--NPN(Funny Protein) NPN Toxicosis--

Hi Ya'll,

These are things the main stream Medicine does not want you to know about!

As some of you may be interested in a more indepth understanding about this subject, I am providing some links for you to study:


http://www.acresusa.com/toolbox/reprints/Brunetti_Protein.pdf




http://www.jem.org/cgi/content/abstract/28/2/243




http://www.usjersey.com/Reference/trueprotfaq.pdf




http://www.innovatewithdairy.com/InnovateWithDairy/Articles/FAQ_NPNitrogen_03...




http://www.westerndairyscience.com/html/DairyNotes/html/f1a1n5.html




http://www.holsteinusa.com/html/trueweb.html




As anyone who has a little bit of "Common Sense" left in their head may be able to Learn after reviewing these links, that NPN is Non-Protein Nitrogen, which is "NOT" True Protein !

Thus NPN is Funny Protein, for it is not True Protein !

NPN is a form of Nitrogen, which has not Complexed into an Amino Acid Complex with the needed Alkaline Minerals and Live Carbons !

And NPN can Cause your body to become Sick and Diseased by eating foods which may have too much of the NPN in it !

And todays Poor Quality Foods, which do not have enough Alkaline Minerals in them may be too high in this Funny Protein(NPN), and this is especially True of foods which are picked too Green, and not allowed to vine ripen !

Try eating apples which have been picked too Green and see how many times they may give you a tummy ache, this may be because of the Funny Protein(NPN) in them !

As usual not everything may be as it may first seem to be !

Also for those Interested in Learning the "Truth" about Funny Protein(NPN)
--Non-Protein Nitrogen being able to Displace Oxygen in the Blood, Specifically
the Isotope of Ammonia :

From the MERCK Veterinary Manual: for the Research has been done on animals to
find the "Truth" about the problem also in Humans !

Nonprotein Nitrogen Poisoning: Introduction
(Ammonia toxicosis)

Poisoning by ingestion of excess urea or other sources of nonprotein nitrogen
(NPN) is usually acute, rapidly progressive, and highly fatal. Sources of NPN
have different toxicities in various species, but mature ruminants are affected
most commonly. After ingestion, NPN undergoes hydrolysis and releases excess
ammonia (NH3) into the GI tract, which is absorbed and leads to hyperammonemia.

Clinical Findings:
The period from urea ingestion to onset of clinical signs is 20-60 min in
cattle, 30-90 min in sheep, and longer in horses. Early signs include muscle
tremors (especially of face and ears), exophthalmia, abdominal pain, frothy
salivation, polyuria, and bruxism. Tremors progress to incoordination and
weakness. Pulmonary edema leads to marked salivation, dyspnea, and gasping.
Horses may exhibit head pressing; cattle are often agitated, hyperirritable,
violent, and belligerent as toxicosis progresses; sheep usually appear
depressed. An early sign in cattle is ruminal atony; as toxicosis progresses,
ruminal tympany is usually evident, and violent struggling and bellowing, a
marked jugular pulse, severe twitching, tetanic spasms, and convulsions may be
seen. Affected cattle with violent or belligerent aberrant behavior may have
produced some 4-MI in vivo through reaction of excessive NH3, released from NPN,
with carbohydrates and reducing sugars in the rumen. The PCV and serum
concentrations of NH3, glucose, lactate, potassium, phosphorus, AST, ALT, and
BUN usually are significantly increased.
As death nears, animals become cyanotic, dyspneic, anuric, and hyperthermic, and
blood pH decreases from 7.4 to 7.0. Regurgitation may occur, especially in
sheep. Death related to excess NPN usually occurs within 2 hr in cattle, 4 hr in
sheep, and 3-12 hr in horses. Survivors recover in 12-24 hr with no sequelae.
Lesions: Carcasses of animals dying of NPN poisoning appear to bloat and
decompose rapidly, with no specific characteristic lesions. Frequently,
pulmonary edema, congestion, and petechial hemorrhages may be seen. Mild
bronchitis and catarrhal gastroenteritis are often reported. Regurgitated and
inhaled rumen contents are commonly found in the trachea and bronchi, especially
in sheep. The odor of NH3 may or may not be apparent in ingesta from a freshly
opened rumen or cecum. A ruminal or cecal pH ≥7.5 from a recently dead animal is
highly suggestive of NPN poisoning. The ruminal pH remains stable for several
hours after death under most circumstances but continues to rise in NPN
toxicosis.


Diagnosis:
Ammonia or NPN poisoning is suggested by signs, lesions, history of acute
illness, and dietary exposure. Exposure to excess NPN may be evaluated through
laboratory analysis for the ammonia nitrogen (NH3-N) in both antemortem and
postmortem specimens and for urea or other NPN in suspected feeds and other
dietary sources. Specimens for NH3-N analysis include ruminal-reticular fluid,
serum, whole blood, and urine. All specimens should be frozen immediately after
collection and thawed only for analysis; alternatively, ruminal-reticular fluid
may be preserved with a few drops of saturated mercuric chloride solution added
to each 100 mL of specimen.

Concentrations of ≥2 mg/100 mL NH3 -N in blood or serum indicate excess NPN
exposure. The concentration of NH3-N in ruminal-reticular fluid is >80 mg/100 mL
in most cases of NPN poisoning and may be >200 mg/100 mL. Acclimated ruminants
fed diets high in legume hay, soybean meal, cottonseed meal, linseed meal, fish
meal, or milk byproducts may have NH3-N concentrations in rumen fluid
approaching 60 mg/100 mL with no apparent toxicity. The pH of ruminal-reticular
fluid should also be determined; a pH of 7.5-8 (at time of death) is indicative
of NPN toxicity.
Differential diagnoses include poisonings by nitrate/nitrite, cyanide,
organophosphate/carbamate pesticides, raw soybean overload, 4-methylimidazole,
lead, chlorinated hydrocarbon pesticides, and toxic gases (carbon monoxide,
hydrogen sulfide, nitrogen dioxide); acute infectious diseases; and
noninfectious diseases such as encephalopathies (eg, leukoencephalomalacia,
hepatic encephalopathy, polioencephalomalacia), enterotoxemia or rumen
autointoxication, protein engorgement, grain engorgement, ruminal tympany, and
pulmonary adenomatosis. Nutritional and metabolic disorders related to
hypocalcemia, hypomagnesemia, and other elemental aberrations should also be
considered.

And there has been much more research to Prove these things I have been sharing
about the Funny Protein(NPN)-- Non-Protein Nitrogen in the foods we eat, whose
Nitrogen Isotope of Ammonia may Displace the Oxygen from our Blood and Cause
"US" to "DIE" , for those willing to open their Closed eyes and see ?

There is also the matter of Potassium Nitrate Poisoning:

The term "nitrate toxicity" is commonly used but the toxic principle is actually
nitrite. When Nitrate is converted to nitrite. Nitrite is absorbed from the
digestive system converting blood hemoglobin to methemoglobin. Methemoglobin
cannot transport oxygen to body tissues, so People and animals die from oxygen
insufficiency.

But, as usual the Worldly Educated, who may have become Educated beyond their
own Intelligence, may not choose to Believe in the "Facts" presented, but those
Seeking the "Truth" may open their eyes and see the "Truth" ?

Choose Life or Death this Day !

Smile Tis your choice.