogenic Potential of Argemone Oil and Isolated Sanguinarine Alkaloid in Mice" (pdf). International Journal of Cancer. 117 (5): 709–717. doi:10.1002/ijc.21234. PMID 15981203.
8) Seifen, E.; Adams, R. J.; Riemer, R. K. (1979). "Sanguinarine: A Positive Inotropic Alkaloid which Inhibits Cardiac Na+, K+ -ATPase". European Journal of Pharmacology. 60 (4): 373–377. doi:10.1016/0014-2999(79)90245-0. PMID 230984.
9) Upreti KK, Das M, Khanna SK (Jun 1991). "Biochemical toxicology of argemone oil. I. Effect on hepatic cytochrome P-450 and xenobiotic metabolizing enzymes.". J Appl Toxicol. 11 (3): 203–9. doi:10.1002/jat.2550110309. PMID 1918795.
10) Eruvaram, N. R.; Das, M. (2009). "Phenotype of Hepatic Xenobiotic Metabolizing Enzymes and CYP450 Isoforms of Sanguinarine Treated Rats: Effect of P450 Inducers on its Toxicity". Toxicology Mechanisms and Methods. 19 (8): 510–517. doi:10.1080/15376510903313825. PMID 19788401.
http://cc.amazingcounters.com/counter.php?i=3190880&c=9572953
https://upload.wikimedia.org/wikipedia/commons/thumb/1/1b/1-s2.0-S0304416504003162-gr1.jpg/488px-1-s2.0-S0304416504003162-gr1.jpg
The seeds of this pretty innocent looking flower are the cause, they often grow in mustard plant fields:
https://upload.wikimedia.org/wikipedia/commons/thumb/5/57/Argemone_mexicana_flower_2.jpg/330px-Argemone_mexicana_flower_2.jpg