Medical Forum / General / General / December 2005
Amoebic dysentery / iron saturation
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ironjustice@aol.com - 14 Dec 2005 02:14 GMT This article seems to give credence to the increasing levels of iron .. leading to .. disease .. proliferation.
Lactoferrin an iron binding protein is able to stop the disease when it is unloaded / no iron on board / apolactoferrin .. but .. when saturated / bound up with iron / holotransferrin .. the pathogen can access the iron.
http://www.brinkzone.com/lacto.html
<<snip>> lactoferrin is hololactoferrin in its iron bound form and apolactoferrin in its iron depleted form <<snip>>
Microbiology. 2005 Dec;151(Pt 12):3859-3871. Links
Human hololactoferrin: endocytosis and use as an iron source by the parasite Entamoeba histolytica.
Leon-Sicairos N, Reyes-Lopez M, Canizalez-Roman A, Bermudez-Cruz RM, Serrano-Luna J, Arroyo R, de la Garza M.
Departamento de Biologia Celular, Centro de Investigacion y de Estudios Avanzados del IPN, Apdo. 14-740, Mexico, D F 07000, Mexico.
Entamoeba histolytica is an enteric protozoan that exclusively infects human beings. This parasite requires iron for its metabolic functions. Lactoferrin is a mammalian glycoprotein that chelates extracellular iron on mucosal surfaces, including the surface of the large intestine, where E. histolytica initiates infection. This work examined the interaction in vitro of E. histolytica trophozoites with human hololactoferrin (iron-saturated lactoferrin). A minimum concentration of 50 muM Fe from hololactoferrin supported growth of the amoeba. Amoebic binding sites for hololactoferrin were different from those for human apolactoferrin, holotransferrin and haemoglobin. One amoebic hololactoferrrin-binding polypeptide of 90 kDa was found, which was not observed after treatment of trophozoites with trypsin. Hololactoferrin-binding-protein levels increased in amoebas starved of iron, or grown in hololactoferrin. Internalization of hololactoferrin was inhibited by filipin. Endocytosed hololactoferrin colocalized with an anti-chick embryo caveolin mAb in amoebic vesicles, and lactoferrin was further detected in acidic vesicles; amoebic caveolin of 22 kDa was detected by Western blotting using this antibody. Cysteine proteases from amoebic extracts were able to cleave hololactoferrin. Together, these data indicate that E. histolytica trophozoites bind to hololactoferrin through specific membrane lactoferrin-binding proteins. This ferric protein might be internalized via caveolae-like microdomains, then used as an iron source, and degraded.
PMID: 16339932 [PubMed - as supplied by publisher]
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<<snip>> Lactoferrin probably exerts its effect at the level of viral adsorption, <<snip>>
: J Infect Dis 2002 Oct 15;186(8):1161-1164 Links Lactoferrin Inhibits Enterovirus 71 Infection of Human Embryonal Rhabdomyosarcoma Cells In Vitro.
Lin TY, Chu C, Chiu CH.
Department of Pediatrics, Chang Gung Children's Hospital, Kweishan, Taoyuan, Taiwan.
Enterovirus 71 (EV71), the newest member of Enterovirudae, is notable for its etiological role in epidemics of severe neurological diseases in children. It appears to be emerging as an important virulent neurotropic enterovirus in the upcoming era of poliomyelitis eradication, whereas no effective vaccine or antiviral agents are available at this moment. Human and bovine lactoferrins, iron-binding proteins belonging to the nonimmune defense system, were assayed in vitro to assess their inhibiting capacity on the cytopathic effect of EV71 on human embryonal rhabdomyosarcoma (RD) cells. Both bovine and human lactoferrins were found to be potent inhibitors of EV71 infection (mean IC(50), 10.5-24.5 &mgr;g/mL and 103.3-185.0 &mgr;g/mL, respectively). Lactoferrin probably exerts its effect at the
level of viral adsorption, since the ongoing infection could not be further inhibited after the EV71 penetrated RD cells.
PMID: 12355368 [PubMed - as supplied by publisher]
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Who loves ya. Tom -- Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking
outsor@citynet.net - 14 Dec 2005 13:34 GMT "This article seems to give credence to the increasing levels of iron .. leading to .. disease .. proliferation."
Or stated another way more in line with biological reality, there is a minimal, an optimal, and a maximal level in all biological processes. The min for there to be an effect, the opt for best outcomes and a max where more adds no benefits and becomes counterproductive. In the case of iron and many other things, moderation in all things is always a wise choice and includes having some animal products in one's diet.
Manky Badger - 14 Dec 2005 22:44 GMT OK Tom - explain this:
Pleasant lady in mid thirties presented a few months ago with pallor and fatigue. Nails appear brittle & indented, and complains of heavy monthly blood loss. Blood count:
Hb 7.2 g/dl MCV 66.3 fl
Prescribed oral ferrous sulphate to be taken daily. Now (a few months later) is feeling on top of the world.
ironjustice@aol.com - 15 Dec 2005 02:58 GMT Actually the post is .. amoebic dysentry ..
You seem to be full of questions ..
Ask your pocketpoolbuddieeeeee .. how / why he .. feels .. justified in falsifying medical studies to .. fit ..
Since he seems to be one of your close .. pals ..
Get him to explain .. it ..
Then I'll explain something much simpler ... to .. you ..
Until then .. I will treat you with the same disdain .. reserved for the likes of you and your pal ..
Step down .. and away .. you little fkg pussy ..
Who loves ya. Tom -- Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking
Manky Badger - 15 Dec 2005 19:07 GMT > Actually the post is .. amoebic dysentry .. > > You seem to be full of questions .. And you have no answers.
> Ask your pocketpoolbuddieeeeee .. how / why he .. feels .. justified in > falsifying medical studies to .. fit .. > > Since he seems to be one of your close .. pals .. > > Get him to explain .. it .. ???
ironjustice@aol.com - 17 Dec 2005 18:48 GMT Scurvy ..
http://www.findarticles.com/p/articles/mi_m0PDG/is_1_2/ai_110152641
Brittle nails: pathogenesis and treatment Journal of Drugs in Dermatology, Jan, 2003 by Hendrik Uyttendaele, Adam Geyer, Richard K. Scher
It is equally important to rule out systemic etiologies for brittle nails. These include infections such as tuberculosis, endocrinopathies (hypo- and hyperthyroidism (7,8), hypoparathyroidism (9), and pituitary disorders (10)), hypochlorhydria, iron deficiency anemia (11), hemochromatosis (12), arsenical intoxication, glucagonoma (13), osteoporosis, osteomalacia, diseases that cause severe arthritic deformities of the distal joints, Sjogren's syndrome and nutritional disturbances such as cachexia (14), vitamin and zinc deficiencies (15).
The treatment of brittle nails is often difficult. If no precipitating or contributing factors can be elucidated and if the brittle nails have been present for many years, available treatments are often ineffective. However, the initial approach to the treatment of brittle nails should focus on the removal of any exogenous factors that may cause or exacerbate nail fragility. Patients should be instructed not to wash hands frequently and to avoid contact with water or other dehydrating chemicals. Rehydration of the nail plate, cuticle and surrounding nail fold can be obtained by soaking the nails in lukewarm water followed by application of an effective moisturizer. Alpha-hydroxy acid containing moisturizer and preparations that contain hydrophilic substances such as phospholipids have been successfully used for this (16). Occasionally, the once a week use of nail enamel is encouraged to slow water evaporation from the nail plate. It is also recommended that the patients keep their nails short, and clip them after soaking them in lukewarm water.
Numerous therapies have been tried for brittle nails. These include application of essential fatty acids, vitamin c, pyridoxine, iron, vitamin D, calcium, and gelatin (17-19). Several systemic therapies for the treatment of brittle nails have also been tried. Oral iron, primrose oil, pyridoxine and ascorbic acid have been suggested to be of some value (20). More recently biotin, a water-soluble B-complex vitamin, has been demonstrated in several studies to be beneficial in the treatment for brittle nails (21-23). The initial rational for this treatment came from the field of veterinary medicine where biotin had been used for the treatment of pathologic hoof changes in horses (24). An association between deficiency of B-complex vitamins had also been proposed as early as 1940 (25). The recommended daily oral biotin dose is 2.5 mg, with two months being the average time before clinical improvements are observed and the recommended time of treatment is 3-6 months. An increase in nail thickness, decreased lamellar splitting, and decreased irregularities of the dorsal nail plate surface were observed in patients with brittle nails treated with Biotin (21). It is not known how long the improvement in nail strength lasts after cessation of biotin treatment. It also remains unclear how biotin-dependent biochemical mechanisms are responsible for nail plate strength, and whether they are necessary for nail keratin or intercellular cement substance production. Lastly, treatments that would increase the rate of nail growth would be beneficial in the treatment of brittle nails. ------------------------------------------------------------------------------------------------------------ If you notice in this article .. the treatment of scurvy resulted in alleviation of .. anemia. Anemia is considered to be THE 'greatest' nutritional problem in the world? Anemia in India is treated successfully with vitamin C. Therefore accordig to these stats on vitamin C deficiency .. the percentage of anemic individuals seems to parallel those with vitamin C deficiency.
Lack of vitamin C and NOT ..iron deficiency?
J Med Assoc Thai 2001 Jun;84 Suppl 1:S106-10
Scurvy: a case report.
Chatproedprai S, Wananukul S
Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
An 8-year-old child with cerebral palsy came with progressive purpuric rash affecting the trunk and legs. He had tenderness on palpation of
his extremities. Physical examination revealed a moderately pale and
cachectic boy. There was bleeding per swollen gums and petichiae on the hard palate. Generalized multiple discrete palpable petichiae spots at hair follicles along the whole body, more on both legs, were observed. He also had tenderness on palpation of his extremities. His hemoglobin was 6.6 g/dl. Platelet count and coagulogram were normal.
Roentgenographic findings showed generalized osteoporosis, metaphyseal white line of distal femur, proximal tibia. proximal fibula, distal radius, and distal ulna with submetaphyseal lucency bilaterally. Skin biopsy showed dilated hair follicles, filled with keratinous material and a small corkscrew hair. A diagnosis of scurvy was made; and vitamin C at a dosage of 300 mg per day was given. His swollen gums,
bleeding per gums and muscle tenderness improved within 2 days. Perifollicular hemorrhage, follicular hyperkeratosis, and anemia improved in 2 and 3 weeks respectively.
PMID: 11529321, UI: 21420014 _________________________________________________________________
Studies in India have shown anemia to be far more easily corrected by the inclusion of vitamin C than supplementing iron. This study shows the 'anemia' present and considered by most doctors to be 'iron deficient' anemia .. is NOT .. and is due to lack of vitamins.
: Food Nutr Bull 2002 Mar;23(1):94-105 Related Articles, Links Iron-deficiency anemia in young working women can be reduced by increasing the consumption of cereal-based fermented foods or gooseberry juice at the workplace.
Gopaldas T.
Tara Consultancy Services, Bangalore, India.
This efficacy for both employers and employees (young working women 18 to 23 years of age) was undertaken to determine whether culturally acceptable dietary changes in lunches in the workplace and at home could bring about a behavioral change and improvement in their iron-deficiency anemia status. Maximum weight was given to increasing consumption of iddli, a popular cereal-based-fermented food, or of gooseberry juice. Four small factories were selected in periurban Bangalore, with a sample of 302 women. The 180-day interventions were supervised at the workplace. In unit 1 (72 women), the intervention consisted of iddli four times a week plus information, education, and communication (IEC) related to iron-deficiency anemia. Unit 2 (80 women) received 20 ml of gooseberry juice (containing 40 mg of vitamin C) three times a week plus IEC once a month. Women in unit 3 (70 women), the positive control, received 400 mg albendazole once plus ferrous sulfate tablets (60 mg elemental iron) two times a week. No IEC was given. Unit 4 (70 women) served as the negative control and received no intervention. The pre-post impact measures were dietary and
nutrient intake, knowledge and practice, and hemoglobin status. In units 1, 2, and 3, the hemoglobin status of the women improved significantly from 11.10 to 12.30 g/dl, 11.20 to 12.70 g/dl, and 11.50 to 13.00 g/dl, respectively. In unit 4 there was no change: the values were 10.90 g/dl before and after intervention. The results show that the type of workplace lunch was of greater significance than IEC. Knowledge gains were impressive, but behavioral change was not sustained. It was concluded that the hemoglobin levels of the workers can easily be improved by cost-effective workplace lunches that also lead to better employer-employee relations.
PMID: 11975375 [PubMed - indexed for MEDLINE]
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CORRECTION OF ANEMIA AND IRON DEFICIENCY IN VEGETARIANS BY ADMINISTRATION OF ASCORBIC ACID
DINESH C. SHARMA* AND RATI MATHUR
*Corresponding Author
Department of Biochemistry S M S Medical College, Jaipur - 302 004
(Received on December 8, 1994)
Abstract: Twenty-eight strict vegetarians were given 500 mg ascorbic
acid twice daily after lunch and dinner for two months. Hemoglobin and certain iron status parameters were measured before and after the treatment. Ascorbate treatment increased mean hemoglobin by 8%, serum iron by 17% and transferrin saturation by 23% and decreased total iron binding capacity by 7%. All these changes were statistically significant. The rise in serum ferritin was 12%. The serum protein or copper level did not indicate their dietary deficiency, while initial serum ascorbate level were low which rose by 60% on therapy. It is concluded that ascorbate supplementation is a better method of improving hematologic and iron status than iron salt administration.
Key words: ascorbic acid, iron deficiency, anemia, vegetarians, hemoglobin, iron, ferritin _________________________________________________________________
INTRODUCTION
Anemia is the second most common affliction in the world and iron deficiency is the most common cause of it (1). The incidence of iron
deficiency anemia is much greater in India than western countries, despite the fact that daily iron intake of Indians is twice that of westerners (2, 3). This apparent paradox is attributed to consumption of predominantly cereal based diet, rich in phytate, oxalates, phosphates, fiber and other inhibitors of iron absorption, by the majority of Indians who practice vegetarianism on account of religion or poverty (4, 5). So we had found significantly lower serum iron in
healthy vegetarians as compared to healthy non-vegetarians (6). Similarly vegetarian parturient women had significantly lower hemoglobin, serum iron and transferrin saturation in comparison to their non-vegetarian counterparts (7). Recently in a closely matched
study all the parameters (hemoglobin, serum iron, transferrin saturation and ferritin) were significantly lower in vegetarian women and their newborns, respectively, despite having received supplemental iron (Ferrous sulphate=60 mg Fe) for about six months during antenatal period (5). The absence of expected response in hemoglobin regeneration was perhaps due to the fact the vegetarian diet was not
deficient in iron but some other nutrient. The dietary survey of vegetarian mothers revealed that their diet was lacking in ascorbic acid as the consumption of fruits and citrus fruits was meagre (5).
The present study was, therefore, undertaken to see the effect of administration of ascorbic acid on hemoglobin and iron status of strictly vegetarian people. _________________________________________________________________
METHODS
The subjects of this study were taken from the staff of the Department of Biochemistry, medical and nursing students, neighbours etc. who volunteered for the study and were vegetarians. All person were known to be healthy so that the drug compliance could be checked frequently and follow up was easy. They were selected on the basis of their dietary habit (vegetarianism) rather than initial hemoglobin level. All the subjects were free from infection and inflammation which are
known to affect serum iron, total iron binding capacity and ferritin
values (3).
The study started with 36 persons but ended with 28; eight persons discontinued vitamin tablets or were erratic in taking them. All the
subjects were asked to take a 500 mg ascorbic acid tablet (Celin, Glaxo) within half an hour after lunch and dinner regularly for two months. Then each person received 1 gm ascorbic acid daily and a total of 60 gm during the study. The dose was not large enough to cause any harmful effect. No one had complained of any side effect. The subjects were not allowed to take any hematinic during this study.
The blood was collected before and after the drug trial. The following estimations were performed on both the samples immediately after the
collection - blood hemoglobin (Hb) (cyanmethemoglobin method), serum
iron (8), total iron binding capacity (TIBC) (8), percent saturation
(PS), (by calculation), serum ferritin (9), serum copper (10), total
proteins (11) and ascorbic acid (12).
An oral questionnaire method was used to find out the details of the
diet intake and dietary habits of all the subjects studied.
The results were statistically analyzed by the paired `t' test (13).
The critical level of significance was 5 percent (probability, 0.05). _________________________________________________________________
RESULTS
Out of 28 subjects of this study, 10 were male, 18 were female, and 28 had initial Hb level below the WHO normal range. Their age ranged between 18-50 years. All were vegetarians and had regularly taken vitamin C tablets. This is confirmed by a rise in ascorbic acid of about 60% in two months time (Table I)
The pre- and post-treatment values are shown in Table I. There was a
statistically significant rise in blood hemoglobin, highly significant rise in serum iron and a significant fall in total iron binding capacity. The rise in transferrin saturation of plasma was highly significant. Interestingly, the response to therapy was better in those who were iron deficient/anemic. Serum ferritin level also showed a rise but statistically insignificant. It may be because (i) the normal range of serum ferritin is very wide, (ii) increased iron was
preferentially utilized for hemoglobin regeneration rather than storage, and (iii) ferritin reflects storage iron which was not expected to rise appreciably in such a short time.
TABLE I. : Hematalogic and iron status of vegetarians before and after ascorbate treatment
Parameter
Pre-treatment level
Post-treatment level
"t" (paired)
"P"
Percent rise Hemoglobin (g/dl) 10.10 01.80 10.90 01.40 5.81 <0.001 07.90 Iron (g/dl) 63.70 13.70 74.50 13.00 6.36 <0.001 16.90 Total Iron Binding Capacity (g/dl) 325.30 49.60 301.70 55.40 -3.62 <0.010 -07.20 Percent Saturation (%) 19.90 05.40 24.40 04.90 4.32 <0.001 22.60
Ferritin (ng/ml) 39.90 39.30 44.70 40.80 1.23 NS 12.00 Ascorbic Acid (mg/dl) 00.47 00.10 00.75 00.20 7.03 <0.001 59.50 Total Proteins (g/dl) 08.33 00.47 06.42 00.43 0.09 NS 01.40 Copper (g/dl ) 80.90 18.00 81.40 19.30 0.53 NS 00.60
All values are Mean SD; NS-Indicates Not Significant _________________________________________________________________
DISCUSSION
The improvement in iron status and correction of anemia in vegetarians by giving only ascorbic acid is a very important finding. Such studies were also conducted in the past but the results were not conclusive (14), because the studies were multifactorial (14).
The role of ascorbic acid in iron metabolism is manyfold. It reduces
ferric iron to ferrous form which is then absorbed, lowers the pH which is conducive to iron absorption, reverses the inhibitory effect of phytate, oxalate, phosphate etc., and also forms chelate with iron for absorption (15).
As dietary proteins and copper also affect iron absorption and utilization, so in this study total serum proteins and serum copper were also estimated. Their levels were within normal range (16) suggesting nutritional adequacy of these nutrients. On the other hand ascorbate level in serum was low or on the lower side of normal (16)
indicating inadequate vitamin C nutrition. This confirms our contention of Vitamin C nutritional inadequacy in vegetarian population on account of meagre intake of fruits, especially citrus fruits (5). The intake of fruits by subjects of present study was also very bow, as revealed by diet survey during oral questionnaire.
The control of nutritional anemia is one of the national health programme of Government of India (17) and pregnant women are advised
to take ferrous sulphate tablets. As iron preparations did not give desired response in our previous study (5) and are not well tolerated by many persons we instead suggest vitamin C tablets (500 mg) to be given twice daily after every major meal. This will improve iron status and correct anemia as shown in this study. In contrast to iron preparations ascorbic acid is well tolerated, quite palatable and harmless. The risk of forming oxalate stones was reported with only megadoses of vitamin C (18), and even this was not confirmed in experimental animals (19). In addition, the daily consumption of vitamin C may confer following benefits (20) - prevent common cold and other viral infections, retard atherosclerosis, decrease risk of cancer, slow down ageing and reduce toxicity of metals.
It is hoped that this study will stimulate further work in this field and that physicians will see the need for prescribing vitamin `C' tablets instead of iron tablets for amelioration of anemia or iron deficiency, especially because men and women need to absorb only 1.14 to 2.38 mg of iron per day (21) while the actual intake iron vegetarian diet in this region is calculated to range from 22.0 to 37.0 mg per day (22). _________________________________________________________________
ACKNOWLEDGEMENTS
This work was supported by a Research Grant from S.M.S. Medical College, Jaipur for which we are thankful to the Principal, Dr. P. L. Nawalakha.
REFERENCES
1. DeMeayer EM, Adiels-Tegman M. The prevalence of anemia in the world. World Health Stat Q 1985;38:302-316. 2. Baker SJ, DeMeayer EM. Nutritional anemia: Its understanding and
control with special reference to the work of the World Health Organisation. Am J Clin Nutr 1979; 32:368-417. 3. Sharma DC, Mathur R, Singh PP. Iron metabolism: A review. Ind J Clin Biochem 1993;8:80-101. 4. Dwyer JT. Nutritional consequences of vegetarianism. Ann Rev Nutr 1991;11:61-91. 5. Sharma DC, Kiran R, Ramnath, V, Khushlani K, Singh PP. Iron deficiency and anemia in vegetarian mothers and their new-borns.
Ind J Clin Biochem 1994;9:100-102. 6. Sharma DC, Khalsa JK, Soni BL, Singh PP, Simlot MM. Some observations on serum iron level in health. J Indian Med Assoc 1972;58:204-207. 7. Sharma DC, Pendse V, Sahay K, Soni BL. The changing pattern of maternal and neonatal anemia at Udaipur during 2 decades in relation to poverty, parity, prematurity and vegetarianism. Asia-Oceania J Obstet Gynaec 1991;17: 13-17. 8. Tietz NW. Fundamentals of clinical chemistry. Philadelphia, Saunders 1976:926-928. 9. Franco RS. Ferritin. In Pesce AJ, Kaplan LA, eds, Methods in clinical chemistry. St. Louis Mosby 1987;1240-1242. 10. Zak B. Simple procedure for single sample determination of serum
copper and iron. Clin Chim Acta 1958;34:328-334. 11. Varley H. Practical clinical biochemistry. New Delhi, Heinemann 1976:236-238. 12. Natelson S. Techniques of clinical chemistry. Springfield, C.C. Thomas 1971:162-165. 13. Mahajan B.K. Methods in biostatistics for medical students and research workers. New Delhi, Jaypee Brothers 1991:146-151. 14. Hunt JE, Mullen LM, Lykken GI, Gallagher SK, Neilsen FH. Ascorbic acid: effect on ongoing iron absorption and status in iron depleted young women. Am J Clin Nutr 1990;51:649-655. 15. Siegenberg D, Baynes RD, Bothwell TH, Macfarlane BJ, LamParelli RD, Car NG, Mac-Phail P, Schmidt U, Tal A, Mayet F. Ascorbic acid prevents the dose-dependent inhibitory effects of polyphenols and phytates on nonheme iron absorption. Am J Clin Nutr 1991;53:537-541. 16. Behrman RE, Kliegman RM. Nelson text book of pediatrics. Philadelphia, Saunders 1987:1536-1558. 17. Ministry of Health & Family Welfare. Policy on control of nutritional anemia. New Delhi Ministry of Health & Family Welfare, Government of India 1991:1-8 18. Chalmers AH, Cowley DM, Brave JM. A possible etiological role for ascorbate in calculi formation. Clin Chem 1986;32:333-336. 19. Singh PP, Sharma DC, Rathore V, Surana SS. An investigation into
the role of ascorbic acid in renal calculogenesis in albino rats. J Urol 1988;139:156-157. 20. Krupp MA, Chatton MJ, Tierney Jr LK. Current medical diagnosis and Treatment. Los Altos, Lange 1986;816&987. 21. FAO. Food and Nutrition Series No.23, Rome, F.A.O. 1988. 22. Soni BL, Sharma DC. Total and ionizable iron in common Indian Cooked foods Am J Clin Nutr 1974;27:455-457. _________________________________________________________________
From Indian Journal of Physiology and Pharmacology, October 1995, Volume 39, Number 4, pp. 403-406
HTML Revised 16 January, 2000. Corrections and formatting 2000 AscorbateWeb
Who loves ya. Tom -- Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking
Manky Badger - 17 Dec 2005 20:20 GMT >Scurvy .. Very interesting hypothesis. Please forgive me for snipping most of it since otherwise the message becomes too long to read. But be assured I'm impressed with it. There's only one really contentious issue. At the risk of upsetting our new-found detente the bit:
>The results show that the type of workplace lunch was of greater >significance than IEC. Knowledge gains were impressive, but behavioral >change was not sustained. would show that there is one symptom of what I would consider the iron deficiency that wasn't corrected by the vitamin C. However I'm willing to suppose that more vitamin C (hence more dietary iron absorbed) might sort this one out.
But I have a reservation
Effectively what the articles are saying is that there is a deficiency of iron which is corrected by vitamin C. If one has an iron deficient anaemia, it is very easy to measure iron status in a laboratory, either directly as iron, as TIBC, as ferritin, as a rise to normal in the MCV. OK - I concede that the "normal" ranges might be subject to debate, but there are several markers all of which are readily measurable in the routine hospital laboratory. As I fully appreciate the dangers of iron overload, I would monitor iron treatment in this variety of ways until I felt replenishment had been achieved. That is I am directly monitoring that which is being administered.
I cannot do this with vitamin C therapy as vitamin C assays are not readily available in routine hospital laboratories. And as I'm sure you're aware, too much vitamin C gives intestinal hurry, and then we're back to the malabsorbtion problems again. There's also renal damage implicit in overdosing on vitamin C which can give a false diagnosis of diabetes. I can see when to stop iron therapy from the lab results. I don't have such information for vitamin C therapy. I can monitor the results of the treatment, but when to stop? I have no way of knowing if vitamin C is reaching dangerous levels until the patient becomes symptomatic.
However, the idea is intriguing It would be interesting to find a clinical trial that directly compares giving citrus fruits and the prescription of oral ferrous sulphate
outsor@citynet.net - 17 Dec 2005 22:20 GMT "Effectively what the articles are saying is that there is a deficiency of iron which is corrected by vitamin C."
Just so, the high fitic acid and other substances in grains and legumes retards absorption of the iron in them and other foods. Vit c increases it. This is well known and our friend mr. justice has posted other bits about htis and thinking the vit c "cured" anemia and it was not due to not having enough iron after all. One was as you suggest where iron and vit c were given to two groups of children and the vit c also increased the iron levels. Of course, in most parts of the world where low iron is a problem and cultural food preferences allow, they would rather increase animal sources and the low iron problem would also disappear.
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