Organic Researcher

I few months ago I posted an piece of work by Josef and sadly the obituaries of Mark Purdey. Since that time these posts have attracted constant attention. So with this new article by Josef I’ve decided it deserves a page.

These are Josef’s words and arguments, you can get in touch via his web page.

Why CWD can be a naturally (not infectious) occurring disease?

The “chronic waste disease” (CWD) was first discovered in 1967 in a
state-owned research facility at Fort Collins, Colorado. After 35 years of
research, no one can say for sure how it started and how it spreads. Even
Beth Williams (who discovered CWD) states, “It’s equally as plausible that
CWD is a naturally occurring disease.”

The known natural hosts of CWD are mule deer, white-tailed deer, elk,
and moose. CWD was first identified as a fatal wasting syndrome in captive
mule deer in Colorado in the late 1960s and in the wild in 1981. It was
recognized as a spongiform encephalopathy in 1978. To date (January 4,
2007), no strong evidence of CWD transmission to humans has been reported.
By the mid-1990s, CWD had been diagnosed among free-ranging deer and elk in
a contiguous area in northeastern Colorado and southeastern Wyoming, where
the disease is now endemic. The geographic range of diseased animals
currently includes 11 U.S. states and two Canadian provinces and is likely
to continue to grow. Surveillance studies of hunter-harvested animals
indicate the overall prevalence of the disease in northeastern Colorado and
southeastern Wyoming from 1996 to 1999 was estimated to be approximately 5%
in mule deer, 2% in white-tailed deer, and cattle and human .

However, recent research (October, 2006) shows for the first time that
chronic wasting disease may spread through saliva and blood of infected
deer, which poses new possibilities that the disease may spread by
blood-sucking insects or social contact between animals. The study also
reinforces that no tissue from an infected animal can be considered free of
prions, the disease-causing agent. The research, released in the Oct. 6
edition of the journal Science, tested the blood, saliva, feces and urine of
deer infected with CWD to determine ways the disease may be transmitted from
animal to animal, which has remained a mystery to scientists...

However, according to the recent article “Should we still be worried?”
(January 10, 2007) there is a different view about the BSE infectiosity -
see following text from this article; “But despite billions spent on efforts
to save Britain’s beef industry and protect its citizens, all the major
questions remain unanswered. The origin of the disease? A mystery. The
number of people infected with vCJD? A mystery. The risk that those
harbouring the disease will infect others? Again, a mystery… At the end of
1986, pathologists at the Central Veterinary Laboratory were analysing
slivers of brain tissue sliced from cattle that appeared to have contracted
a new disease. It left the cattle uncoordinated and jerky, and ultimately
proved fatal. Under a microscope, the brain damage resembled scrapie, a
disease caused by rogue proteins known as “prions” that had been endemic in
the national sheep flock for nearly 200 years. Without publicity, an
investigation was launched to find the cause of the outbreak. It revealed an
alarmingly widespread disease. One year later, 95 cases of BSE had been
confirmed on 80 farms. By February 1988, 264 cases had been tracked back to
223 farms. The number of cases began to grow exponentially. It was turning
into a major crisis and there was all sorts of wild guesswork going on
because no one understood it, says Chris Higgins, who now chairs the
government’s advisory committee on spongiform encephalopathy diseases. The
politicians didn’t know what to do and the scientists didn’t know what to
do. We didn’t know where it came from, what caused it, how bad it might be.
We didn’t know anything.. “The danger now is not from cattle, it’s from
other human beings,” says another expert in vCJD ..”. “The story of BSE in
Britain is a case study in the ruthless efficiency of intensive farming, the
self-serving behaviour of government departments and the patronising caution
extended to the public when explaining risk. It reveals the impotence of the
scientists involved – at least at the outset, when they were being called
upon to give meaningful advice while still battling to understand a disease
they had never encountered before.”- say britain scientists, who had been
summoned to an emergency meeting in London.

The story of CWD in the U.S. is also a case study in the ruthless
efficiency of intensive farming ?

1. Elk digestive anatomy (small stomach disagned for more rapidly digestible
feed)
To properly understand the nutrient requirements of elk, and how
various crops and storage methods may work with elk, a brief examination of
their digestive anatomy is useful. Elk have been described as intermediate
or mixed feeders that will naturally select a mixture of food from grasses
to browse material such as leaves. This is different from cattle or bison,
which are classified as roughage/grass eaters and will select almost
exclusively grass. The implications this has when considering feeds for elk
is that they have a smaller stomach size relative to body weight and their
digestive systems are designed for more rapidly digestible feed. Conversely,
cattle and bison hold feed in their rumens for a longer time to allow for
digestion of more fibrous plant material. These anatomical differences
should be considered when making feed decisions for elk based on information
from cattle research. Cattle are easier to feed since they have been bred
and adapted over hundreds of generations to farm production. However, deer
have a digestive system that remains more closely linked to their
environment. Feeding them on a farm requires a careful balance of rations
(http://www.deer-library.com/artman/publish/article_133.shtml).

2. High nitrogen intake and nitrogen fertilization recommendations

White-tailed deer in most southern habitats have access to adequate
amounts of forage most of the year. However, white-tailed deer need a
minimum of 17% crude protein in their forage year-round for maximum body and
antler-growth and other natural deer forages do not contain this minimal
amount of protein. Thus food quality, not quantity, may be the limiting
factor in producing high quality white-tails on a sustainable basis.

There probably is no better off-season forage that one can plant for
deer than soybeans. Soybean foliage is high in protein, the soybean seed is
extremely high in protein and other nutrients. Soybean plants are utilized
heavily from sprouting through seed production. Cowpeas are annual legumes
like soybeans and produce high protein forage during the off-season. It has
been our experience that cowpeas often are not browsing by deer until they
reach a certain stage of maturation. However, when this stage is reached,
deer may direct their attention to these plantings and eliminate them in a
matter of a week or so. This may defeat the intended purpose of supplying
deer high-quality forage throughout the summer season.

Generally speaking, areas selected for natural forage enhancement on
most Alabama soils would benefit from an application of the equivalent of
1-3 tons of lime per acre before fertilization. These areas, whether fallow
fields, roadsides, honeysuckle patches, etc. should then receive a broadcast
treatment of 13-13-13 at a rate of 4-500 pounds per acre (an acre is about
the size of a football field). Fertilization should coincide with spring
green-up or about mid-March. Around the first to the middle of May apply
ammonium nitrate at a rate of 100 pounds per acre. Natural forage production
can be doubled and crude protein content of many plants can be pushed well
beyond the basic requirements of white-tailed
deer(http://www.pfmt.org/wildlife/deer_nutrition.htm). In addition, fallow
and whitetail deer are very selective eaters, choosing to consume only the
most succulent and digestible plants and plant parts. Reindeer are selective
feeders and, if conditions permit, eat only the top (younger) portion of
plants (so, naturally higher protein intake).

About high protein recommendations into the practice – see one exaple
as the ” protein feeders offer”
(http://www.sweeneyfeeders.com/home.php?cat=5); “Nutrition is the key to
successful wildlife and game management. And nothing is more important than
protein. Protein is absolutely essential to the health of your entire herd
and to the potential for trophy bucks. Whitetail deer need protein all year
round… Automatic Protein Feeders are totally dependable, providing protein
on time, every time, all year round.are ideal for free choice protein
feeding”.

3. Official nutrition requirements for deer and elk (recommendations for
the captive deer herds)

Crudeprotein(CP)

Protein is needed for maintenance, muscle and bone growth, and tissue
repair. Elk that are rapidly growing or lactating and bulls recovering from
the rut have higher protein needs. To some extent, greater protein
requirements can be met by increased intake. However, the percentage of
protein in diets designed for these animals is usually increased as well.
Maintenance rations should be at 10 – 12% crude protein, whereas rations for
lactation or antler growth should provide 14 – 18% crude protein. Growing
rations should contain 16 – 20% crude protein. If a single diet is fed to
all gender and age groups, a 16 – 17% crude protein level is optimal. Total
dietary protein content must be determined to follow these general
guidelines.

Calcium and phosphorus

The actual amount of calcium and phosphorus required by elk increases
greatly during growth, lactation and antler growth. A minimum of 0.7%
calcium and 0.4% phosphorus is suggested for elk rations. Of equal
importance is ensuring a calcium to phosphorus ratio of at least 1.5 to 1.
How wide a ratio is tolerated by elk has not been researched although other
ruminant species can tolerate calcium to phosphorus ratios as high as 5:1.
Calcium levels are relatively high in hay, especially legumes, but
phosphorus content is quite low. Access to browse (twigs and leaves)
improves natural mineral intake on pastures. Check trace element levels for
copper, zinc and manganese. Elk, unlike sheep, require supplemental copper.
Next check the levels of vitamins A, D, E, and
selenium.(http://www.deer-library.com/artman/publish/article_117.shtml).

4. Conclusions

A/ High dietary crude protein intake;

The high dietary crude protein (CP) for “adult deer” (16- 18%),
recommended by “deer nutrition scientists” is significantly higher-
compared with “high yielding dairy cows”. So, for example dairy cow; milk
yield 55 kg/ day, according to the NRC (1989 and 2001) – requires only
17,5 and 16,7% of CP recommendation , respectively. In addition, recent
research (during 1990s) resulted to the decrease of CP content in dairy cow
ration – compared NRC (1989) and NRC (2001)-
(http://www.nap.edu/catalog/9825.html)- and significant or “dramatic”
decrease in “early lactation”( 19 and 15.9%, respectively).

Lush grass innately has an increased level of crude protein. This
factor, combined with increased use of nitrogenous fertilizers in the soil,
causes an increase in ammonia in ruminal fluid, leading to a decrease in the
availability and absorption of magnesium. So in high crude protein (CP)
intake; deer rumen ammonia (NH3) levels are excessively high, the NH3 is
absorbed into the blood and either recycled or excreted in the urine as
urea. Excess NH3 in the portal system can readily pass through the liver and
enter the arterial system. Brain tissue rapidly extracts NH3 from the
arterial blood. Ammonia then builds up in bloodstream (hyperammonemia) and
more and more NH3 accumulates in tissue cells. The CNS is first to
malfunction because it has a large requirement for energy. Behavioral and
nervous signs do seem to appear first, cellular energy and respiration
deficits probably cause ultrastructural damage and the degenerative changes
in the CNS.

B/ High dietary calcium intake (magnesium deficit in “intracellular fluid”);

The above recommended high dietary calcium level for the “adult deer”
(minim. 0.7 %) – it is the same example- compared with the requirements for
high yielding dairy cow ( 55 kg milk yield/ day) (see; NRC, 2001;
http://www.nap.edu/catalog/9825.html).

A high content of calcium in the ration increases the magnesium
requirements of the animal. The lower the magnesium level in the animal
ration (and in the tissue cells); the more marked is “calcium effect
excitotoxicity” in the CNS. It can be also accentuated; a low temperature
raises magnesium requirements. Impairment of neuronal energy metabolism may
sensitize neurons to excitotoxic cell death. However, calcium in cells is
tightly regulated and mostly unrelated to necessary dietary calcium.

C/ Higher dietary potassium intake (magnesium deficit in “extracellular
fluid”);

In addition, potassium (K) concentrations were found with a high
positive correlation with crude protein content in forages. So, if the
mule deer;

(a) naturally select a mixture of food from grasses to browse material such
as leaves (higher CP content)

(b) have a smaller stomach size relative to body weight and their digestive
systems are designed for more rapidly digestible feed, choosing to consume
only the most succulent and digestible plants and plant parts (young plant-
higher CP content)

(c) prefer legumes (higher protein and potassium content) over grasses
because they are higher quality,

there is not only higher protein but also higher potassium intake.

While non-ruminants absorb magnesium (Mg) primarily from the small
intestine, ruminants are able to absorb much of their Mg requirement from
the rumen. In fact, the reticulum and rumen can account for up to 80% of the
Mg absorption along the entire digestive tract. Probably, the nutrient
having the greatest adverse effect on Mg absorption is an excess of
potassium (K) in the ration, as shown by at least four sheep experiments. In
addition, experiments demonstrated that younger cows are better able to
mobilize Mg from the body reserves than older cows (see the BSE occurrence
only in older cattle.).

5. Summary

Hyperammonemia plus hypomagnesaemia “simultaneous” action
(www.bse-expert.cz)

There is the possibility that these mechanisms have a strong influence
on CNS, and that the CWD has its roots in a more common nutritional
problem- and not an “infectious disease”. This alternative ” ammonia-
magnesium” theory is based on the chronic Mg-deficiency potentiated by
hyperammonemia in ruminants. So various clinical symptoms can be observed
because the nervous system controlling both voluntary and unvoluntary
muscles is affected (Mg and Ca disturbances). It seems, that during the
chronic hypomagnesemic disease, the heavy weather changes (cold- rainy,
windy…) or nutrition (high intake of crude protein…) stress – these
episodes of acute abruptions, may accelerate the nervous, like to “CWD”
disease. If the CWD is involved; a longer- chronic action of corresponding
biochemical changes in the blood (CSF) is necessary, to rise irreversible
neurodegenerative changes. So, prions are a symptom of the metabolic
“chronic wasting disease” and do not cause the disease. The sad twist to
this tale is that straightforward magnesium supplementation of deer in CWD
risk areas may be all that is required to prevent CWD. However, also dietary
protein should be lowered.

There is the evidence that the story of BSE in Britain and the story of
CWD in U.S. can be a consequence of “intensive farming” (metabolic
disease and “neurotoxicity”) and belongs in the “Organic Research”
(http://organicresearcher.wordpress.com/2007/01/06/bse-an-alternative-theory/).
So, I described an alternative “BSE ammonia-magnesium” theory
(http://www.agriworld.nl/feedmix/headlines.asp?issue=3). See also my
“opinion- article”; about the link between BSE and Alzheimer´s disease
(http://www.medicalnewstoday.com/youropinions.php?opinionid=11677). This
theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia
(high protein intake.). These mechanisms have a strong influence on CNS,
especially in ruminants and carnivora animals. My alternative “BSE
ecological view” can be well documented concerning the example about
“Chronic Wasting Disease” (CWD). More details about it – see one Chapter
in my website ( www.bse-expert.cz.).

Recent supporting views about the BSE (CWD) “not infectiosity”

In general, I think that beef – deer meat “is safe in the all world”,
because the BSE (CWD) is not an infectious disease- as I for example sent
to “Iowa Farmer Today” in October, 2006
(http://iowafarmertoday.com/articles/2006/10/05/livestock/47bse_ap.txt#e3f6832db08c10a952fa2a8cf99030cc).
Really, also according to the recent research; BSE can be “not infectious
disease”. Why? At first, authors in “Journal of Pathology” (March, 2006)
found that prion proteins implicated in the development of transmissible
spongiform encephalopathies, such as vCJD, may be markers for disease rather
than the infectious agents. So, under laboratory circumstances prion-protein
can be absorbed across the gut, it also shows that this is unlikely to occur
in real life
(http://www3.interscience.wiley.com/cgi-bin/abstract/112568745/ABSTRACT).
Other authors in “Journal Biol. Chem.” (November, 2006) found that small
amounts of detergent-insoluble PrP aggregates are present in uninfected
human brains, so insoluble aggregates and protease-resistant conformers of
prion protein in uninfected human brains
(http://www.jbc.org/cgi/content/abstract/281/46/34848).

More recently (February, 2007); Authors in “Neuron” wrote; “Early
functional impairments precede neuronal loss in prion disease.they occur
before extensive PrPSc deposits accumulate.supporting the concept that they
are caused by a transient neurotoxic species, distinct from aggregated PrPSc
.”
(http://www.neuron.org/content/article/abstract?uid=PIIS0896627307000086).
The prion protein infection from transmissible BSE is then thought to travel
to the brain via peripheral nerves, perhaps with assistance from the
lymphoreticular system. In 2004, a study of 13,000 appendix and tonsil
samples revealed that thousands of people may be unknowingly harbouring vCJD
(http://news.bbc.co.uk/2/hi/health/6334215.stm). However, recently
scientists find connection between nerve cells and immune system. They have
made visible an astounding number of contacts between immune and nerve
cells. These include some of the most important immune cell types, such as
B-lymphocytes, T-lymphocytes and dendric cells – all of which form
connections to the nerves (http://www.news-medical.net/?id=21792). The new
findings, offer significant insights into normal folding mechanisms as well
as those that lead to abnormal amyloid fibril conversion
(http://www.sciencedaily.com/releases/2007/02/070212182836.htm). Until about
five or six years ago, everyone assumed that the large amyloid plaques, or
neurofibrillary tangles, that were found in the brains of Alzheimer’s
victims were the cause of the disease. However, recent scientific
discoveries indicate that these large, insoluble aggregates might merely be
markers of the disease- they do not cause the disease
(http://www.sciencedaily.com/releases/2007/02/070215110558.htm).

Josef Hlasny, Bludov, Czech Republic