Feedstock for prepartum dairy cattle

Drug – bio-affecting and body treating compositions – Preparations characterized by special physical form – Food or edible as carrier for pharmaceutical

Reexamination Certificate

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C424S400000, C424S438000, C424S439000, C424S489000, C426S074000, C426S072000, C426S807000

Reexamination Certificate

active

06521249

ABSTRACT:

BACKGROUND OF THE INVENTION
This invention generally relates to dietary factors with respect to prepartum dairy cattle nutrition. More specifically this invention relates to the effects of dietary cation-anion difference (DCAD) and essential fatty acid nutrients on calcium homeostasis in prepartum dairy cattle.
Metabolic problems with periparturient dairy cattle are numerous and interrelated. The majority of these problems involve subclinical and clinical hypocalcemia beginning from a few days prior to parturition through several days postpartum. This hypocalcemia, in the clinical form, is termed “milk fever” (parturient paresia) and manifests itself in cows with them becoming anorexic and, in its final stages, with cows having paralysis. While the onset of lactation is a precipitating factor for this disease, the root cause is the cow's inability to effectively regulate calcium metabolism via the hormonal cascade controlling bone calcium mobilization and deposition. Normally the blood serum of a dairy cow contains 9-12 mg of calcium per 100 ml. If the level decreases to about 5 mg per 100 ml, milk fever symptoms usually develop.
In its subclinical form, the hypocalcemia causes a cascade of disorders associated with muscle contraction, such as displaced abomasums and retained placentas. This subclinical hypocalcemia also leads to a reduced feed intake in the periparturient period. The reduced feed intake leads to the mobilization of body fat reserves and weight, which is known to be a causative factor in excess liver fat accumulation prior to the onset of lactation. Aside from the immediate veterinary costs associated with these disorders, there is a decided reduction in productivity for the remainder of the lactation.
Other dietary factors are of concern with respect to dairy cattle nutrition. Dietary macromineral elements are necessary for proper health and productive performance of lactating dairy cattle. As a class of nutrients, these elements have been the subject of extensive research, and considerable information exists about individual effects of each macromineral element. Information on interrelationships of macromineral elements in diets for lactating dairy cows, however, is relatively limited.
An early publication was the first to propose that mineral interrelations were related to acid-base status [J. Biol. Chem., 58, 235 (1922)]. It was proposed further that maintenance of normal acid-base equilibrium required excretion of excess dietary cations and anions. It was hypothesized that consumption of either excess mineral cations relative to anions or excess anions relative to cations resulted in acid-base disturbances in animals (A. T. Shohl. Mineral Metabolism. Reinhold Publishing Corp., New York. 1939).
Once animal nutritionists began to test this hypothesis, mineral interrelationships were found to affect numerous metabolic processes, and there was evidence that mineral interrelationships had profound influences. It was theorized that for an animal to maintain its acid-base homeostasis, input and output of acidity had to be maintained. It was shown that net acid intake was related to the difference between dietary cations and anions. The monovalent macromineral ions Na, K and Cl were found to be the most influential elements in the interrelationship (P. Mongin. Page 1, Third Ann. Int. Mineral Conf. Orlando, Fla. 1980).
Nutrient metabolism in animals results in the degradation of nutrient precursors into strong acids and bases. In typical rations fed to dairy cattle, inorganic cations exceed dietary inorganic anions by several milliequivalents (meq) per day. Carried with excess dietary inorganic cations are organic anions which can be combusted to HCO
3

. Consequently, a diet with excess inorganic cations relative to inorganic anions is alkaline, and a diet with excess inorganic anions relative to cations is acidogenic.
Chloride is the most acidogenic element to be considered. An excess of dietary chloride can lead to a respiratory and/or metabolic acidosis. This is critical in ruminant nutrition because of salt (NaCl) feeding both in the diet and on an ad libitum basis. The acidogenic influence of chloride can be negated by sodium and potassium which are alkalogenic elements. Conversely, excess intake of sodium or potassium can induce metabolic alkalosis.
Blood pH ultimately is determined by the number of cation and anion charges absorbed in the blood. If more anions than cations enter the blood from the digestive tract, blood pH will decrease. It was proposed that a three-way interrelationship among dietary Na, K and Cl, i.e., the sum of Na plus K minus Cl [in meq per 100 g diet of dry matter (DM)], could be used to predict net acid intake. The term “dietary cation-anion difference (DCAD)” was coined to represent the mathematical calculation (W.K. Sanchez and D. K. Beede. Page 31, Proc. Florida Rum. Nutr. Conf. Univ. of Florida. 1991). Expressed in its fullest form, DCAD is written as follows:
meq [(Na
+
+K
+
+Ca
+2
+Mg
+2
)−(Cl

+SO
4
−2
+PO
4
−3
)]/100 g of dietary dry matter (DM).
A problem with including the multivalent macrominerals (Ca, Mg, P and S) in the DCAD expression for ruminants relates to the variable and incomplete bioavailability of these ions compared to Na, K and Cl. The expression employed most often in ruminant nutrition is the monovalent cation-anion difference:
meq (Na
+
+K
+
−Cl

)/100 g dietary DM
Because of the additional use of sulfate salts in prepartum rations, the expression that has gained most acceptance in ruminant nutrition is as follows:
meq(Na
+
+K
+
)−(Cl

+SO
4
−2
)/100 g dietary DM
For a calculation, mineral concentration are first converted to milliequivalents:
meq
-
/
100



g
=
(
milligrams
)
/
(
valence
)
(
g



atomic



weight
)
The following illustrates a calculation of the meq Na+K−Cl−S value of a diet with 0.18% Na, 1.0% K, 0.25% Cl and 0.2% S. There are 180 mg Na (0.18%=0.18 g/100 g or 180 mg/100 g), 1000 mg K (1.0% K), 250 mg Cl (0.25% Cl) and 200 mg S (0.2% S) per 100 g dietary DM. The SO
4

entity is calculated as atomic sulfur.
meq



Na
=
(
180



mg
)

(
1



valence
)
(
23



g



atomic



weight
)
=
7.8



meq



Na
meq



K
=
(
1000



mg
)

(
1



valence
)
(
39



g



atomic



weight
)
=
25.6



meq



K
meq



Cl
=
(
250



mg
)

(
1



valence
)
(
35.5



g



atomic



weight
)
=
7.0



meq



Cl
meq



S
=
(
200



mg
)

(
2



valence
)
(
32



g



atomic



weight
)
=
12.5



meq



S
The calculated DCAD value is as follows:
meq
(Na+K−Cl−S)=7.8+25.6−7.0−12.5=13.9
meq/
100
g
dietary
DM
A simpler expression is as follows:
DCAD
=
(
0.18

%



Na
/
0.023
)
+
(
1.0

%



K
/
0.039
)
-
(
0.25

%



Cl
/
0.0355
)
-
(
0.2

%



S
/
0.016
)
=
+
13.9



meq
/
100



g



dietary



DM
The macrominerals in a feedstock have other significant metabolic interrelationships relative to the health and performance of dairy cattle. Animal trials have indicated that a magnesium deficiency results in failure to retain potassium, which can lead to a potassium deficiency. Also, excessive levels of potassium interfere with magnesium absorption. Because sodium and potassium must be in balance, excessive use of salt depletes an anim

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