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Medical Forum / Diseases and Disorders / Arthritis / January 2007Porphyria caused by iron cured by vitamin C
<<snip>> ascorbate suppresses hepatic URO accumulation at low, but not high hepatic iron levels <<snip>> Effect of iron and ascorbate on uroporphyria in ascorbate-requiring mice as a model for porphyria cutanea tarda. Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM, Balestra D, Sinclair JF, Sinclair PR Hepatology. 2006 Dec 22; 45(1): 187-194 Excess hepatic iron is known to enhance both porphyria cutanea tarda (PCT) and experimental uroporphyria. Since previous studies have suggested a role for ascorbate (AA) in suppressing uroporphyria in AA-requiring rats (in the absence of excess iron), the present study investigated whether AA could suppress uroporphyria produced by excess hepatic iron. Hepatic URO accumulation was produced in AA-requiring Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered either sufficient AA (1000 ppm) in the drinking water to maintain near normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70 % lower hepatic AA levels. The higher AA intake suppressed hepatic URO accumulation in the absence of administered iron, but not when iron dextran (300-500 mg Fe/kg) was administered. This effect of iron was not due to hepatic AA depletion since hepatic AA content was not decreased. The effect of iron to prevent AA suppression of hepatic URO accumulation was not observed until a high hepatic iron threshold was exceeded. At both low and high AA intakes, hepatic malondialdehyde (MDA), an indicator of oxidative stress, was increased three-fold by high doses of iron dextran. MDA was considerably increased even at low iron dextran doses, but without any increase in URO accumulation. The level of hepatic CYP1A2 was unaffected by either AA intake. Conclusion: In this mouse model of PCT, AA suppresses hepatic URO accumulation at low, but not high hepatic iron levels. These results may have implications for the management of PCT. (HEPATOLOGY 2007;45:187-194.). Abstract · PubMed FullText · SFX · GS Clip Export InterDB · Terms Related · Graph Tag · Scopus · Cites 10.1002/hep.21474 Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk The iron loading diseases .. hemochromatosis and hepatitis C .. may CAUSE .. porphyria .. Sooo .. eating .. meat .. that highly absorbable form of iron FOUND in meat .. then raises iron levels .. and therefore may CAUSE .. porphyria. http://exchange.healthwell.com/news.cfm?news=1746 <<snip>> "it is probable that a chronically high intake of heme iron can lead to high body iron stores and thus may elevate the risk of diabetes," the authors said. " <<snip>> http://en.wikipedia.org/wiki/Porphyria <<snip>> Some liver diseases may cause porphyria even in the absence of genetic predisposition. These include hemochromatosis and hepatitis C. Treatment of iron overload may be required. <<snip>> Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk numbnutz wrote: > The iron loading diseases .. hemochromatosis and hepatitis C .. may > CAUSE .. porphyria .. ferroprotein: a protein combined with an iron-containing radical. Ferroproteins are important oxygen-transferring enzymes (e.g., nicotinamide, adenice dinucleotide dehydrogenase, cytochrome osidase). ferrotherapy: the use of iron in treating anemia. ... Numbnutz Tom suffers from ferropexia. Blah, Blah, Blah.... all very well, but PCT causes a tiny amount of pain when compared to its nastier siblings....acute intermittent, Variegate, coproporphyria (my personal affliction) and others. ...is this telling me that by restricting protein (which I kinda do anyway) and loading up on ascorbic acid (which I don't do, but I don't avoid it either) will "cure" my HCP, which is caused by a genetic defect and leads to a 50% reduction in a key enzyme that turns heme precursors into hemoglobin? I hope so.....If this is true, then Ovation Pharmaceuticals will be out of business in weeks....no need for Panhematin when ascorbic acid will cure all of us. I won't have to take more narcotics than Elvis and Jim Morrison combined and I can crawl out of my basement and see the sun again. In all fairness, I don't really know what they mean by "uroporphyria" as it is not a human disease....maybe I just am too uninformed to understand what I'm reading.....say, do you have a link for the entire article??? ............... Excess hepatic iron is known to enhance both porphyria cutanea tarda (PCT) and experimental uroporphyria. Since previous studies have suggested a role for ascorbate (AA) in suppressing uroporphyria in AA-requiring rats (in the absence of excess iron), the present study investigated whether AA could suppress uroporphyria produced by excess hepatic iron. Hepatic URO accumulation was produced in AA-requiring Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered either sufficient AA (1000 ppm) in the drinking water to maintain near normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70 % lower hepatic AA levels. The higher AA intake suppressed hepatic URO accumulation in the absence of administered iron, but not when iron dextran (300-500 mg Fe/kg) was administered. This effect of iron was not due to hepatic AA depletion since hepatic AA content was not decreased. The effect of iron to prevent AA suppression of hepatic URO accumulation was not observed until a high hepatic iron threshold was exceeded. At both low and high AA intakes, hepatic malondialdehyde (MDA), an indicator of oxidative stress, was increased three-fold by high doses of iron dextran. MDA was considerably increased even at low iron dextran doses, but without any increase in URO accumulation. The level of hepatic CYP1A2 was unaffected by either AA intake. Conclusion: In this mouse model of PCT, AA suppresses hepatic URO accumulation at low, but not high hepatic iron levels. These results may have implications for the management of PCT. (HEPATOLOGY 2007;45:187-194.). Abstract · PubMed FullText · SFX · GS Clip Export InterDB · Terms Related · Graph Tag · Scopus · Cites 10.1002/hep.21474 Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk >>Blah, Blah, Blah.... all very well, but PCT causes a tiny amount of pain when compared to its nastier siblings....acute intermittent, Variegate, coproporphyria (my personal affliction) and others. ...is this telling me that by restricting protein (which I kinda do anyway) and loading up on ascorbic acid (which I don't do, but I don't avoid it either) will "cure" my HCP, which is caused by a genetic defect and leads to a 50% reduction in a key enzyme that turns heme precursors into hemoglobin?<< You seem to have forgotten the iron .. How could you have forgotten the iron .. The iron is why the vitamin C doesn't work .. Increased iron doesn't happen until one .. bypasses .. the bodies natural mechanism for .. control .. the NON - absorption OF .. iron .. WHEN .. not .. NEEDED .. >> I hope so.....If this is true, then Ovation Pharmaceuticals will be out of business in weeks....no need for Panhematin when ascorbic acid will cure all of us. I won't have to take more narcotics than Elvis and Jim Morrison combined and I can crawl out of my basement and see the sun again.<< That is the .. goal .. You are very .. astute .. >> In all fairness, I don't really know what they mean by "uroporphyria" as it is not a human disease....maybe I just am too uninformed to understand what I'm reading.....<< Must .. be .. Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk You seem to have forgotten the iron .. How could you have forgotten the iron .. The iron is why the vitamin C doesn't work .. Increased iron doesn't happen until one .. bypasses .. the bodies natural mechanism for .. control .. the NON - absorption OF .. iron .. WHEN .. not .. NEEDED ..<< The steady increase of iron .. **stores** FROM eating meat / blood .. leads .. toooooo .. ---------------------------------------------- Role of iron in the hydrogen peroxide-dependent oxidation of hexahydroporphyrins (porphyrinogens): a possible mechanism for the exacerbation by iron of hepatic uroporphyria F De Matteis MRC Toxicology Unit, Medical Research Council Laboratories, Carshalton, Surrey, United Kingdom. The hypothesis that the accumulation of uroporphyrin, characteristic of uroporphyria, arises at least in part from oxidation of uroporphyrinogen and the molecular basis for the potentiation of the disorder by iron have been investigated. The iron chelates of ethylenediaminetetraacetic acid (EDTA) and nitrilotriacetic acid were very active at promoting the hydrogen peroxide-dependent oxidation of porphyrinogens, and a similar role of iron was found for the NADPH- dependent oxidation of porphyrinogens by liver microsomes in vitro. In contrast, neither the iron chelate of desferrioxamine (DES) nor ferritin iron possessed prooxidant activity, but the latter could be mobilized in an active form by incubation with EDTA. Iron was also found to promote further modification of the porphyrin pigment, leading to marked loss of its Soret absorbance. This latter effect, which could also be inhibited by DES, suggested further oxidative conversion of the accumulating uroporphyrin, but further work is necessary to establish the relevance of this (or similar) reaction to the inhibitor of uroporphyrinogen decarboxylase which has recently been reported. These results suggest a possible mechanism for the exacerbation of uroporphyria by excess iron and also for its marked improvement when the iron stores are diminished, for example, by DES treatment. Volume 33, Issue 4, pp. 463-469, 04/01/1988 Copyright ? 1988 by American Society for Pharmacology and Experimental Therapeutics -------------------------------------------------------------------------------- http://www.foxriverwatch.com/liver_hepatic_damage_pcbs_1e.html Study #22 iron greatly sensitizes mice to PCB induced hepatic porphyria and liver tumor formation Treatment of Ah-responsive C57BL/10ScSn mice with iron greatly sensitizes them to induction of hepatic porphyria and tumour formation by the polychlorinated biphenyl mixture Aroclor 1254. In the present studies, male C57BL/10ScSn mice received a single dose of iron-dextran (600 mg Fe/kg) and were fed a diet containing 0.01% Aroclor 1254 for 1, 3 and 5 weeks. By use of HPLC with electrochemical detection, 8-hydroxydeoxyguanosine (8-OHdG) was then measured in liver DNA as a marker for oxidative damage. Treatments with iron or Aroclor alone did not result in a significant increase in 8-OHdG except at 3 weeks following iron treatment. At 1 and 3 weeks 8-OHdG levels were induced approximately 3- and 5-fold above control groups respectively in iron- and Aroclor-treated animals. Although there was an apparent 5- to 10-fold increase in the level of 8-OHdG at 5 weeks, this was partially attributed to the in vitro effects of porphyrins, levels of which were massively elevated in liver at this time point. The iron/Aroclor-induced synergistic elevation of 8-OHdG at 1 and 3 weeks was concluded to be due to in vivo damage, thus suggesting the importance of DNA oxidation in the early events of carcinogenesis in this system. (Faux et al, 1992) Study #23 PCBs induce liver enzymes (cytochrome P-450), which increases the oxidative stress caused by iron, which leads to porphyria. PCB-induced uroporphyria may be linked to liver tumors Possible mechanisms of drug induced uroporphyrias were discussed with particular reference to the role of iron (7439896) and the possibility that accelerated uroporphyrinogen (UROgen) oxidation may be important and serve as an indicator of oxidative stress involving iron. One hypothesis was that reactive metabolites of polyhalogenated chemicals, formed by cytochrome-P-450 (P450) isozymes, inhibited uroporphyrinogen-decarboxylase (UDC). Increased porphyria was induced by chlorinated compounds when animals or cells were pretreated with inducers of P450 isozymes, particularly 3-methylcholanthrene (MC) (56495) (P448). Hexachlorobenzene (118741) (HCB), 2,3,7,8-tetrachlorodibenzo-p-dioxin (1746016) (TCDD) and polyhalogenated biphenyls were known inducers of P450s. Responsiveness of two mouse strains to porphyria induction by TCDD correlated with inducibility of P448. HCB and TCDD did not inhibit UDC directly but an inhibitor could be isolated from treated cells. HCB could be metabolized to a protein binding reactive product, although this did not correlate with in-vivo toxicity. This hypothesis did not account for known synergism of iron nor for porphyria induced by chemically unrelated compounds. A theory was presented in which chemicals caused chronic induction of the P450 system, greater production of reduced oxygen metabolites that mobilized iron, and subsequent direct or indirect inhibition of UDC. Liver microsomes from MC pretreated chick embryos catalyzed UROgen oxidation in the presence of NADPH, especially with addition of a uroporphyria inducing biphenyl. A structure activity relationship was noted for uroporphyria induction, P448 induction, and microsomal NADPH dependent UROgen oxidation by two tetrachlorobiphenyls. Increased levels of reduced oxygen species were produced in liver microsomes from animals treated with HCB or MC. Iron alone could induce uroporphyria in-vivo and in-vitro, and there was an apparent association between chemically induced uroporphyria and liver tumor development. (Smith et al, 1990) Study #24 PCBs and iron together increase the incidence of porphyria and liver cancer A study was conducted examining mechanisms underlying the synergistic effects of iron (7439896) and polychlorinated biphenyl compounds on the induction of porphyria. The incidence of porphyria and liver cancer were assessed in mice fed diets containing Aroclor-1254 (11097691) with or without pretreatment with subcutaneous injections of an iron-dextran solution. Pretreatment with iron markedly exacerbated the induction of hepatic porphyria. The porphyria was characterized by decreased hepatic uroporphyrinogen-decarboxylase and accumulation of uroporphyrin-I and uroporphyrin-III. Iron pretreatment also potentiated increases in liver weight, the mitotic rate, oval cell and bile duct proliferation, and cholangiofibrosis in C57BL/10ScSn-mice compared with aryl hydrocarbon nonresponsive DBA-mice. An accelerated development of a mononucleated diploid cell population characteristic of many hepatocarcinogenic regimes in rodents was also identified in C57BL/10ScSn-mice treated with both iron and Aroclor-1254. Based on these results a possible biochemical basis for the synergistic effect of iron involving uncoupling of an induced cytochrome-P450-1A system was described. (Smith et al, 1995) Study #25 PCB-induced cytochrome P450 (particularly the 1A2 isozyme) plays a key role in uroporphyria ascorbic acid (Vitamin C) prevents this uroporphyria The purpose of this project is to determine the mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related planar polychlorinated aromatic hydrocarbons such as polychlorinated biphenyls (PCBs) cause massive liver accumulation of uroporphyrin (URO). This phenomenon is also seen in human Porphyria Cutanea Tarda (PCT). PCT is usually associated with alcohol consumption, use of the contraceptive pill, hemodialysis or diabetes. An additional goal of this project is to determine the relationships of the uroporphyrias caused by TCDD and other conditions. However most of the work has centered on that caused by TCDD and related compounds. Liver cells in tissue culture are used as models for the human and intact animal conditions. A focus was to find suitable culture models and to determine the mechanism of the process of URO accumulation. FINDINGS: We have shown a key role in the uroporphyria of TCDD and PCB-induced cytochrome P450 particularly the 1A2 isozyme. We have shown that the role of the P450 is to catalyze the oxidation of uroporphyrinogen (UROgen). Recently, we demonstrated that ascorbic acid prevents URO accumulation by the chick hepatocytes and isolated microsomes. The site of action of the ascorbate was the first step of the UROgen oxidation and ascorbate was competitive with UROgen. The mechanism of the oxidation is not completely understood. Our results suggest that UROgen is a substrate of the P450 and that ascorbate somehow competes for the oxidizing moiety of the P450. More recently, we have used a rat strain (ODS) that requires ascorbate in its diet to test whether normal levels of ascorbate suppress uroporphyria and deficiency increases uroporphyria. Rats were treated with 3-methylcholanthrene (MC) and 5-aminolevulinate (ALA) and were maintained on 3 different dietary levels of ascorbate. We found that low levels of dietary ascorbate (50 and 200 ppm) resulted in a large accumulation of hepatic uroporphyrin in animals treated with MC plus ALA. At 800 ppm, hepatic uroporphyrin was quite low, similar to that in normal rats that synthesize their own ascorbate. The levels of dietary ascorbate did not affect the induction of P450 1A2 that is an essential participant in the uroporphyrin accumulation. These data suggest that ascorbate has an important role in regulating uroporphyrin in vivo, and validates results obtained in tissue culture and in vitro systems for studying the mechanism of the effect of ascorbate. Recent investigations determined whether iron loading of the ODS rat decreased liver ascorbate. The effect of iron loading was quite small. We also found that 11/13 of a group of PCT patients had plasma levels of ascorbate that were clearly in the deficient range. This was probably due to a poor diet. Smoking, an inducer of P4501A2, was quite common. The relationship of the TCDD/PCB caused uroporphyria to the more common human PCT is not yet known. Our results suggest that the potential role of P4501A2 in this disease needs to be investigated. Furthermore, our work suggests that ascorbic acid prevents this condition. In fact our data suggests that PCT is not more common because UROgen oxidation is prevented in humans by normal levels of ascorbate. This represents a new and specific role of ascorbate in human disease. (Sinclair, 1999) Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk numbnutz wrote: > Effect of iron and ascorbate on uroporphyria in ascorbate-requiring > mice as a model for porphyria cutanea tarda. http://digestive.niddk.nih.gov/ddiseases/pubs/porphyria/index.htm Porphyria Porphyria is a group of different disorders caused by abnormalities in the chemical steps leading to the production of heme, a substance that is important in the body. The largest amounts of heme are in the blood and bone marrow, where it carries oxygen. Heme is also found in the liver and other tissues. Multiple enzymes are needed for the body to produce heme. If any one of the enzymes is abnormal, the process cannot continue and the intermediate products, porphyrin or its precursors, may build up and be excreted in the urine and stool. The porphyria disorders can be grouped by symptoms-whether they affect the skin or the nervous system. The cutaneous porphyrias affect the skin. People with cutaneous porphyria develop blisters, itching, and swelling of their skin when it is exposed to sunlight. The acute porphyrias affect the nervous system. Symptoms of acute porphyria include pain in the chest, abdomen, limbs, or back; muscle numbness, tingling, paralysis, or cramping; vomiting; constipation; and personality changes or mental disorders. These symptoms appear intermittently. The porphyrias are inherited conditions, and the genes for all enzymes in the heme pathway have been identified. Some forms of porphyria result from inheriting an abnormal gene from one parent (autosomal dominant). Other forms are from inheriting an abnormal gene from each parent (autosomal recessive). The risk that individuals in an affected family will have the disease or transmit it to their children is quite different depending on the type. Attacks of porphyria can develop over hours or days and last for days or weeks. Porphyria can be triggered by drugs (barbiturates, tranquilizers, birth control pills, sedatives), chemicals, fasting, smoking, drinking alcohol, infections, emotional and physical stress, menstrual hormones, and exposure to the sun. Porphyria is diagnosed through blood, urine, and stool tests. Diagnosis may be difficult because the range of symptoms is common to many disorders and interpretation of the tests may be complex. Each form of porphyria is treated differently. Treatment may involve treating with heme, giving medicines to relieve the symptoms, or drawing blood. People who have severe attacks may need to be hospitalized. For More Information American Porphyria Foundation P.O. Box 22712 Houston, TX 77227 Phone: 713-266-9617 Email: porphyrus@aol.com Internet: www.porphyriafoundation.com National Organization for Rare Disorders Inc. (NORD) 55 Kenosia Avenue P.O. Box 1968 Danbury, CT 06813-1968 Phone: 1-800-999-6673 or 203-744-0100 Fax: 203-798-2291 Email: orphan@rarediseases.org Internet: www.rarediseases.org American Liver Foundation (ALF) 75 Maiden Lane, Suite 603 New York, NY 10038-4810 Phone: 1-800-GO-LIVER (465-4837), 1-888-4HEP-USA (443-7872), or 212-668-1000 Fax: 212-483-8179 Email: info@liverfoundation.org Internet: www.liverfoundation.org Additional Information on Porphyria The National Digestive Diseases Information Clearinghouse collects resource information on digestive diseases for National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Reference Collection. This database provides titles, abstracts, and availability information for health information and health education resources. The NIDDK Reference Collection is a service of the National Institutes of Health. To provide you with the most up-to-date resources, information specialists at the clearinghouse created an automatic search of the NIDDK Reference Collection. To obtain this information, you may view the results of the automatic search on Porphyria. If you wish to perform your own search of the database, you may access and search the NIDDK Reference Collection database online. -------------------------------------------------------------------------------- National Digestive Diseases Information Clearinghouse 2 Information Way Bethesda, MD 20892-3570 Email: nddic@info.niddk.nih.gov The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health of the U.S. Department of Health and Human Services. Established in 1980, the Clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. The NDDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases. Publications produced by the Clearinghouse are carefully reviewed by both NIDDK scientists and outside experts. This publication is not copyrighted. The Clearinghouse encourages users of this publication to duplicate and distribute as many copies as desired. -------------------------------------------------------------------------------- NIH Publication No. 03-4632 March 2003 > Man Is A Herbivore! > http://tinyurl.com/a3cc3 Created with canine teeth to rip apart and eat MEAT. ... P.E.T.A.: People Eating Tasty Animals numbnutz wrote: > Effect of iron and ascorbate on uroporphyria in ascorbate-requiring > mice as a model for porphyria cutanea tarda. http://www.porphyriafoundation.com/about_por/diet/diet03.html Nutritional recommendations for the acute porphyrias The following are general recommendations that may not apply to all patients with acute porphyria. Individual nutritional needs vary and are affected by the nature and severity of a disease. Therefore, a physician should be consulted and the advice of a dietitian sought before implementing dietary recommendations for a complex medical condition such as porphyria. Other recommendations may need to be added or substituted to meet the needs of an individual patient. These general nutritional recommendations for acute porphyrias are very similar to those for diabetes mellitus. Therefore, physicians and dietitians may find that dietary instructions given for a patient with acute porphyria are not very different from that given for a disease they encounter much more frequently than porphyria. Nutritional recommendations for acute intermittent porphyria, hereditary coproporphyria and variegate porphyria emphasize a high carbohydrate intake as part of a balanced diet that provides all essential nutrients. The recommendations include an adequate intake of dietary fiber, vitamins and minerals. The goals are to prevent acute attacks of porphyria that may be related to diet, avoid deficiencies of nutrients and maintain a normal body weight. The following dietary guidelines are recommended. Energy intake should be prescribed at a level to maintain a desirable body weight. Carbohydrate intake should be 55 to 60 percent of total energy intake. Protein intake should follow the RDA. (Recommended Daily Allowance.) This may be increased in elderly subjects, and reduced if there is kidney impairment. Total fat intake should be less than 30 percent of total calories. In individuals with high blood cholesterol levels, saturated fat should be less than 10 percent of total energy intake, polyunsaturated fat 6 to 8 percent, and the remainder monounsaturated fat. Cholesterol intake should be less than 300 milligrams per day. Artificial sweeteners are acceptable. Salt intake need not be restricted unless it is important for controlling hypertension.(The management of hypertension high blood pressure may include salt restriction. This is not discussed here because most patients with porphyria do not have persistent hypertension.) Intakes of vitamins and minerals should meet the RDAs. Calcium intake in women should be at least one gram daily. ---------------------------------------------- NOTE BELOW------------------------------------------ Iron intake should be adequate to avoid iron deficiency. Women with heavy menstrual blood loss and patients who have had frequent blood drawings due to illness and hospitalization may require greater intakes of iron. (Iron is a component of heme. Iron deficiency can compromise heme synthesis and may exacerbate porphyria. Therefore, iron deficiency should be avoided in porphyria. Early iron deficiency occurs before there is anemia (low blood count). Early iron deficiency can be detected by tests such as serum iron and iron-binding capacity and serum territin.) Alcoholic beverages should be avoided. Alcohol stimulates the heme biosynthetic pathway in the liver and can itself exacerbate porphyria. Alcohol has other harmful effects and can lead to weight gain. Some experts feel that small amounts of alcohol are not harmful in porphyria while others feel that even small amounts should be avoided. Fiber intake should be about 40 grams per day but should not be increased above 50 grams per day. A high-fiber diet may increase the requirements for calcium, iron and trace minerals. High dietary fiber intakes should be avoided in patients with upper gastrointestinal problems (abnormalities in the esophagus or stomach) because sometimes excess fiber can accumulate in the form of "bezoars." Increasing dietary fiber intake sometimes causes abdominal cramping, diarrhea and flatulence. These can be minimized by increasing fiber intake gradually. Foods contain many natural chemicals that can stimulate the heme biosynthetic pathway. Although none have been definitely linked to attacks of porphyria, the possibility that these chemicals might contribute should be kept in mind especially when attacks of porphyria recur in the absence of a definite inciting factor. Some of the dietary factors that might have an adverse effect on porphyria include charcoal-broiled meats (which contain chemicals similar to those found in cigarette smoke), certain vegetables (such as cabbage and brussel sprouts which may contain chemicals that in large amounts can stimulate heme and porphyrin synthesis), and high intakes of protein. Probably, none of these foods need to be completely avoided in porphyria. However, it is important to consume a well-balanced diet and not to consume any particular type of food in excess. The best way to maintain a well-balanced diet is to learn to eat a variety of foods from what are commonly referred to as the four major food groups. Detailed advice on how to do this should be sought from a dietitian > Man Is A Herbivore! > http://tinyurl.com/a3cc3 Created with canine teeth to rip apart and eat MEAT. ... Why are animals made of meat if we're supposed to be vegans? I suppose since you seem to be .. intent .. upon .. eating meat .. then THAT which you posted seems to go against .. everything you RECOMMEND .. WHY would you post stuff that goes .. contrary to what you .. 'say' .. ? That wouldn't be because you are .. stupid .. ? Eh chief .. It would be because you didn't .. bother .. to READ your postings .. ? The food intake is recommended to be .. same as diabetes .. and since THEY have now been recommended to have LOW meat intake .. means .. no / low meat for .. porphyria .. >>These general nutritional recommendations for acute porphyrias are very similar to those for diabetes mellitus. << Iron-rich foods raise heart risks for diabetics. http://www.nlm.nih.gov/medlineplus/news/fullstory_43613.html >>Therefore, physicians and dietitians may find that dietary instructions given for a patient with acute porphyria are not very different from that given for a disease they encounter much more frequently than porphyria. << That would be .. ? .. low meat intake .. / but logically .. NO meat intake .. because .. ? .. meat has a MUCH higher level of absorbable iron than any other source of iron.. therefore .. NO MATTER WHAT .. meat is HIGH in iron. >>Nutritional recommendations for acute intermittent porphyria, hereditary coproporphyria and variegate porphyria emphasize a high carbohydrate intake as part of a balanced diet that provides all essential nutrients.<< High carb .. ? That again .. eliminates .. meat .. You see chief .. carbs and meat are .. mutually .. EXCLUSIVE .. That means .. meat .. does not contain .. carbs .. Those with porphyria .. need .. carbs .. It seems you have come onto a thread and are attempting to convince people to do .. OPPOSITE of what is recommended by .. doctors .. ? Do you have an article or two which may .. **explain** why you seem to be trying to .. kill .. people .. ? >> The recommendations include an adequate intake of dietary fiber, vitamins and minerals. The goals are to prevent acute attacks of porphyria that may be related to diet, avoid deficiencies of nutrients and maintain a normal body weight.<< No fiber in meat .. there .. chief .. >>Porphyria cutanea tarda. Even though porphyrins in this condition originate from the liver, carbohydrate and energy intakes have not been described as major determinants of disease activity. Restriction of dietary iron is usually not necessary.<< "Restriction of dietary iron is usually not necessary" I wonder WHY they said that .. ? Could it be because ALL the .. other .. porphyrias' .. MUST restrict .. dietary .. iron .. ? Nah .. Of course that is why they said it .. Because iron seems to be .. bad / b-a-d .. Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk numbnutz tom, aka ironjustice, wrote: > Effect of iron and ascorbate on uroporphyria in ascorbate-requiring > mice as a model for porphyria cutanea tarda. http://www.porphyriafoundation.com/about_por/diet/diet09.html Nutrition in other types of porphyria A balanced diet that provides all essential nutrients is important for everyone. Otherwise, only a few specific dietary recommendations are justified for types of porphyria other than the acute porphyrias. ALAD porphyria (porphyria due to a deficiency of 8-aminolevulinic acid dehydratase). Effects of diet on this extremely rare condition have not been reported. However, because it bears some resemblances to the acute porphyrias, at least some of the same nutritional considerations may apply. Congenital erythropoeitic porphyria. Diet does not appear to play a specific role in this condition. The excess porphyrins in this condition originate from the bone marrow. The heme biosynthetic pathway in the bone marrow seems to be much less sensitive than in the liver to changes in carbohydrate and energy intakes. Because patients with this condition may be severely ill, however, their diets may be inadequate. Such nutritional deficiencies should be prevented because they may contribute to anemia and other manifestations. Porphyria cutanea tarda. Even though porphyrins in this condition originate from the liver, carbohydrate and energy intakes have not been described as major determinants of disease activity. Restriction of dietary iron is usually not necessary. Erythropoeitic protoporphyria. Excess protoporphyrin in this condition originates primarily from the bone marrow, which as noted above is not highly sensitive to changes in energy and carbohydrate intakes. The bone marrow is sensitive to iron deficiency which, therefore, should be prevented by assuring an adequate intake of iron. Occasionally, the liver seems to contribute significantly to excess protoporphyrin production in erythropoietic protoporphyria and there can be significant liver damage. For this reason, patients with this condition may be advised to follow dietary recommendations similar to those for patients with the acute forms of porphyria. > Man Is A Herbivore! Created with canine teeth to rip apart and eat MEAT. ... I love animals, especially with a good gravy and a baked potato. I suppose since you seem to be .. intent .. upon .. eating meat .. then THAT which you posted seems to go against .. everything you RECOMMEND .. WHY would you post stuff that goes .. contrary to what you .. 'say' .. ? That wouldn't be because you are .. stupid .. ? Eh chief .. It would be because you didn't .. bother .. to READ your postings .. ? The food intake is recommended to be .. same as diabetes .. and since THEY have now been recommended to have LOW meat intake .. means .. no / low meat for .. porphyria .. >>These general nutritional recommendations for acute porphyrias are very similar to those for diabetes mellitus. << Iron-rich foods raise heart risks for diabetics. http://www.nlm.nih.gov/medlineplus/news/fullstory_43613.html >>Therefore, physicians and dietitians may find that dietary instructions given for a patient with acute porphyria are not very different from that given for a disease they encounter much more frequently than porphyria. << That would be .. ? .. low meat intake .. / but logically .. NO meat intake .. because .. ? .. meat has a MUCH higher level of absorbable iron than any other source of iron.. therefore .. NO MATTER WHAT .. meat is HIGH in iron. >>Nutritional recommendations for acute intermittent porphyria, hereditary coproporphyria and variegate porphyria emphasize a high carbohydrate intake as part of a balanced diet that provides all essential nutrients.<< High carb .. ? That again .. eliminates .. meat .. You see chief .. carbs and meat are .. mutually .. EXCLUSIVE .. That means .. meat .. does not contain .. carbs .. Those with porphyria .. need .. carbs .. It seems you have come onto a thread and are attempting to convince people to do .. OPPOSITE of what is recommended by .. doctors .. ? Do you have an article or two which may .. **explain** why you seem to be trying to .. kill .. people .. ? >> The recommendations include an adequate intake of dietary fiber, vitamins and minerals. The goals are to prevent acute attacks of porphyria that may be related to diet, avoid deficiencies of nutrients and maintain a normal body weight.<< No fiber in meat .. there .. chief .. >>Porphyria cutanea tarda. Even though porphyrins in this condition originate from the liver, carbohydrate and energy intakes have not been described as major determinants of disease activity. Restriction of dietary iron is usually not necessary.<< "Restriction of dietary iron is usually not necessary" I wonder WHY they said that .. ? Could it be because ALL the .. other .. porphyrias' .. MUST restrict .. dietary .. iron .. ? Nah .. Of course that is why they said it .. Because iron seems to be .. bad / b-a-d .. Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk I suppose since you seem to be .. intent .. upon .. eating meat .. then THAT which you posted seems to go against .. everything you RECOMMEND .. WHY would you post stuff that goes .. contrary to what you .. 'say' .. ? That wouldn't be because you are .. stupid .. ? Eh chief .. It would be because you didn't .. bother .. to READ your postings .. ? The food intake is recommended to be .. same as diabetes .. and since THEY have now been recommended to have LOW meat intake .. means .. no / low meat for .. porphyria .. >>These general nutritional recommendations for acute porphyrias are very similar to those for diabetes mellitus. << Iron-rich foods raise heart risks for diabetics. http://www.nlm.nih.gov/medlineplus/news/fullstory_43613.html >>Therefore, physicians and dietitians may find that dietary instructions given for a patient with acute porphyria are not very different from that given for a disease they encounter much more frequently than porphyria. << That would be .. ? .. low meat intake .. / but logically .. NO meat intake .. because .. ? .. meat has a MUCH higher level of absorbable iron than any other source of iron.. therefore .. NO MATTER WHAT .. meat is HIGH in iron. >>Nutritional recommendations for acute intermittent porphyria, hereditary coproporphyria and variegate porphyria emphasize a high carbohydrate intake as part of a balanced diet that provides all essential nutrients.<< High carb .. ? That again .. eliminates .. meat .. You see chief .. carbs and meat are .. mutually .. EXCLUSIVE .. That means .. meat .. does not contain .. carbs .. Those with porphyria .. need .. carbs .. It seems you have come onto a thread and are attempting to convince people to do .. OPPOSITE of what is recommended by .. doctors .. ? Do you have an article or two which may .. **explain** why you seem to be trying to .. kill .. people .. ? >> The recommendations include an adequate intake of dietary fiber, vitamins and minerals. The goals are to prevent acute attacks of porphyria that may be related to diet, avoid deficiencies of nutrients and maintain a normal body weight.<< No fiber in meat .. there .. chief .. >>Porphyria cutanea tarda. Even though porphyrins in this condition originate from the liver, carbohydrate and energy intakes have not been described as major determinants of disease activity. Restriction of dietary iron is usually not necessary.<< "Restriction of dietary iron is usually not necessary" I wonder WHY they said that .. ? Could it be because ALL the .. other .. porphyrias' .. MUST restrict .. dietary .. iron .. ? Nah .. Of course that is why they said it .. Because iron seems to be .. bad / b-a-d .. Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk numbnutz tom wrote (posted THREE TIMES) > WHY would you post stuff that goes .. contrary to what you .. 'say' .. ?> > That wouldn't be because you are .. stupid .. ? > It would be because you didn't .. bother .. to READ your postings .. ? Let's see who is stupid. Let's see who doesn't read what is posted. Iron intake should be adequate to avoid iron deficiency. Women with heavy menstrual blood loss and patients who have had frequent blood drawings due to illness and hospitalization may require greater intakes of iron. (Iron is a component of heme. Iron deficiency can compromise heme synthesis and may exacerbate porphyria. Therefore, iron deficiency should be avoided in porphyria. Early iron deficiency occurs before there is anemia (low blood count). Early iron deficiency can be detected by tests such as serum iron and iron-binding capacity and serum territin.) Fiber intake should be about 40 grams per day but should not be increased above 50 grams per day. A high-fiber diet may increase the requirements for calcium, iron and trace minerals. High dietary fiber intakes should be avoided in patients with upper gastrointestinal problems (abnormalities in the esophagus or stomach) because sometimes excess fiber can accumulate in the form of "bezoars." Increasing dietary fiber intake sometimes causes abdominal cramping, diarrhea and flatulence. These can be minimized by increasing fiber intake gradually. Foods contain many natural chemicals that can stimulate the heme biosynthetic pathway. Although *** NONE *** have been definitely linked to attacks of porphyria, the possibility that these chemicals might contribute should be kept in mind especially when attacks of porphyria recur in the absence of a definite inciting factor. Some of the dietary factors that might have an adverse effect on porphyria include charcoal-broiled meats (which contain chemicals similar to those found in cigarette smoke), certain *** vegetables *** (such as cabbage and brussel sprouts which may contain chemicals that in large amounts can stimulate heme and porphyrin synthesis), and high intakes of protein. *** Probably, none of these foods need to be completely avoided in porphyria. *** > The food intake is recommended to be .. same as diabetes .. and since > THEY have now been recommended to have LOW meat intake .. means > .. no / low meat for .. porphyria .. Take the above to your kindergarten teacher or mommy and have them read the above to you, since you have demonstrated a canny inability to comprehend what others are posting. > That would be .. ? .. low meat intake .. / but logically .. NO meat > intake .. because .. ? .. meat has a MUCH higher level of absorbable > iron than any other source of iron.. therefore .. NO MATTER WHAT .. > meat is HIGH in iron. *** PROBABLY NONE OF THESE FOODS NEEDS TO BE COMPLETELY AVOIDED IN PORPHYRIA. *** Iron intake should be adequate to avoid iron deficiency. Women with heavy menstrual blood loss and patients who have had frequent blood drawings due to illness and hospitalization may require greater intakes of iron. (Iron is a component of heme. Iron deficiency can compromise heme synthesis and may exacerbate porphyria. Therefore, iron deficiency should be avoided in porphyria. Early iron deficiency occurs before there is anemia (low blood count). Early iron deficiency can be detected by tests such as serum iron and iron-binding capacity and serum territin.) > High carb .. ? > That again .. eliminates .. meat .. > You see chief .. carbs and meat are .. mutually .. EXCLUSIVE .. Sez you, numbnuts. > Man Is A Herbivore! Created with CANINE TEETH to chew and eat meat. > DEAD PEOPLE WALKING Brain dead, like numbnutz tom. ... numbnutz tom is a mental tourist. His mind wanders! |
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