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Medical Forum / General / General / December 2005

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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]

--------------------------------------------------------------------------------

<<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]

---------------------------------------------------------------------------­-

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]

--------------------------------------------------------------------------

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

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      copper and iron. Clin Chim Acta 1958;34:328-334.
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Ascorbic
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      RD, Car NG, Mac-Phail P, Schmidt U, Tal A, Mayet F. Ascorbic
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      phytates on nonheme iron absorption. Am J Clin Nutr
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  16. Behrman RE, Kliegman RM. Nelson text book of pediatrics.
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      nutritional anemia. New Delhi Ministry of Health & Family
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      Government of India 1991:1-8
  18. Chalmers AH, Cowley DM, Brave JM. A possible etiological role
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      ascorbate in calculi formation. Clin Chem 1986;32:333-336.
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      the role of ascorbic acid in renal calculogenesis in albino
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      J Urol 1988;139:156-157.
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      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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