The most recent evidence meat eating causes disease in a herbivore is from a medical study conducted by researchers in the United States.
The researchers discovered their work was being skewed and they narrowed it down to the food they were / are feeding their mice.

The researchers found by eliminating the purchased NIH recommended pelleted food and substituting this food for a chow prepared by the researchers themselves eliminated this problem.

I wondered whether this could be the study I was waiting for .. a study in which they fed their herbivore animals meat and the consequences of said action.
I predicted a herbivore would manifest iron toxicity.

The pelleted foods contain fish and other meat products.
I believe it has finally been proven man is a herbivore eating meat and this easily absorbed form of iron .. heme iron builds to toxic levels and causes iron poisoning in EVERYONE who eats meat.

Iron reduction therapy / iron removal has now been shown to be more effective in more diseases than any intervention in history.

I have been trying to prove this hypothesis for a few years which is .. man is a herbivore eating meat and this leads to all disease.
A .. herbivore hypothesis.
It is PROVEN by the fact the iron levels in the body rise due to eating meat and it causes disease PROVING the consumption of meat kills humans.

The study below illustrates the fact of porphyria being induced in the mouse by eating fish.

I believe this was proven by these men . They accidentally found there was / is something in the .. chow .. of the mice the chow used by the NIH .. and it gives them porphyria.

Below is a study .. the second study by these men in which they show uroporphyria is suppressed by diet.
Their first study the second study below showed ascorbate could not suppress uroporphyria WHEN iron was high in the cell.
This study they found some ‘unknown factor’ in the mouse chow that was / is causing .. uroporphyria.
They created their own diet and the mouse does NOT manifest uroporphyria no matter how much iron is supplemented.

I have always predicted meat given to a herbivore / mouse the mice would become polycythemic.
I did not have the wherewithall to conduct or have this study conducted.
It seems these men accidentally did the study.
Their mouse does NOT manifest uroporphyria WHEN given their own prepared diet but when given the NIH diet the mouse manifests porphyria .

The study was done backwards .. the hypothesis was raised by me .. then they just so happened to find something ‘weird’ .. in the food .. THEY ‘wondered’ out loud when they finished their study.

I had already predicted porphyria if a mouse was given meat I wondered if there could be some type of meat in the diet since they have been KNOWN to feed meat to herbivores.

I began to research a bit and looked and found FISH in the diet provided and used by the NIH.

Voila ..

One can surmise the meat / fish caused the .. uroporphyria .

Here the researchers wondered WHY the mice were getting uroporphyria when eating the ‘chow’ but not when given a diet they made up for them.

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defined iron-deficient diets, rather than chow diets, did not develop
uroporphyria
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Hepatology. 2007 Sep 13; [Epub ahead of print] Links
Effect of an oral iron chelator or iron-deficient diets on
uroporphyria in a murine model of porphyria cutanea tarda.
Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM,
Balestra D, Sinclair JF, Sinclair PR.
Veterans Affairs Medical Center, White River Junction, VT.
Porphyria cutanea tarda is a liver disease characterized by elevated
hepatic iron and excessive production of uroporphyrin (URO).
Phlebotomy is an effective treatment that probably acts by reducing
hepatic iron. Here we used Hfe(/) mice to compare the effects on
hepatic URO accumulation of two different methods of hepatic iron
depletion: iron chelation using deferiprone (L1) versus iron-deficient
diets. Hfe(/) mice in a 129S6/SvEvTac background were fed 5-
aminolevulinic acid (ALA), which results in hepatic URO accumulation,
and increasing doses of L1 in the drinking water. Hepatic URO
accumulation was completely prevented at low L1 doses, which partially
depleted hepatic nonheme iron. By histological assessment, the
decrease in hepatic URO accumulation was associated with greater
depletion of iron from hepatocytes than from Kupffer cells. The L1
treatment had no effect on levels of hepatic cytochrome P4501A2
(CYP1A2). L1 also effectively decreased hepatic URO accumulation in
C57BL/6 Hfe(/) mice treated with ALA and a CYP1A2 inducer. ALA-
treated mice maintained on defined iron-deficient diets, rather than
chow diets, did not develop uroporphyria, even when the animals were
iron-supplemented either directly in the diet or by iron dextran
injection.
Conclusion:
The results suggest that dietary factors other than iron are involved
in the development of uroporphyria and that a modest depletion of
hepatocyte iron by L1 is sufficient to prevent URO accumulation.
(HEPATOLOGY 2007.).
PMID: 17854053 [PubMed – as supplied by publisher]

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This is the effect of meat in a frugivore.

http://tinyurl.com/nfftd

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The remainder of the diet (50%) was a gelatinised product containing
chopped fruit and some meat blended with a vitamin supplement (SA-37,
Rogar-STB, London, ON, Canada) and minerals, that is allowed to
solidify and then cut into pieces.
CONCLUSIONS 1. Egyptian fruit bats will develop hemochromatosis when
fed high levels of dietary iron. 2. Iron absorption and toxicity was
likely enhanced by excessive vitamin C intake. 3. Pathologic findings
in bats resembles secondary hemochromatosis in man. 4. Toxicity may
result from the use of food supplements which contain high
concentrations of iron or other minerals.
It is recommended that dietary iron and ascorbic acid levels in diets
for frugivorous bats be closely monitored and maintained at required
levels only.
<>

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This is the diet provided and used by the NIH for their mice.

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http://www.dyets.com/613038.htm
Dyets Version of the NIH-07 Open Formula Rodent Diet
Fish Meal
100.00

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http://tinyurl.com/2z2bww
Product Description
The Rodent NIH-07 Open Formula diet is formulated for reproduction and
lactation of both rats and mice.
It has been used at the National Institutes of Health as the standard
reference diet for biological and biomedical research. It is also
recommended for use in production and research rodent colonies.
Guaranteed
Fish Meal (60%)

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Here the researchers had proven that ascorbate acid CAN prevent uroporphyria BUT only if the iron is low.
I believe the above study shows HOW the iron gets high.
ONLY by eating meat / dietary factor does the iron get high .. and is UNABLE to get high by any other means.

When the iron rises past the point of normal the vitamin C in the animals body is no longer able to quench the oxidation.

<>
ascorbate suppresses hepatic URO accumulation at low, but not high hepatic iron levels
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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

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