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OCR for page 162
7 vitamins
Vitamins are classified as either fat-soluble or water-
soluble. Vitamins A, D, E, and K are fat-soluble and the
B-vitamins and vitamin C are water-soluble. Vitamins have
diverse functions including involvement in many metabolic
pathways, immune cell function, and gene regulation. A
clinical deficiency of a vitamin results in a specific def~-
ciency disease such as rickets when vitamin D is deficient.
Subclinical deficiencies may occur in which clinical signs
of the deficiency are not evident but performance or overall
animal health is less than optimal.
FAT-SOLUBLE VITAMINS
Dairy cattle require vitamins A, D, E, and K; however,
vitamins A and E are the only ones with an absolute dietary
requirement. Vitamin K is synthesized by ruminal and
intestinal bacteria. Vitamin D is synthesized by ultraviolet
radiation of the skin. Many natural foodstuffs contain vita-
min A precursors and vitamin E, and under certain situa-
tions these will not need to be supplemented. However,
relying solely on vitamins contained within foodstuffs and
on synthesis of vitamin D via exposure to sunlight has risk
because of the large variability in vitamin concentrations
in feeds and exposure to sunlight. As management systems
for dairy cattle trend toward more confinement with less
exposure to sunlight and fresh forages, there is an increased
need to add supplemental sources of vitamins A, D, and E.
Vitamin A
SOURCES
Vitamin A activity is defined in retinal equivalents. An
IU of vitamin A corresponds to 0.3 fig of all-trans retinal
(0.344 fig of all-trans retinyl acetate or 0.550 fig of all-
trans palmitate). Retinal is not found in plants, but many
feeds contain p-carotene (provitamin A). Other carot-
enoids can be converted to vitamin A by animals, but
conversion efficiency appears to be poor and most common
feeds do not contain substantial amounts of those carot-
enoids. Most of the p-carotene in plants is found in vegeta-
tive material; therefore, forages can contain substantial
amounts of p-carotene but most grains and grain byprod-
ucts are practically void of p-carotene (corn gluten meal
contains moderate concentrations of p-carotene). Beta-
carotene concentrations decrease as forages mature (Park
et al., 19831. Beta-carotene is easily oxidized and once
plants are cut, concentrations decrease quickly so that
stored forages (silage and hay) have significantly lower
concentrations of p-carotene than do fresh forage (Bruhn
and Oliver, 1978; Park et al., 19831. The length of time
forages are stored is negatively correlated with p-carotene
concentrations (Bruhn and Oliver, 19781. Even when
known sources of variation are considered, the p-carotene
concentrations in foodstuffs are highly variable.
The common forms of supplemental vitamin A used in
the United States are all-trans retinyl acetate and all-trans
retinyl palmitate. When these forms of vitamin A are stored
properly, vitamin A activity is relatively stable with losses
of about 1 percent/month. When these retinyl esters are
stored in combination with minerals or other foodstuffs or
are pelleted, storage losses increase to 5 to 9 percent/
month (Coelho, 19911.
BIOAVAILABILITY
Studies on the bioavailability of various forms of vitamin
A and p-carotene for dairy cattle are extremely limited.
Bioavailability of vitamin A is dependent upon the degree
of ruminal destruction and on absorption efficiency by the
small intestine. In addition to those factors, the bioavailabil-
ity of p-carotene also depends on the efficiency of convert-
ing it to retinal. Beta-carotene is converted to retinal by
enzymes located in intestinal mucosal cells. Dairy cattle
also absorb and store p-carotene. Blood and milk of Guern-
sey and Jersey cattle contain more p-carotene than that
from other breeds because they are either more efficient
162
OCR for page 163
Vitamins 163
at absorbing p-carotene or less efficient at converting
p-carotene to retinal. The vitamin A activity of p-carotene
for cattle is defined as 1 mg of p-carotene = 400 IU of
vitamin A (equivalent to 120 fig of retinal), and is much
lower for cattle than for rats (1 mg p-carotene = 1800 IU
of vitamin A). The defined activity of p-carotene for cattle
is based largely on experiments using lambs fed corn silage
(Martin et al., 19681.
Ruminal destruction of vitamin A can be extensive.
Approximately 60 percent of supplemental vitamin A was
destroyed in the rumen of steers fed hay and corn grain
diets (Warner et al., 19701. Similar values have been
obtained using in vitro rumen systems (Rode et al., 1990;
Weiss et al., 19951. In vitro data suggest that ruminal
destruction of vitamin A was approximately 20 percent
when cattle were fed high forage diets, but it increased to
about 70 percent when cattle were fed diets with 50 to
70 percent concentrate. Limited studies with p-carotene
suggest that between 0 and 35 percent of dietary p-caro-
tene is destroyed in the rumen (Potanski et al., 19741.
Essentially no reliable data are available on the intestinal
absorption of retinyl esters in cattle. Data collected from
humans and rats suggest 20 to 60 percent of dietary retinyl
esters are absorbed (Blomhoff et al., 19911. Absorption in
those species is dependent on the amount and type of
dietary fat. Apparent digestibility of p-carotene from a
variety of forages averaged 77 percent in dairy steers (Wing,
1969), but Cohen-Fernandez et al. (1976) reported that
fecal recovery (indigestibility) of radiolabeled p-carotene
was about 90 percent in sheep.
FUNCTIONS AND ANIMAL RESPONSES
Vitamin A (retinaldehyde) is necessary for the produc-
tion of rhodopsin (a vision pigment) that is necessary for
low light vision. Vitamin A also is needed for normal growth
and development (including fetal growth), spermatogene-
sis, and for maintenance of skeletal tissue and epithelial
tissue. Abortions, increased prevalence of retained fetal
membranes, and increased calf morbidity and mortality
are indicators of vitamin A deficiency in gestating cows.
Ross and Ternus (1993) reported that retinoic acid indi-
rectly regulates gene expression which may explain the
many diverse functions of vitamin A. Vitamin A also
increases disease resistance and has stimulatory effects on
cell-mediated immunity (Chew, 1987; Bendich, 19931. A
deficiency of vitamin A often results in increased preva-
lence of infectious diseases. Beta-carotene, independent
of its provitamin A function, is an antioxidant and can
enhance the killing ability of neutrophils (Chew, 19931. In
some (Chew, 1987) but not all (Michal et al., 1994) studies,
and mastitis. These studies were conducted with cows at
dry-off or peripartum cows.
Vitamin A is clearly needed for good reproduction and
some data suggests that p-carotene also may be involved
with reproduction. In a review, Hurley and Doane (1989)
reported that supplemental p-carotene (usually at 300 to
400 mg/day) improved some measure of reproductive eff~-
ciency in 12 of 22 studies. When studies conducted only
in North America were summarized, p-carotene had no
effect on reproduction in 4 of 5 studies.
FACTORS THAT AFFECT REQUIREMENTS
Since the actual p-carotene content of diets is highly
variable and almost never known in commercial situations,
the vitamin A requirements presented in this publication
are for supplemental vitamin A, not total dietary vitamin
A. Fresh forage (e.g., pasture) has relatively high concen-
trations of p-carotene. Therefore the amount of supple-
mental vitamin A needed when fresh forage is fed will
be less than for cattle consuming conserved forages. The
requirements presented below assume conserved forages
are fed and are probably in excess of requirements for
grazing cattle.
Based on a reevaluation of older data, the vitamin A
requirement for growing dairy animals was increased to
80 IU/kg of body weight (BW). In the previous Nutrient
Requirements of Dairy Cattle (National Research Council,
1989), the requirement for vitamin A of growing dairy
animals was 42 IU/kg of BW. That requirement for growing
cattle was based on the amount of vitamin A needed to
maintain cerebrospinal fluid pressure below 120 mm Hg
in calves (Rousseau et al., 19541. Other data (Rousseau et
al., 1954; Eaton et al., 1972) using different criteria (i.e.,
a statistically significant increase in cerebrospinal fluid
pressure or the presence of papillary edema of the eye)
suggests that the vitamin A requirement for growing dairy
animals was between 60 and 100 IU/kg of BW. The sub-
committee decided that rather than discounting these stud-
ies, a compromise using all the data was appropriate.
The vitamin A requirement for adult dairy cattle has
been increased to 110 IU/kg of BW. In Nutrient Require-
ments of Dairy Cattle (National Research Council, 1989),
the vitamin A requirement for adult animals (76 IU/kg of
BW) was based largely on a long-term reproduction study
(Ronning et al., 1959~. The sole source of vitamin A in that
study was p-carotene, and cows were fed low concentrate
diets. The previous requirement (National Research Coun-
cil, 1989) also was based on data from a study (Swanson
et al., 1968) that indicated the amount of vitamin A deemed
adequate by Ronning et al. (1959) was adequate to maintain
supplementing between 15O,OOO and 25O,OOO IU/day of- milk production. In that study, cows produced approxi-
vitamin A or feeding 300 to 600 mg of p-carotene/day mately 3500 kg of milk during a 40-week lactation. Mean
reduced the incidence of intramammary gland infections milk production is currently about twice as high and many
OCR for page 164
164 Nutrient Requirements of Dairy Cattle
herds have mean milk production that is more than four
times higher. Furthermore, in a more recent study, milk
production increased from about 35 kg/day to 40 kg/day
when cows in early lactation were fed diets that provided
approximately 280 IU of vitamin A/kg of BW compared
with cows fed approximately 75 IU/kg of BW (Oldham et
al., 19911. The new requirement for lactating cows (110
IU/kg of BW) was based on data used by the previous
Nutrient Requirements of Dairy Cattle (National Research
Council, 1989) and on data showing that the bioavailability
of vitamin A (retinyl esters) may be as much as 50 percent
less than that of p-carotene when fed in high concentrate
diets because of ruminal destruction. Dry cows are typically
fed diets with lower amounts of concentrate and bioavail-
ability of vitamin A should be higher than for lactating cows.
The previous National Research Council requirement for
dry cows (76 IU/kg of BW) may be adequate, but in light
of potential improvements in mammary gland health and
data showing increased milk production after dry cows
were supplemented with vitamin A in amounts greater
than National Research Council (1989) requirements, the
vitamin A requirement for dry cows was kept the same as
that for lactating cows (110 IU/kg of BOO).
Presently available data are not adequate to define a
specific requirement for p-carotene for any class of dairy
cattle. Conditions that may warrant additional supplemen-
tation of vitamin A include:
· low forage diets (more ruminal destruction and less
consumption of p-carotene);
· diets that contain larger amounts of corn silage and
smaller amounts of haycrops (lower concentrations of
p-carotene and potentially lower bioavailability of basal
p-carotene);
· diets that contain lower quality forages (lower basal
concentrations of p-carotene);
· increased exposure to infectious pathogens (increased
demands on the immune system); and
· times when immunocompetence maybe reduced (per-
ipartum period).
Vitamin A toxicosis should not be a problem under most
practical situations. The presumed safe limit for vitamin
A is 66,O00 IU/kg of diet for both lactating and nonlactating
cattle (National Research Council, 19871.
Vitamin D
PHYSIOLOGY
Vitamin D is a pro-hormone, a necessary precursor for
the production of the calcium regulating hormone 1,25-
dihydroxyvitamin D. Vitamin D can be produced within
the skin of most mammals, including cattle, as a result of
the photochemical conversion of 7-dehydrocholesterol to
vitamin D3. In plants, ultraviolet irradiation causes photo-
chemical conversion of ergosterol to vitamin D2. Vitamin
D, supplied by the skin or the diet, is rapidly transported
to and sequestered by the liver. The rapid removal of
vitamin D from circulation prevents concentrations of vita-
min D in blood from becoming very high; the normal
concentration is 1 to 2 ng vitamin D/ml plasma (Horst
and Littledike, 19821. Within the liver, vitamin D can be
converted to 25-hydroxyvitamin D by vitamin D 25-hydrox-
ylase and released into the blood. The production of 25-
hydroxyvitamin D within the liver is dependent on the
vitamin D content of the diet. Thus plasma 25-hydroxy-
vitamin D concentration is the best indicator of vitamin D
status of an animal (Horst et al., 19941.
The 25-hydroxyvitamin D then circulates to the kidney
where it can be converted to the hormone 1,25-dihydroxy-
vitamin D. This hormone acts to increase the active trans-
port of calcium and phosphorus across the intestinal epithe-
lial cells, end potentiates the action of parathyroid hormone
to increase bone calcium resorption. Both functions are
vital for calcium and phosphorus homeostasis. In addition
to calcium and phosphorus homeostasis, 1,25-dihydroxyvi-
tamin D is involved in maintaining immune function (Rein-
hardt and Hustmyer, 19871; generally it promotes Th2
(humoral) immunity while inhibiting Th1 (cell mediated)
immunity (Daynes et al., 19951.
Renal production of 1,25-dihydroxyvitamin D is tightly
regulated. The 25-hydroxyvitamin D-1-`x-hydroxylase
activity of the kidney is stimulated by parathyroid hormone,
which is released in response to declining concentrations
of calcium in blood (DeLuca, 19791. In the absence of
parathyroid hormone, when an animal is in positive Ca
balance, 25-hydroxyvitamin D can be hydroxylated in the
kidney to 24,25-dihydroxyvitamin D as a primary step in
the inactivation and catabolism of vitamin D. The vitamin
D catabolic enzymes also function to deactivate 1,25-dihy-
droxyvitamin D. These catabolic enzymes exist in tissues
throughout the body. In these tissues the catabolic pathway
is generally stimulated by 1,25-dihydroxyvitamin D as a
negative feedback to reduce high concentrations of 1,25-
dihydroxyvitamin D in plasma (Goff et al., 1992; Reinhardt
and Horst, 19891.
A low concentration of phosphorus in blood also can
enhance renal production of 1,25-dihydroxyvitamin D,
even when the concentration of calcium in plasma is normal
or above normal (Tanaka and DeLuca, 1973; Gray and
Napoli, 19831. A1SO, higher than normal concentrations of
phosphorus in blood can inhibit renal production of 1,25-
dihydroxyvitamin D, which can be a factor contributing to
milk fever in the periparturient cow (Barton et al., 19871.
Pharmacologic doses of vitamin D have been utilized with
limited success to prevent milk fever. This is discussed in
the section on milk fever (Chapter 91.
OCR for page 165
Vitamins 165
Vitamin D2, the form associated with plants, and vitamin
D3, the form associated with vertebrates are both used for
supplementation of diets. The biologic activity of the two
forms is generally considered equal in cattle; however
Horst and Littledike (1982) demonstrated an apparent dis-
crimination against the vitamin D2 form in cattle. Presum-
ably this discrimination is the result of reduced binding of
vitamin D2 metabolites to vitamin D-binding proteins in
blood leading to more rapid clearance of vitamin D2 metab-
olites from plasma. However, the subcommittee does not
recommend adjusting the vitamin D requirement based
on the form of vitamin D used as a supplement.
Vitamin D deficiency reduces the ability to maintain
calcium and phosphorus homeostasis, resulting in a decline
for phosphorus and less often a decrease for calcium in
plasma. This eventually causes rickets in young animals
and osteomalacia in adults; both are bone diseases in which
the primary lesion is failure to mineralize the organic matrix
of bone. In young animals rickets causes enlarged and
painful joints; the costochondral joints of the ribs are often
readily palpated. In adults, lameness and pelvic fracture
are a common sequelae of vitamin D deficiency.
REQUIREMENT
The amount of dietary vitamin D required to provide
adequate substrate for production of 1,25-dihydroxyvita-
min D is difficult to define. Animals exposed to sunlight
at the lower latitudes may not require any dietary vitamin
D. Sun-cured hay also may provide enough vitamin D to
prevent symptoms of vitamin D deficiency (Thomas and
Moore, 19511.
The movement away trom pasture leeching systems anct
toward confinement and feeding of stored feeds and by-
products has increased the need for dietary supplementa-
tion of vitamin D for dairy cows. As a general rule, the
contribution of sunlight and forage to the supply of vitamin
D for the cow is not considered when describing the vita-
min D requirement. The vitamin D requirement in this
publication will consider the "requirement" to be the
amount of supplemental vitamin D that should be added
to the diet.
Horst et al. (1994) determined that plasma 25-hydroxyvi-
tamin D concentrations below 5 ng/ml are indicative of
vitamin D deficiency and concentrations of 200 to 300 ng/
ml would indicate vitamin D toxicosis. Normal cows have
concentrations of 25-hydroxyvitamin D in plasma between
20 and 50 ng/ml.
Dry, pregnant cows housed indoors and fed a corn silage
based diet had plasma concentrations of 25-hydroxyvitamin
D in plasma of 19 ng/ml at 14 days prior to parturition
and 10.5 ng/ml at 35 days into lactation. Supplementation
of the diet with 5,000 (7.5 IU vitamin D/kg BW) or lO,OOO
IU vitamin D (15 IU vitamin D/kg BW) maintained plasma
concentrations between 25 and 31 ng/ml throughout the
dry period and early lactation (Vines et al., 19851.
Ward et al. (1971) reported that cows fed an alfalfa hay-
concentrate diet receiving 30O,OOO IU vitamin D3 once
each week (~ 43,000 IU/day) returned to estrus 16 days
earlier than cows given no supplement. Ward et al. (1972)
also demonstrated that cows receiving 30O,OOO IU vitamin
D3/week had improved absorption of dietary calcium.
Hibbs and Conrad (1983) summarized the results of several
Ohio State University trials and concluded that cows sup-
plemented with 4O,OOO IU vitamin D2/day (50 to 70 IU
vitamin D/kg BW) produced more milk and generally ate
more than cows fed the same diets with no vitamin D
supplementation or supplemented with 8O,OOO or more IU
vitamin D/day. Reduced milk production, which could be
interpreted as the beginning of vitamin D intoxicosis, was
observed when cows were fed 8O,OOO IU vitamin D/day
(120-140 IU/kg BOO).
McDermott et al. (1985) fed an orchard grass-corn silage
based ration supplemented with O. lO,00O, 5O,00O, or
25O,OOO IU vitamin D3/day to Holstein cows in late gesta-
tion and for the first 12 weeks of lactation. Cows had no
access to sunlight from 2 weeks before calving until 4 days
postpartum. Thereafter they were outside and exposed to
sunlight 1 to 2 in/day. Plasma 25-hydroxyvitamin D concen-
trations in unsupplemented cows were below 20 ng/ml
during late gestation and the first 4 weeks of lactation.
Plasma 25-hydroxyvitamin D concentrations in cows
receiving lO,OOO or 5O,OOO IU vitamin D3/day (16-80 IU/
kg) were similar (between 30 and 45 ng 25-hydroxyvitamin
D/ml). Cows receiving 25O,OOO IU vitamin D/day had ele-
vated plasma 25-hydroxyvitamin D concentrations (60-80
ng/ml). The rapid changes in plasma concentrations of 25-
hydroxyvitamin D, 24,25-dihydroxyvitamin D, and vitamin
D suggested that at 25O,OOO IU/day the capacity of the
liver to store vitamin D had been exceeded, which was
interpreted as excessive vitamin D supplementation though
no outward clinical signs of vitamin D intoxication were
noted.
Under most circumstances lO,OOO IU/day (16 IU vitamin
D/kg BW) should provide adequate vitamin D for dairy
cows during late gestation. Astrup and Nedkvitne (1987)
reported that lactating cows producing about 20 kg of milk/
day required about 10 IU vitamin D/kg body weight to
maintain normal concentrations of calcium and phosphorus
in blood. These studies were conducted in Norway in win-
ter and spring when effective sunlight exposure should
have been minimal.
The 1989 Nutrient Requirements of Dairy Cattle
(National Research Council, 1989) requirement forvitamin
D for adult dairy cows was set at 30 IU/kg body weight.
This is more vitamin D than many studies suggest is neces-
sary for maintenance of normal plasma concentrations of
25-hydroxyvitamin D (17 IU/kg BW) (McDermott et al.,
OCR for page 166
166 Nutrient Requirements of Dairy Cattle
1985) or calcium and phosphorus (10 IU/kg BW) (Astrup
and Nedkvitne, 1987) in plasma. However, Ward et al.
(1971, 1972) and Hibbs and Conrad (1983) suggested that
milk production and reproductive and health benefits were
potentially improved when diets were supplemented with
as much as 70 IU/kg BW. Based on all available data,
the requirement of 30 IU/kg BW established previously
(National Research Council, 1989) seems justified.
TOXICITY
The maximum tolerable amount of vitamin D is inversely
related to dietary concentrations of calcium and phospho-
rus. The studies of McDermott et al. (1985) suggest that
5O,OOO IU D3/day (80 IU/kg BW) is well tolerated while
25O,OOO IU vitamin D3/day (400 IU/kg BW) is not. Hibbs
and Conrad (1983) reported a slight decline in milk produc-
tion when cows were fed 8O,OOO IU D2/day (~ 160 IU/kg
BOO). The 1987 National Research Council committee on
vitamin tolerance of animals (National Research Council,
1987) suggested the maximal tolerable level of vitamin D
is 2,200 IU/kg diet when fed for long periods (more than
60 days) and 25,OOO IU/kg diet when fed for short periods
of time. Vitamin D intoxication is associated with reduced
feed intake, polyuria initially followed by anuria, dry feces,
and reduced milk production. Upon necropsy calcification
of kidneys, aorta, abomasum, and bronchioles is evident
(Littledike and Horst, 19801.
Some of the dietary vitamin D is degraded in the rumen
by bacteria to inactive metabolites (Sommerfeldt et al.,
1983; Gardner et al., 19881. Injection of vitamin D avoids
this problem; however, the maximal tolerable dose of par-
enterally administered vitamin D is at least 100-fold lower
than the maximal tolerable oral dose and repeated injec-
tions can be especially toxic (Littledike and Horst, 19801.
Vitamin E
SOURCES
Vitamin E is a generic name for a series of lipid-soluble
compounds called tocopherols and tocotrienols. The most
biologically active form of vitamin E is oc-tocopherol; it is
also the most common form of vitamin E found in feed-
stuffs. Eight different stereoisomers of oc-tocopherol can
exist, and the isomer that has the highest biologic activity
is RRR-oc-tocopherol. The vitamin E content of foodstuffs
is highly variable (coefficients of variation are often 50
percent). Depending on species and maturity (Tramontano
et al., 1993; cupola et al., 1996), fresh forage plants contain
between 80 and 200 IU of vitamin E/kg of DM. Alpha-
tocopherol concentrations in forages decrease quickly after
the plant is cut; prolonged exposure to oxygen and sunlight
exacerbates the loss in vitamin E activity (Thafvelin and
Oksanen, 19661. Silage and hay contain 20 to 80 percent
less oc-tocopherol than does fresh forage. In general, con-
centrations of vitamin E in concentrates are low; possible
exceptions are raw whole soybeans and whole cottonseeds.
Heat treatment of whole soybeans destroys essentially all
the oc-tocopherol (Weiss, unpublished). Alpha-tocopherol
concentrations in feeds generally decrease as storage
. .
time Increases.
The commercial form of supplemental vitamin E usually
fed to dairy cows is all-rac-oc-tocopheryl acetate (previously
designated DL-oc-tocopheryl acetate). The esterified form
of the vitamin is more stable than the alcohol form;
expected losses in biologic activity from premixes contain-
ing all-rac-oc-tocopheryl acetate are less than 1 percent
per month under most storage conditions, but extruded
products containing all-rac-oc-tocopheryl acetate may have
storage losses of 6 percent per month (Coelho, 19911. RRR-
oc-tocopherol is available commercially but is not com-
monly fed to ruminants.
BlOAVAlLABlLITY
Early data (Alderson et al., 1971) suggested that signifi-
cant amounts of supplemental vitamin E were destroyed
in the rumen and that destruction increased as the amount
of concentrate in the diet increased. More recent studies
(Leedle et al., 1993; Weiss et al., 1995) found that vitamin
E (all-rac-oc-tocopheryl acetate) was not destroyed during
in vitro fermentation. The authors of these studies sug-
gested that poor extraction of tocopherol from digesta was
the reason early reports indicated that vitamin E was
destroyed by ruminal fermentation. Based on the new data
using better analytic techniques, ruminal metabolism of
. .
vitamin ~ appears mlmma .
The USP defines 1 IU of vitamin as equal to 1 mg of
all-rac-oc-tocopheryl acetate, and 1.49 IU of vitamin E is
equal to 1 mg of RRR-oc-tocopherol. Those conversion
factors are based largely on research with laboratory ani-
mals. Data from cows comparing bioavailability of various
tocopherol stereoisomers is contradictory. Hidiroglou et
al. (1988, 1989) reported no or only slight differences in
concentrations of oc-tocopherol in plasma and tissue
between cows and heifers fed similar IU amounts of vita-
min E as all-rac-oc-tocopherol or all-rac-oc-tocopheryl ace-
tate. Concentrations of oc-tocopherol in tissue and plasma
were 20 to 60 percent higher in beef cows fed RRR-°'-
tocopherol than those fed all-rac-oc-tocopheryl acetate
(Hidiroglou et al., 19881. Based on that study 1 mg of RRR-
oc-tocopherol would be equal to 1.8 to 2.4 IU of vitamin
E. Different formulations of all-rac-oc-tocopheryl acetate
(silica adsorbate, oil, or a microencapsulated form) did not
greatly affect concentrations of oc-tocopherol in plasma
suggesting equivalent bioavailability (Bald) et al., 19971.
Insufficient consistent data are available currently to war-
OCR for page 167
Vitamins 167
rant changing IU conversion factors for vitamin E for rumi-
nants. The current USP factors will be used for describing
vitamin E requirements in this publication.
FUNCTIONS AND ANIMAL RESPONSES
The best understood function of vitamin E is as a lipid-
soluble cellular antioxidant (Hogan et al., 19931. Via this
function and perhaps other functions, vitamin E is involved
in maintenance of cellular membranes, arachadonic acid
metabolism, immunity, and reproductive function.
White muscle disease is a classic sign of a clinical def~-
ciency of vitamin E. White muscle disease was prevented
in preweaned calves when 50 IU of vitamin E/day (all-rac-
oc-tocopheryl acetate) were supplemented to a vitamin E-
free diet based on skim milk (Blaxter et al., 19521. Presum-
ably those data were used to formulate the vitamin E
requirements for all classes of dairy cattle in the last Nutri-
ent Requirements of Dairy Cattle (National Research
Council, 19891. More recent experiments with vitamin E
have focused on its relationship with reproductive disor-
ders, mastitis, and immune function.
Dietary or parenteral supplementation of vitamin E to
dairy cows during the peripartum period has consistently
improved the function of neutrophils and macrophages
(Hogan et al., l99O, 1992; Politis et al., 1995, 19961. In
those studies, the amount of supplemental vitamin E fed
per day during the prepartum period was either 1000 IU/
day or 3000 IU/day. In three of those studies (Hogan et
al., 1992; Politis et al., 1995, 1996) vitamin E also was
injected (3000 or 6000 IU on approximately day 7 prepar-
tum). During the postpartum phase, cows were fed either
500 or 3000 IU/day of supplemental vitamin E. Cows in
all studies were fed stored forages.
Clinical studies have been conducted to evaluate the
effect of supplemental vitamin E on prevalence of retained
fetal membranes, intramammary infections, and clinical
mastitis. Feeding approximately 1000 IU/day of supple-
mental vitamin E (usually all-rac-oc-tocopheryl acetate) to
dry cows when adequate selenium was supplemented
reduced the prevalence of retained fetal membranes in
some (Harrison et al., 1984; Miller et al., 1993) but not all
(Wichtel et al., 1996) studies. When vitamin E was injected
(usually in combination with selenium) rather than fed,
about half the time there was no effect for prevalence of
retained fetal membranes and about half the time there
was a positive response (Miller et al., 19931. The typical
treatment was a single injection of approximately 700 IU
of vitamin E and 50 mg of selenium given about 3 weeks
before calving. Relative to the amount of vitamin E nor-
mally consumed, 700 IU of vitamin E over 21 days is trivial.
Most likely, selenium, not vitamin E, was the nutrient
responsible for the positive effect.
Two clinical studies conducted in Ohio (Smith et al.,
1984; Hogan et al., 1993) reported that feeding supplemen-
tal vitamin E significantly reduced the incidence and dura-
tion of intramammary gland infections and clinical mastitis.
In those studies, approximately 1000 IU/day of supplemen-
tal vitamin E was fed during the 60-day prepartum period
and 500 IU/day was fed during lactation. Conversely, a
study conducted in Canada (Batra et al., 1992) found that
similar amounts of supplemental vitamin E did not reduce
the incidence of clinical mastitis. Based on the concentra-
tions of selenium in the plasma (~35 ng/ml), cows in that
study (Batra et al., 1992) were deficient in selenium.
Another study (Weiss et al., 1997) using diets low in total
selenium (0.15 ppm) but with animals in better selenium
status (plasma selenium >50 ng/ml) than cows in the Batra
et al. (1992) study found that feeding 1000 IU/day of vita-
min E during the dry period reduced clinical mastitis at
calving by 30 percent but did not affect prevalence of
intramammary gland infections. In that same study, feeding
4000 IU of supplemental vitamin E/day during the last 2
weeks of the dry period resulted in an 80 percent reduction
in clinical mastitis at calving and a 60 percent reduction
in intramammary gland infections (Weiss et al., 19971.
REQUIREMENTS AND FACTORS THAT AFFECT
REQUIREMENTS
The vitamin E requirement (15 IU/kg of DMI) in the
previous Nutrient Requirements of Dairy Cattle (National
Research Council, 1989) was for total, not supplemental,
vitamin E and the basis for that requirement was not given.
The previous vitamin E requirement should prevent classic
signs of vitamin E deficiency. The vitamin E content of
the basal diet is highly variable and will not be known in
most situations; therefore, vitamin E requirements in this
edition are presented for supplemental vitamin E. The
requirements presented assume that cattle are consuming
conserved forages. Because fresh forage is an excellent
source of vitamin E the requirements for supplemental
vitamin E for grazing cattle are probably substantially less
than those presented for cattle fed conserved forages.
Because titration studies are lacking, a specific requirement
cannot be defined. The subcommittee concluded that there
were adequate data available on the effect of vitamin E
on mastitis and reproductive disorders to justify an increase
in the vitamin E requirement. Based on health and immune
function in cows, plasma concentrations of oc-tocopherol
in peripartum cows should be approximately 3 ~g/ml
(Weiss et al., 1994, 19971. To maintain these blood values,
dry cows and heifers fed stored forages during the last 60
days of gestation require approximately 1.6 IU of supple-
mental vitamin E/kg of body weight (approximately 80 IU/
kg of DMI). An additional benefit on calf health may be
observed by increasing vitamin E intake by cows and heif-
OCR for page 168
168 Nutrient Requirements of Dairy CattIe
ers in late gestation. Only minor amounts of vitamin E can
pass the placenta (Van Saun et al., 19891; hence newborn
calves rely on colostrum for vitamin E. Increased intake
of vitamin E during the prepartum period significantly
elevates vitamin E in colostrum. For lactating cows, the
recommended amount of vitamin E (supplemental) was
changed to 0.8 IU/kg of body weight (approximately 20
IU/kg of DMI) when stored forages are fed. This recom-
mendation is based on a reduction in mastitis. The differ-
ence between the recommendations for vitamin E for the
two classes of cattle is mainly caused by expected differ-
ences in intake of vitamin E from basal foodstuffs and
perhaps reduced absorption of vitamin E by cows fed con-
ventional dry cow diets. Based on typical feed intakes and
average vitamin E concentrations in feedstuffs, the recom-
mended amount of total vitamin E (supplemental plus
vitamin provided by feedstuffs) is approximately 2.6 IU/
kg of body weight during late gestation and for lactating
dairy cows. Of that amount, the basal diet will provide on
average about 1.8 IU/kg of body weight for lactating cows
(ranges from about 0.8 for cows fed diets based on severely
weathered hay to about 2.8 IU/kg of body weight for cows
fed diets based on pasture) and about 1 IU/kg body weight
(ranges from 0.5 to about 2.3 IU/kg of body weight) for
dry cows.
Although several factors are known to influence vitamin
E requirements, limited data make quantifying the neces-
sary adjustments difficult. The amount of supplemental
vitamin E fed may need to be changed during the follow-
ing situations:
· When fresh forage is fed there should be less need
for supplemental vitamin E. A diet based on fresh forage
(ca. 50 percent of dietary DM) would require about 67
percent less supplemental vitamin E to meet the cows
requirements compared with a diet that contained a similar
amount of stored forage. Requirements for supplemental
vitamin E is reduced 67 percent in the accompanying soft-
ware when animals are fed pasture.
· The amount of supplemental vitamin E probably
should be increased when low forage diets are fed (forages
typically have more vitamin E than do concentrates). The
requirements listed above were generated from studies
using diets with 50 to 60 percent forage (lactating cows)
and 60 to 80 percent forage (animals in late gestation).
· Cows in suboptimal selenium status probably require
more vitamin E.
· Milk is not a major excretion route for oc-tocopherol
(0.4 to 0.6 ~g/ml) but colostrum contains high concentra-
tions of oc-tocopherol (3 to 6 ~g/ml). Additional vitamin E
may be useful during colostralgenesis.
· Intake of polyunsaturated fatty acids increases the
vitamin E requirement of nonruminants. As methods for
protecting fats from biohydrogenation in the rumen
improve, additional vitamin E may be required when pro-
tected unsaturated fats are fed.
· Additional vitamin E may be useful during periods of
immunosuppression (peripartum period).
· Large amounts of supplemental vitamin E (~1000
IU/day) can reduce oxidative flavors in milk (St.-Laurent
et al., 19901.
TOXICITY
Vitamin E is one of the least toxic vitamins due in part
to its relatively low absorption. Toxicity studies have not
been conducted with ruminants but data from rats suggest
an upper limit of approximately 75 IU/kg of body weight
per day (National Research Council, 19871.
Vitamin K
Vitamin K is a generic term used to describe a group
of quinone compounds exhibiting antihemorrhagic effects.
The basic form of vitamin K is 2-methyl-1,4-naphthoqui-
none. Isomers of vitamin K differ in the length and nature
of the side chain (Frye et al., 19911. The three most com-
mon isomers or vitamers of K are: phylloquinone (vitamin
Kit, menaquinones (vitamin K2 ~ and menadione (vitamin
Kay. The phylloquinones are commonly found in the chloro-
plast of green plants and have side chains consisting of
several isoprenoid units. Menaquinones are synthesized by
bacteria flora and have isoprene side chains containing
double bonds. Menadione (2-methyl-1,4-napthoquinone
without a side chain) does not exist naturally. Menadione
and its derivatives are the synthetic forms of vitamin K
used in feed supplements (Combs, 19921.
Cattle require vitamin K for the synthesis of at least a
dozen proteins. Among these are four blood clotting fac-
tars; prothrombin (factor II), and factors VII, IX and X.
These vitamin K dependent protein factors are components
of a complex system that functions to prevent hemorrhage
by activation of thrombin and ultimately clot formation
(Combs, 19921.
Because large quantities of menaquinones are synthe-
sized by ruminal bacteria and ruminant diets generally
contain green forages and/or pasture plants high in phyllo-
quinones, a deficiency of vitamin K rarely occurs. The only
reported deficiencies have occurred when moldy sweet
clover hay was fed (National Research Council, 19891.
Dicoumarol is a fungal metabolite produced from sub-
stances in sweet clover that inhibits the synthesis of clotting
factors. Holstein calves were shown to develop dicoumarol
toxicosis when fed sweet clover hay containing 18 mg/kg
of dicoumarol for two weeks or longer (Yamini et al., 19951.
Early signs of vitamin K deficiency include stiffness and/
or lameness and hematoma of tissues. Prolonged feeding
of dicoumarol leads to uncontrolled bleeding. Dicoumarol
OCR for page 169
Vitamins 169
can pass placental barriers resulting in the fetus or newborn Folic Acid
animals being affected (Frye et al., 19911. Vitamin K3 was
found to be ineffective in preventing the anticoagulant
effects of dicoumarol (Casper et al., 1989~.
Toxicity data for either naturally occurring or synthetic
forms of vitamin K are extremely limited. For humans and
laboratory animals the presumed upper safe level for oral
ingestion of menadione (K3) is 1,000 times the dietary
requirement (National Research Council, 1987), but toxic-
ity data for cattle are not available.
WATER-SOLUBLE VITAMINS
Ruminal microorganisms synthesize most water-soluble
vitamins (biotin, folic acid, niacin, pantothenic acid, pyri-
doxine, riboflavin, thiamin, and vitamin B12) and common
foodstuffs generally contain high concentrations of most
of those vitamins. Vitamin C is synthesized by ruminant
animals. True deficiencies of these vitamins are rare in
animals with a functional rumen. To date, a limited amount
of research has been conducted on most water-soluble
vitamins (niacin is the exception) for adult cattle; however,
research in this area has increased during the past few
years. Adequate data to quantify bioavailability, ruminal
synthesis, and requirements for most water-soluble vita-
mins are not available. Deficiency diseases for most B
vitamins can be induced when preruminant calves are fed
synthetic diets but are rare when calves are fed milk. Milk
replacers should be supplemented with B vitamins as
described in Chapter 10.
B -VITA M I N S
Biotin
Biotin acts as a cofactor for many enzymes involved in
carboxylation reactions. Ruminal bacteria normally synthe-
size biotin and concentrations of the vitamin may exceed
9 ~g/L of strained ruminal fluid (Briggs et al., 1964~. Biotin
is not extensively metabolized in the rumen and increased
intake of dietary biotin results in elevated concentrations
of biotin in serum and milk (Frigg et al., 1993; Midla
et al., 1998~. Unpublished epidemiologic data suggest a
negative relationship between serum concentrations of bio-
tin and the incidence of clinical lameness in dairy cattle.
In controlled long-term field studies, feeding approxi-
mately 20 mg/day of supplemental biotin statistically
improved measures of hoof health (Bergsten et al., 1999;
Fitzgerald et al., 2000; Midla et al., 1998~. However, insuff~-
cient data are available at this time to quantify the require-
ment for biotin of dairy cattle.
Folic acid containing coenzymes are involved in move-
ment of one-carbon units in biochemical pathways. Methi-
onine also serves as a methyl donor; therefore, folic acid
mav snare methionine. Folic acid is necessary for the syn-
thesis of nucleic acids. Growth rate and hematologic
responses have been used to access adequacy in animal
studies. Microbial degradation of supplemental folic acid
can be extensive (Zinn, 1987~. Consequently, parenteral
administration of folic acid is usually used to examine
responses to supplemental folic acid.
Weekly intramuscular injections of 40 mg folic acid from
45 days after mating until 6 weeks after parturition did
not alter blood parameters or influence calf birth weight,
therefore, dietary folic acid and microbial synthesis of this
vitamin appear to supply sufficient amounts to prevent
deficiency symptoms in adult dairy cattle (Girard et al.,
1995~. Young calves that do not have a completely devel-
oped ruminal microflora may be most susceptible to folic
acid deficiency. Calves given weekly intramuscular injec-
tions of 40 mg of folic acid from 10 days of age until 16
weeks of age increased average daily gain by 8 percent
during the 5 weeks following weaning (approximately 7 to
12 weeks of age; Dumoulin et al., 19911. Treatment also
increased serum folates, blood hemoglobin, and packed
cell volume suggesting that folic acid may be deficient in
young calves.
Parenteral supplementation of 160 mg of folic acid each
week from 45 days of gestation until 6 weeks postpartum
tended to increase milk and milk protein production during
mid to late lactation of primi- and multiparous cows. After
calving, milk protein percentage was increased in multipa-
rous cows only during the first 6 weeks of lactation (Girard
et al., 1995~. Milk production during days 1 to 200 of
lactation was increased linearly for multiparous cows but
not for primiparous cows when O. 2, or 4 mg folate/kg BW
were fed (Girard and Matte, 19981. Blood folates were
increased indicating that some dietary folic acid escaped
ruminal degradation. Deficiency symptoms for folate have
not been observed in lactating dairy cattle. The increased
milk production observed when supplemental folate was
fed may be a direct response to the vitamin or may be an
indirect response caused by sparing methionine. Insuffi-
cient data are currently available to quantify the folic acid
requirement of cattle.
Inositol
Inositol is an important nutrient in the metabolism and
transport of lipids, and is a constituent of phospholipids,
and has lipotropic activity. Myo-inositol is found in feeds
as a component otphytic acid (Gerloffet al., 19841. Because
physic acid can be degraded in the rumen, deficiencies of
OCR for page 170
170 Nutrient Requirements of Dairy Cattle
inositol are not likely to occur. However, during periods
of hepatic lipidosis or fatty liver syndrome where feed
intakes may be low, supplementation of inositol has been
investigated as an aid to help minimize triglyceride accu-
mulation in the liver. Gerloff et al. (1984) in a field study
involving 80 multiparious cows reported that the lipid con-
tent of liver was not decreased by feeding 17 grams of
nonphytate myo-inositol for one month pre- and postpar-
tum. Similarly, Grummer et al. (1987) indicated that nei-
ther milk production nor milk fat percentage were
increased with abomasal infusion of 37 grams of myo-
inositol.
Dietary requirements for inositol have not been demon-
strated in dairy animals with normal rumen activity. Bacte-
rial synthesis in the rumen and/or the amounts in feeds
apparently supply adequate amounts to meet metabolic
requirements. The previous edition of Nutrient Require-
ments of Dairy Cattle, (National Research Council, 1989)
cited research from 1940 and 1950 showing deficiencies
in calves after several weeks when fed purified or semi-
purif~ed diets. Because dairy products are generally good
sources of these vitamins (Combs, 1992) and milk replacers
are fortified with additional amounts (Tomkins and [aster,
1991), deficiencies are unlikely to occur under typical calf
. . .
raising practices.
Niacin
Niacin is a generic name for pyridine 3-carboxylic acids
and their derivatives that demonstrate activity similar to
the amide form (i.e., nicotinamide). Niacin functions as
a coenzyme for the pyridine nucleotide electron carriers
NAD(H) and NADP(H). Consequently, niacin plays a criti-
cal role in mitochondrial respiration and the metabolism
of carbohydrates, lipids, and amino acids.
Net synthesis of niacin in the rumen is likely because
supply of niacin to the intestine exceeds intake when
unsupplemented diets are fed to cattle (Zinn et al., 19871.
Rate of niacin synthesis may be inversely related to level
of supplementation (Abdouli and Schaefer, 1986b). During
supplementation, the amount of niacin reaching the intes-
tine may be less than that fed, indicating niacin degradation
or absorption from the rumen (Zinn et al., 19871. Niacin
absorption from the rumen appears to be low, particularly
for nicotinic acid (Erickson et al., 19911. Feeding supple-
mental niacin increases concentrations in ruminal and duo-
denal fluid, which suggests that some supplemental niacin
reaches the small intestine (Zinn et al., 1987; Campbell
et. al., 19941. Estimates are that 17 to 30 percent of supple-
mental niacin reaches the small intestine (Harmeyer and
Kollenkirchen, 1989; Campbell et al., 19941. Nicotinamide
is rapidly converted to nicotinic acid in the reticulorumen
(Harmeyer and Kollenkirchen, 1989; Campbell et al.,
19941.
Niacin may increase microbial protein synthesis (Shields
et al., 1983; Riddell et al., 198O, 19811; however, several
studies indicate no effects (Hannah and Stern, 1985;
Abdouli and Schaefer, 1986a; Doreau and Ottou, 19961.
Differences between these studies, all of which utilized in
vitro systems, may reflect the amount and availability of
niacin in the unsupplemented diet, the niacin status of the
microbes, or both. When niacin was fed in combination
with other B-vitamins to feedlot calves (Zinn et al., 1987),
or nicotinic acid or nicotinamide was fed to lactating cows
(Doreau and Ottou, 1996), there were no treatment effects
on microbial flow to the intestine.
Niacin is requiredin the diet of preweaned calves. Calves
fed synthetic milk that was deficient in niacin developed
scours within 48 hours (Hopperand;[ohnson, 19551. Imme-
diate improvement was observed on the day following oral
(6 mg/head/day) or intramuscular (10 mg/head/day) nico-
tinic acid administration. Niacin supplementation did not
improve growth rates of heifers that began on trial at
approximately 110 or 370 kg (Riddell et al., 19811.
A total of 30 treatment comparisons from peer reviewed
literature (Fronk et al., 1980; Kung et al., 1980; Riddell et
al., 1981; Dufva et al., 1983; [aster et al., 1983a,b; Homer
et al., 1986, 1988; Muller et al., 1986; Skaar et al., 1989;
Driver et al., 1990; Erickson et al., l99O, 1992; Martinez
et al., 1991; Lanham et al., 1992; Zimmerman et al., 1992;
Bernard et al., 1995; Ottou et al., 1995; Madison-Anderson
et al., 1997; Minor et al., 1998) were summarized to exam-
ine niacin effects on lactation; a significant increase or
decrease was declared if P <0.05. One comparison indi-
cated a significant increase in milk production and 29 com-
parisons indicated no significant change in milk production.
For the fourteen comparisons in which niacin administra-
tion began prepartum or prior to two weeks postpartum,
none indicated a positive response. The absence of a
response in many trials may be the consequence of inade-
quate replication. The only positive milk yield response
was from one of the two field trials that have utilized
large animal numbers (Muller et al., 19861. The numbers
of significant positive, neutral, or significant negative
responses were 3, 26, and 1 for milk fat percentage and
5, SO, and 2 for milk protein percentage.
A similar summary by Erdman (1992) indicated that
average milk yield response was 0.3 kg/day; 0.4 kg/day if
studies were restricted to those in which niacin supplemen-
tation began prepartum. A summary of 23 to 30 treatment
comparisons by Drackley (1992) indicated that average
milk production was increased by 0.62 kg/day and milk fat
and protein were increased by 0.033 and 0.002 percentage
units when supplemental niacin was fed. Summaries by
Erdman (1992) or Drackley (1992) indicated that milk
production was decreased 1.1 or 0.42 kg/day when niacin
was added to diets that contained supplemental fat. How-
ever, there have been no significant (P <0.05) interactions
OCR for page 171
Vitamins 171
between fat and niacin for milk yield in the eight studies
that have tested for interactions (Homer et al., 1986; Skaar
et al., 1989; Driver et al., 1990; Martinez et al., 1991;
Erickson et al., 1992; Lanham et al., 1992; Ottou et al.,
1995; Madison-Anderson et al., 19971.
Niacin is antilipolytic and has been examined closely as
a feed additive to prevent or treat fatty liver and ketosis.
Early studies indicated that small (12 g/day until negative
milk acetone test; Fronk and Schultz, 1979) or large (160
grams over 8 hours; Waterman et al., 1972) pharmacologic
doses of niacin reduced blood ketones in ketotic cows. In
these studies, there were no ketotic cows assigned to a
control (no niacin) treatment. Consequently, niacin effects
were confounded with time. A slug dose of 12 or 120 grams
of niacin decreased plasma concentrations of nonesterif~ed
fatty acids but not beta-hydroxybutyrate ([aster et al.,
1983a). A summary of 14 treatment comparisons in which
niacin was fed (Fronk et al., 1980; Dufva et al., 1983; [aster
et al., 1983a; Skaar et al., 1989; Driver et al., 1990; Erickson
et al., 1990; Martinez et al., 1991; Erickson et al., 1992;
Zimmerman et al., 1992; Bernard et al., 1995; Chilliard
and Ottou, 1995; Ottou et al., 1995; Minor et al., 1998)
indicated plasma nonesterif~ed fatty acids were significantly
reduced once, increased twice, and not altered 11 times.
If restricted to studies in which niacin was fed prepartum
or within two weeks postpartum, plasma nonesterif~ed fatty
acids were significantly reduced once, increased twice, and
not altered 8 times. In 10 comparisons (9 of which niacin
treatment began prepartum or prior to two weeks postpar-
tum) plasma ketones were significantly reduced 4 times
and not affected 6 times. However, three of the four com-
parisons in which significant reductions were observed
were from a single experiment and corresponded to con-
trasts between three different doses of niacin to a control
treatment (Dufva et al., 19831. Initiating the feeding of
niacin prepartum did not reduce the amount of fat in liver
of cows at 1 to 2 days or 28 to 35 days postpartum (Skaar
et al., 1989; Minor et al., 19981.
Niacin requirements for dairy cattle are not known. Sup-
plemental niacin may be required by calves fed milk
replacer (Hopper and Johnson, 1955) but not by post
weaned "rowing heifers (Riddell et al., 19811. Data summa-
rized from more than 25 trials does not support routine
use of niacin to enhance lactation performance of dairy
cattle. Data also do not support the routine use of niacin
to minimize the risk of lipid-related metabolic disorders
such as ketosis and fatty liver.
Pantothenic Acid
Pantothenic acid is a constituent of coenzyme A and is
therefore essential for several fundamental reactions in
metabolism including fatty acid oxidation, amino acid
catabolism and acetylcholine synthesis (Smith and Song,
19961. No dietary requirement for pantothenic acid has
been established as synthesis of pantothenic acid by rumi-
nal microorganisms appears to be 20 to 30 times more
than dietary amounts. Net microbial synthesis of panto-
thenic acid in the rumen of steer calves has been estimated
to be 2.2 mg/kg of digestible organic matter consumed per
day and degradation of dietary pantothenic acid in the
rumen is estimated to be 78 percent (Zinn et al., 19871.
Supplementation of pantothenic acid at five to 10 times
theoretic requirements did not improve performance of
feedlot cattle (Cole et al., 1982; Zinn et al., 19871. Def~-
ciency symptoms are very diverse and nonspecific. In non-
ruminants, some generally reported symptoms include: dis-
orders of the nervous, gastrointestinal, and immune sys-
tems, reduced growth rate, decreased food intake, skin
lesions and changes in hair coat, alterations in lipid and
carbohydrate metabolism and death (Smith and Song,
19961.
Riboflavin (B2)
Riboflavin is a constituent of several enzyme systems
associated with intermediary metabolism. No dietary
requirement for ruminants has been established. Tissue
requirements are apparently met through microbial syn-
thesis of the vitamin in the rumen as destruction of dietary
riboflavin in the rumen is nearly 100 percent (Zinn et al.,
19871. Miller et al. (1986) reported ruminal synthesis of
riboflavin to be 148 percent of intake with apparent absorp-
tion from the small intestine averaging 23 percent. Synthe-
sis of riboflavin in the rumen and flow to the small intestine
was unaffected by concentrate content of the diet fed to
steers. Zinn et al. (1987) estimated the flow of riboflavin
from the rumen at 15.2 mg/kg of digestible organic matter
consumed per day and a net absorption from the small
intestine of 25 percent.
Thiamin (Big
Thiamin is a water-soluble vitamin, which in pure form
is white in color, and has a sulfurous odor. It functions
as an important coenzyme in several energy metabolism
pathways and has a role, although not well defined, in
nerve and brain function (Combs, 19921. Sources of thia-
min include grains, grain by-products, soybean meal, and
brewers yeast. Amounts of thiamin synthesized daily in the
rumen (28 to 72 ma) have been reported to equal or exceed
dietary intake (Breves et al., 19811.
A dietary requirement for thiamin has not been estab-
lished for healthy animals with a functional rumen. The
combination of thiamin in feeds and synthesis of thiamin
in the rumen meet or exceed metabolic requirements even
with an estimated 48 percent destruction of dietary thiamin
in the rumen (Zinn et al., 19871. Thiamin is generally
OCR for page 172
172 Nutrient Requirements of Dairy Cattle
nontoxic as the upper safe feeding level for most nonrumi-
nants is 1,000 times the requirement (National Research
Council, 19871. An upper safe feeding level has not been
established for ruminants.
Deficiencies of thiamin have been found when thiamin-
ases associated with either feeds or produced from altered
ruminal fermentation destroy thiamin or produce an anti-
metabolite of thiamin, which blocks thiamin dependent
reactions. Bracken ferns and some raw fish products have
been found to contain thiaminases. Feeding diets high in
sulfate (Gould et al., 1991) or those which cause a sudden
drop in ruminal pH (Zinn et al., 1987) can result in a
thiamin deficiency. Because thiamin is intricately involved
in several of the energy producing Krebs cycle reactions
and because of the importance of glucose as an energy
supply for the brain, any deficiency of thiamin results in
a central nervous system disorder. Polioencephalomalacia
(PEM), is the most common thiamin deficiency disorder.
Symptoms of PEM include a profuse, but transient diar-
rhea, listlessness, circling movements, opisthotonus (head
drawn back over neck), and muscle tremors. If treated
promptly by parenteral injection of thiamin (2.2 mg/kg
of body weight), the condition can be reversed (National
Research Council, 19961.
Vitamin Be
Vitamin Be is a cofactor for two major enzymes; methyl-
malonyl coenzyme A mutase necessary for conversion of
propionate to succinate, and tetrahydrofolate methyl trans-
ferase which catalyzes transfer of methyl groups from 5-
methyltetrahydrofolate to homocysteine to form methio-
nine and tetrahydrofolate. Vitamin B12 is not found in the
tissues of plants. Microbes are the only natural source of
vitamin Be. Ruminal microbes can produce all of the vita-
min Be required by the cow provided adequate available
cobalt is in the diet (see section on cobalt, Chapter 61.
Vitamin Be deficiency has been demonstrated in calves
when fed diets devoid of animal protein (Lassiter et al.,
1953) demonstrating that vitamin B12 is a required nutrient
in dairy cattle. Based on this work, it was suggested that
the vitamin Be requirement for dairy cattle was between
0.34 and 0.68 ~g/kg of live weight. Vitamin Be deficiency
is the principle manifestation of cobalt deficiency (See
section on cobalt).
Significant quantities of vitamin Be are synthesized in
the rumen. Vitamin Bl2 activity in the rumen tends to be
greater in animals either grazing or fed high forage diets
compared with animals fed high concentrate diets (Sutton
and Elliot, 1972; Walker and Elliot, 19721. Data from beef
cattle (Zinn et al., 1987) suggest more than adequate syn-
thesis of vitamin Be to meet expected requirements for
lactating dairy cows (Erdman, 1992), although exact
requirements have not been established.
In the mature ruminant, vitamin Be is of interest because
of its roles in propionate metabolism (gluconeogenesis)
and in methionine synthesis. It was suggested that inade-
quate Be may be related to the low-milk fat syndrome in
cows fed high grain diets (Frobish and Davis, 19771. Studies
using both supplemental (Elliot et al., 1979) and injected
(Croom et al., 1981) vitamin Be failed to show any response
in fat test from cows fed high grain diets. There is no
evidence that lactating dairy cows fed adequate amounts
of cobalt will respond to dietary or intramuscular injections
of vitamin Be
Vitamin Be also is required as part of the enzyme com-
plex methionine synthase in which methionine is synthe-
sized from S-adenosylhomocysteine and 5-methyl tetrahy-
drofolate. Methionine is used as a methyl donor for synthe-
sis of choline, carnitine, and others compounds; therefore,
a deficiency of vitamin Be is likely to affect methionine
and methyl donor metabolism. Methyl donor requirements
are not defined in ruminants and again it is unlikely that
vitamin Be deficiency is of practical significance except
during cobalt deficiency.
B-Vitamins General
In general, B-vitamin requirements can be met through
synthesis by ruminal microorganisms and escape of dietary
sources from the rumen. Table 7-1 illustrates potential
requirements extrapolated from swine requirements and
average vitamin concentrations found in milk. Based on
these estimated requirements and limited research on B-
vitamins of Miller et al. (1986) and Zinn et al. (1987) only
folio acid and pantothenic acid appear to be limiting based
on ruminal synthesis and escape of these vitamins occurring
naturally in feeds. In contrast, some studies have demon-
strated production and/or health benefits to dairy cows
when diets have been supplemented with B-vitamins, most
notably niacin, biotin, and folio acid. At the present time,
almost no research is available on requirements of B com-
plex vitamins for gestation, health, and milk production of
high producing dairy cows.
VITAMIN C
Vitamin C or ascorbic acid is synthesized from L-gulonic
acid within the cells of ruminants. Calves cannot synthesize
ascorbic acid until approximately 3 weeks of age (Cummins
and Brunner, 19911. Therefore, vitamin C is not considered
an essential nutrient for healthy cattle that are older than
about 3 weeks. Some studies, however, have reported ben-
ef~cial responses when supplemental vitamin C is adminis-
tered to cattle, particularly calves. Ascorbic acid functions
as awater-soluble cellular antioxidant. Specifically, ascorbic
acid is thought to be involved in regulation of steroid syn-
thesis and the concentration of ascorbic acid is high in
OCR for page 173
Vitamins 173
TABLE 7-1 Estimated Absorption of Selected B-vitamins From the Small Intestine Compared with Estimated
Requirements for Tissue and Milk Synthesis of a 650-kg Cow Producing 35 kg of 4 Percent Fat-Corrected Milk/Day
Dally Estimated Requirement
Rumlnal Rumlnal
Tissuea MilLb Total Synthesist Escaped from
Vitamin (mg/day) (mg/day) (mg/day) (mg/day) diet (%)
Biotin 5 1 6 14 100
Folic acid 33 2 35 7 3
Niacin 256 33 289 1804 6
Pantothenic acid 304 121 425 38 22
Riboflavin 95 61 156 261 1
Thiamin 26 15 41 143 52
Be 26 22 48 96 100
Be 0.4 0.2 0.6 70 10
aBased on lactating sow (175 kg) requirements (NRC, 1998) adjusted to 650 kg lactating cow weight.
bAdapted from Jenness (1985) and adjusted to 35 kg milk production.
Readapted from Miller et al. (1986)C and Zinn et al. (1987)d and adjusted to digestible organic matter intake of 17.2 kg/day (total DM intake 22.9 kg/day).
steroid secreting cells. Plasma concentrations of ascorbic
acid were lower in calves (Cummins and Brunner, 1991)
and growing steers (Hidiroglou et al., 1977) reared under
stressful (i.e., slatted floors, cold stress) conditions than
animals housed in better environments. That effect may
be mediated by cortisol. Oral supplementation of 1 or 2
grams of vitamin C/day to preruminant calves elevated
plasma concentrations of ascorbic acid compared with no
supplemental vitamin C (Hidiroglou et al., 19951. The 2
grams supplementation rate tended to increase plasma con-
centrations of ascorbic acid above the 1 gram rate but the
difference was not statistically consistent during the 35
day experiment. Data are lacking on the effect of oral
supplementation of vitamin C with cattle. Most orally
ingested ascorbic acid is destroyed in the rumen, but newer
formulations of vitamin C may provide some protection
from ruminal metabolism. With sheep, oral supplementa-
tion of 4 g/day of various forms of vitamin C for 28 days
significantly increased plasma ascorbic acid concentrations
(Hidiroglou et al., 19971.
No growth response has been reported when calves were
supplemented with vitamin C. Because of its antioxidant
function, most research has concentrated on the effects of
vitamin C on immune function. Immunoglobulin titers in
calves were generally not affected by vitamin C supplemen-
tation (Cummins and Brunner, 1989; Hidiroglou et al.,
19951. Steers injected subcutaneously with 20 mg of
ascorbic acid/kg of BW had improved neutrophil function
compared with uninjected controls (Roth and Kaeberle,
19851. In the same study, an injection of 40 mg of ascorbic
acid/kg of BW counteracted the negative effects on neutro-
phil function induced by dexamethasone. Current data do
not support routine supplementation of vitamin C to calves
or adult cattle.
CHOLINE
Choline is not a vitamin in a traditional sense because
it is not a part of an enzyme system, and is required in
gram rather than milligram amounts as for true vitamins.
Johnson et al. (1951) produced a choline deficiency in
week-old dairy calves using synthetic milk replacer diets
containing 15 percent casein. Choline requirements esti-
mated from that experiment were 260 mg/L of milk
replacer (1733 mg/kg DM). Current estimates of require-
ments for the calf are 1000 mg/kg dry matter (DM) (Chap-
ter 101. The predominant sign of choline deficiency in most
animals is fatty liver. In calves, reported deficiency signs
included muscular weakness, fatty infiltration of the liver,
and renal hemorrhage; similar to those observed in
other species.
Both naturally occurring choline in feeds, predominantly
found in phospholipids (lecithin) and dietary choline from
supplements such as choline chloride have been shown to
be extensively degraded in the rumen (Neil et al., 1979;
Sharma and Erdman, 1988a,b, 1989b). Microbial degrada-
tion of choline in the rumen results in the production of
acetaldehyde and trimethylamine. Methyl group carbon
from trimethylamine is subsequently degraded to methane
(Neil et al., 19781. Supplementation of dietary choline in
an unprotected form is useless because of extensive ruminal
degradation (Erdman, 19921.
Because of extensive degradation of dietary choline,
methyl group requirements for synthesis of methyl-con-
taining metabolites in the dairy cow are presumably pro-
duced via methylation pathways involving methionine and
the enzyme, S-adenosylmethionine methyl transferase.
Sources of methyl groups for ruminants would include
dietary methionine, betaine resulting from degradation of
choline, and de nova synthesized methyl groups produced
through 5-methyl tetrahydrofolate. Approximately one-
third of the methionine methyl groups were transferred to
choline in studies with lactating dairy goats (Emmanuel
and Kennelly, 19841. Intravenous infusion of choline and
carnitine reduced the irreversible loss of methionine by
18 to 25 percent in sheep suggesting that methionine could
be spared with the addition of methyl-group-containing
metabolites (Lobley et al., 19961.
OCR for page 174
174 Nutrient Requirements of Dairy Cattle
Choline content of whole milk varies substantially (43
to 285 mg/L; Hartman and Hayden, 1974) with about 25
mg/L in the form of phospholipids. More recently, Deu-
chler et al. (1998) found that the concentration of choline
in milk ranged from 70 to 90 mg/L with an average secre-
tion rate of choline into milk of between 2 to 3 g/day.
Secretion of choline into milk was increased by either
post~uminal infusion of choline chloride (Aliev and Bur-
kova,1987; Deuchler et al., 1998) or by dietary supplemen-
tation of ~umen-protected choline. This suggests that secre-
tion of choline into milk could be used as a qualitative
indicator of post~uminal choline supply.
Choline requirements for lactating daily cows have not
been established. As a ruminant animal, the daily cow has
evolved under circumstances where intestinally absorbed
choline is almost nonexistent because of extensive Nominal
degradation of dietary choline. Experiments where choline
has been supplemented either by feeding in a ~umen-
protected form or by post~uminal infusion of choline chlo-
ride have produced variable results. Milk production
increased O to 3 kg/day in experiments where 15 to as much
as 90 grams of choline chloride were infused post~uminally
(Glummer et al., 1987; Erdman and Sharma, 1991; Sharma
and Erdman, 1989a). In an experiment where methyl trans-
fer from methionine was inhibited but choline was pro-
vided, 4 percent FCM production was increased by 3.4
kg/day suggesting the importance of methionine in methyl
group metabolism in the dairy cow (Sharma and Erd-
man, 1988b).
Lactational responses to choline are likely to be affected
by methionine supply. Daily cows that are fed diets that
supply adequate amounts of intestinally absorbed methio-
nine are less likely to respond to supplemental choline than
when methionine is limiting. Because of the relationship
between fatty liver and ketosis, it has been speculated
that choline could play a role in ketosis treatment and
prevention, but there is no direct evidence to date to sup-
port this theory (Erdman, 19921. The establishment of a
choline requirement, either for the lactating daily cow, or
for the transition cow in the late dry period and in early
lactation, will require more extensive feeding experiments
than were available at the time of this publication.
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Representative terms from entire chapter:
dairy cattle
