06: Minerals

Macrominerals

Minerals present in the body in higher amounts

Macromineral list

Ca, P, Na, Cl, K, Mg, S

Trace minerals

Minerals present in the body in lower amounts

Trace minerals list

Co, I, Zn Fe, Cu, Mn, Se, Mo, F

Uses of macrominerals

Structure, activity, Ion (acid/base) balance

Sites of Calcium storage

Bone (99%), muscle, plasma (free and bound)

Ca:P range in ruminants

2:1-6:1

Calcium deficiency diseases

Milk fever, urinary calculi

Mechanics of urinary calculi

Ca:P ratio becomes <1:1, and crystals form in the urinary tract

When does balancing for Ca and P quantity not matter the most

When the Ca:P ratio is off

When diagnosing a calcium deficiency, why won’t a blood sample work

The Ca in plasma is kept in a very narrow homeostatic range, even in deficiencies

Use of calcium in muscle tissue and nervous system

Used for contractions and nerve excitement

Signs of subclinical Calcium deficiency

Placenta retention

How does vitamin D affect calcium metabolism

Increases Calcium uptake from the gut, triggers bone resorption

How does PTH affect calcium metabolism

Triggers activation and biosynthesis of vitamin D, triggers bone resorption

How does calcitonin affect calcium metabolism

Slows down calcium absorption and bone resorption

How do the hormones and coenzymes work together in calcium metabolism

Low BCa → PTH released from parathyroid → Bone resorption and activation of vitamin D → bone resorption and increased calcium uptake from the gut → higher BCa → calcitonin released → slows down calcium absorption and bone resorption

Bone accretion

Calcium deposition

Bone resorption

Calcium mobilization

Bone malformation diseases

• Rickets: bowed bones in young animals due to low calcium during development

• Osteomalacia: Demineralization in adults

• Osteoporosis: Demineralization in elderly

When does milk fever occur

Early lactation in dairy cows and high producing sows

Signs of milk fever (hypocalcemia)

Muscle tetany, cow goes down, muscles contract and can’t relax, retained placenta, decreased feed intake

How can hypocalcemia lead to acidosis

Low calcium → decreased feed intake → negative energy balance → ketosis → diet change to provide more E → acidosis

Milk fever treatment

IV calcium and oral calcium citrate gel

How does the modern strategy for diet change in the close up dry period prevent milk fever

The Cation/Anion imbalance fed primes the system for increased absorption and mobilization by mimicking the calcium excretion in lactation

Reason feeding more calcium right before lactation doesn’t work

There is a saturation max for the active calcium transporters in the gut, and % absorption doesn’t really go up

What minerals are fed in the modern diet strategy to prevent milk fever

Cl-, S

What type of ration is fed in the modern strategy to prevent milk fever

A negative Dietary Cation Anion Difference diet

What are the cations and anions involved in the DCAD ration

• cation: K+, Na+

• Anion: Cl-, S

How does feeding a negative DCAD diet work to prevent milk fever

Feeding a diet with high anion content (say, adding NH4Cl) will lead to the excretion of Cl- andNH4 (as urea) in the urine. This creates metabolic acidosis → acidic urine, which will take a lot of Calcium with it. This large excretion of Ca makes the body think there is a deficiency, and increases the absorption from the gut. When lactation starts, the diet is switched back to a positive DCAD, but there is still a lot of Ca loss through milk. To the body, the amount of Ca outflow hasn’t really changed, we’ve just swapped in a different avenue for Calcium to lead the body. The system for absorbing Ca has already been primed, so the cow continues to absorb lots of Calcium to supply the large outflow through lactation.

Metabolic state caused by feeding a negative DCAD ration

Metabolic acidosis

Calcium content in grain

Low, <1%

Calcium content in forage

Moderate to high, 0.5-1.5%

If alfalfa is fertilized with CaCO₃, what is a problem that can arise

CaCO₃ is a neutral fertilizer, and the increase in soil pH causes an increase in molybdenum uptake by the alfalfa, which can be a problem because it ties up copper

Inorganic sources of calcium

CaCO₃ (limestone), CaCl₂ (not common unless DCAD diets)

Sites of phosphorous storage

Bone (80%), membranes, macromolecules, D/RNA, salts, ATP, bone ash

What hormone is involved in phosphorous regulation

PTH and active vit D

Phosphorous hormonal regulation pathway

Low blood P → PTH release → vit D is activated → decrease in P excretion

Functions of phosphorous in the body

Structure, cell mechs, membranes

Phosphorous absorption in the gut

Both passive and active transport

How is phosphorous absorption tied to calcium absorption

An excess of P will lead to a decrease in Ca absorption

Minerals that negatively impact phosphorous absorption

Excess Ca, Mg, Fe oxide

Phytate phosphates

Have less bioavailability for non-ruminants, can lead to an underestimation of provided P if not accounted for. Very little effect on ruminants

Phosphorous excretion

Mostly through the kidneys

Consequences of phosphorous deficiencies in ruminants

Lower P in saliva, less P for microbes in the rumen, decrease in fiber digestion

Symptoms of clinical phosphorous deficiency

• Pica: chewing on wood and objects

• Decreased bone density in adults

Symptoms of subclinical phosphorus deficiency

Impaired reproduction, poor heats, poor conception

Prevalence of subclinical phosphorous deficiency

Not common; high producing animals are pushed so hard that any deficiency usually manifests as an issue

Phosphorous content in grain

Moderate, 0.6%

Phosphorous content in forage

Low, 0.2%

Inorganic sources of phosphorous

Dicalcium phosphate, monocalcium phosphate, monoammonium phosphate

Sites of Magnesium in the body

Bone (50%), liver, brain, muscle, cofactors, structures, blood (75% in RBCs and 25% in serum)

Function of Magnesium

Normal skeletal development, metabolic processes, coenzymes and enzyme systems

Magnesium mineral interactions

K, Ca, P

Magnesium deficiency syndromes

Grass Tetany, subclinical hypomagnesia

Grass tetany symptoms

Hyperirritability, incoordination, muscle tetany, hyperemia (decreased blood flow) of ears and extremities

Symptom that distinguishes grass tetany from milk tetany

Hyperemia

Common cause of grass tetany

Cool season grasses grown in cool moist conditions (spring and fall) uptake K a lot more, which decreases magnesium metabolism

Common tx for grass tetany (or any downed cow)

Ca-Mg-dextrose

Symptoms of subclinical hypomagnesia

Decreased butterfat

During what seasons does Mg supplementation need to be higher

Spring and Fall, watch your fresh cool season grasses

Magnesium content in grain

Low, 0.12-0.15%

Magnesium content in forage

Low, 0.17%

Inorganic sources of Mg

MgO, dolomitic limestone

Magnesium toxicity symptoms

Decreased feed intake (because supplement isn’t palatable), diarrhea, loss of reflexes, cardiorespiratory depression

Electrolytes

K, Na, Cl

Function of electrolytes

Maintains osmotic pressure and A/B balance

Site of electrolytes in body

Tissues, blood, interstitial fluid, cellular fluids

Site of most K

Intracellular

Site of most Na

Extracellular

Specific function of K

Enzyme reactions, AA and GL transport

Specific function of Na

Nerve impulse transmission

Specific function of Cl

HCl

Losses of electrolytes

Urine, sweat, diarrhea

Signs of K deficiency

Abnormal EKG

Signs of Na or Cl deficiency

low salt → low water intake → low feed intake → decreased growth

When would be the only case an electrolyte toxicity could happen

Short term bulk with limited water

Sources of K

Alfalfa and grasses, KCl, K carbonate (low reactivity, works well in mixes)

Sources of Na

NaCl, Na₂CO₃, Na sesquicarbonate

Sources of Cl

NH₄Cl, MgCl, CaCl₂

In what types of diets would K and Na be higher

Lactating rations to maintain a positive DCAD

Types of salts

Block, loose, plain, trace mineral

Electrolytes per head of cattle per day

0.25 lbs

How to modify mineral intake

Modify salt content in mix, ensuring adequate water

Site of sulfur in body

AA, some vitamins, mucopolysaccs (in joint fluid), CoA

Why do diets high in NPN need higher sulfur supplementation

Production of AA and CoA will require S

Signs of sulfur deficiency

Lower microbe synthesis of sulfur containing AA → poor performance and growth

Sulfur sources

MgKSO₄, CaSO₄, S containing proteins

When are trace mineral deficiencies seen

If there is negative mineral interactions

Cobalt function

Component of vitamin B12

Sites of cobalt in the body

Areas of high metabolism: liver, adrenals, bone

Sign of cobalt deficiency

B12 deficiency

Cobalt source

B12

Why is nonruminant cobalt requirement lower than ruminant requirement

?? ask McCarthy

Iodine function

Component of thyroid hormones

Site of iodine in the body

70-80% in the thyroid gland

Sign of iodine deficiency

Low iodine → TSH from anterior pituitary → triggers production of thyroxine → not enough thyroxine available because low iodine → TSH is still released → thyroid hypertrophy to try to make more thyroxine → goiter

Iodine sources

Calcium iodate, iodized salt, sea kelp, EDDI (organic)

Zinc function

Immune system, metalloenzymes

Sites of zinc in the body

Liver, bone, kidney, muscle, pancreas, skin, hair, wool