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Banning Animal Protein Products from rhea and ostrich feed is WRONG!!!
Certain marketing by a feed company is calling for a ban on animal protein products in ratite feed, absurdly linking the problem with a cow disease: BSE.
Meat Protein in the diet helps
detoxify
Link to study on higher levels of
meat protein protecting against osteoporosis
Contrary to what you may be hearing, abolishing animal protein from ratite diets is a
horrible, scientifically unfounded idea. Clean animal protein helps the
body detoxify and therefore mitigate fading chick syndrome.
The adulterated animal protein products that are made from meat by-products, dead animals, the plastic cartons the old meat is packaged in, etc. are terrible and do not belong in ratite feed. BUT, and this is the big difference--good quality animal protein will save the chicks by helping the chicks to detoxify. Insects or organ meats from pastured or organically raised animals should be in our ratite feed.
The best way to produce beautiful chicks is to include high quality protein in their diets. Fading Chick Syndrome is an autoimmune disorder, not a generic nutritional deficiency. It must be treated as such.
After harvesting our pastured poultry and rheas we process the byproducts into a nutritious supplement for the chicks. Along with ratite egg this provides the chicks with the high quality protein they need to detoxify and overcome the syndrome. We monitor progress by checking blood glucose. Study the other pages under "about rheas" for more information on dealing with this problem in rheas and ostriches.
In this study CP is crude protein. The casein (milk protein) diet
allowed the chicks to better survive the monensin dose. In other words,
animal protein helps the body detoxify whereas soy protein did not.
Any product or drug that kills some organism is a poison of some sort,
even if only a mild posion to the animal receiving the dose. It is far safer
to build the immune system than to kill the invader, and in this case it was
done with an extracted animal protein, which we consider to be less
effective than whole clean meat, eggs, or insects.
Further investigation of the dietary protein level-monensin
interrelationship in broiler chicks: influence of dietary protein source and
type of anticoccidial drug
Welch, C. C., Parsons, C. M., Baker, D. H.
1988 Poult Sci 67:4 652-659
Three experiments were conducted to evaluate the influence of dietary
protein source on the monensin response in healthy chicks fed diets varying
in CP. The interrelationship between dietary CP level and four different
anticoccidial drugs was evaluated in a fourth experiment. The experiments
were conducted from 8 to 21 or 22 days posthatching. In Experiment 1,
crossbred chicks were fed corn-soybean meal (SBM) diets containing either 24
or 16% CP or casein-dextrose diets containing 20, 15, or 10% CP in the
presence or absence of 160 mg/kg monensin. When CP level was decreased in
the corn-SBM treatments, the resulting monensin- induced growth depression
was greater. However, this interaction was not observed in chicks fed
casein-dextrose diets. Experiments 2 and 3 were conducted to determine if
the monensin-protein level interrelationship is influenced by the source of
dietary soybean protein or by high levels of animal protein (AP). Monensin
at 140 mg/kg produced a much greater growth depression at 16 than at 24% CP
in chicks fed a corn-SBM diet, whereas amounts of monensin depression in
chicks fed a corn-isolated soy protein diet were similar for both CP levels.
As dietary protein was reduced from 24 to 16% in Experiment 3, 140 mg/kg
monensin caused growth depressions of 10 and 40%, and 14 and 28%,
respectively, in broiler chicks fed corn-SBM and corn-AP diets.(ABSTRACT
TRUNCATED AT 250 WORDS)
About BSE and birds: NOT
The idea that we have to worry about BSE-(BOVINE) is ridiculous. There is no such disease in avians nor are avians ruminants. These people advocating these ideas need to provide data that their diet is preventing or treating fading chick syndrome.
They have not done so yet and probably cannot. From what we have learned over the last 7 years it CANNOT help fading chick syndrome!!!
From a citation below:
Bovine
spongiform encephalopathy is, by definition, only seen in bovine species, not
in sheep, humans, or any other host species. If the agent of BSE in cattle
jumps species, the disease (= unfortunate outcome of the relationship between
the host and the infectious agent), must have another name.
We have long held the position that BSE is not a meat transmitted infectious disease but a toxin induced disorder.
From a list:
http://agbioview.listbot.com
Date: May 22 2000 14:03:49 EDT
From: Andrew Apel <agbionews@earthlink.net>
Subject: BSE
Colleagues,
The method of transmission of bovine spongiform encephalopathy (BSE, or 'mad cow disease') has not yet been nailed down, nor, even, its cause.
Some have long suspected that the prions implicated in BSE are not infective in the sense in which bacteria and virii are infective.
Suspicion has, for instance, fallen on the use of organophosphates for the control of warble fly in cattle, which by some mechanism cause a proliferation of malformed prions (which are normally benign) in the bovine nervous system. The same, accordingly, could possibly account for the advent of new-variant Creutzfeldt-Jakob syndrome in humans, an account which has nothing whatsoever to do with eating beef, but with ingesting a certain chemical instead.
I would point out that Europeans are singularly lax in allowing toxics to escape into the food chain.
This recently appeared in the journal Science:
Charles Weissmann of the Imperial College School of Medicine in London and colleagues at Biogen in Cambridge, Mass., and the University of Zurich in Switzerland have worked to find ways to prevent the mutated prions from spreading through the nervous system. Writing in the journal Science, they said prions seem to be produced by immune cells in the spleen known as follicular dendritic cells (FDCs).
If we take these new findings at face value, could this indicate that the assumptions behind the response to the 'mad cow' epidemic were erroneous, and that there might be not merely a different causative agent, but a different 'mode' of 'transmission?'
and another from the same list months later:
A ProMED-mail post
<http://www.promedmail.org>
Date: Sat, 22 Jul 2000 15:29:47 -0700
From: Dr. Raymond G. Whitham <zoonotic@pacbell.net>
Like the description of many zoonoses, the various
reports of transmissible spongiform encephalopathies in various host species I
have read in ProMED-mail and other newsgroups are plagued with the same problem.
There is confusion as to the need to distinguish between the variables
"host species", "infectious agent", and "disease"
involved.
Bovine
spongiform encephalopathy is, by definition, only seen in bovine species, not in
sheep, humans, or any other host species. If the agent of BSE in cattle jumps
species, the disease (= unfortunate outcome of the relationship between the host
and the infectious agent), must have another name.
To the casual observer, this may seem picky, but to an
epidemiologist, this results in utter confusion to properly report possible
outbreaks, creating a valid scientific database, and making sense of the
situation so as to properly address the situation.
- --
Dr. Raymond G. Whitham ,
Epidemiology Team Leader, County of Los Angeles Health Services, Los Angeles, California
<zoonotic@pacbell.net>
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