Learning Center / nutrition

Micronutrients

 

 

Chromium
Diabetes, glucose tolerance factor , insulin and chromium are vitally connected. There has not been enough research on the dietary requirements of chromium in any mammal and that includes diabetic humans. The only known biological use of chromium is its function with glucose and insulin. There is preliminary research showing that diabetic and obese humans might have better weight loss with chromium picolinate in their diet.
Cobalt

Vitamin B12 or cobalamin is synthesized from cobalt. And without Vitamin B12, the metabolism of propionic acid, a volatile fatty acid doesn’t take place and the amount of ATP (remember your Krebs cycle) is reduced. Which reduces the amount of “energy” to run the cells and therefore the whole body is slowly running down. Excess propionic acid in the blood depresses appetite.

Since there are many areas of cobalt deficient soils in the world, including the southeastern Atlantic coast of the United States, cobalt deficiency is a possibility. Cobalt deficiency has the usual decreased appetite and failure to grow symptoms. Advance stages of deficiency are severe unthriftiness, rapid weight loss, fatty degeneration of liver, impairment of neutrophils to kill yeast , reduced disease resistance and pale skin and mucous membranes.

The bad news is that the toxicity symptoms are nearly the same! The only way to test for toxicity / deficiency is by determining the cobalt concentration in the liver.

There are some species’ differences- in ruminants, the rumen microorganisms require the cobalt to manufacture Vitamin B12. So ruminants require more cobalt than horses or rabbits (chinchillas ???). Horses and rabbits have less need of cobalt because their microorganisms don’t synthesize nonactive cobalt containing compounds like the ruminant one do. Also ruminant animals are more dependent on volatile fatty acid metabolism than hindgut fermentation species. Vitamin B 12 absorption in rabbits is more efficient than in humans, rats or sheep due to coprophagy ( the eating of the “night feces”). Let us hope chinchillas are closer to rabbits and horses in their needs for cobalt.

Feed grade cobalt can be fed in free-choice mineral mixtures or by adding cobalt sulfate or cobalt carbonate as a premix. In cattle, they use a controlled release glass pellet containing cobalt or pellets containing cobalt oxide and finely divided iron to add cobalt to the diet.

Copper

Gene Roddenberry was very clever to have made Mr. Spock’s blood based on copper instead of iron. Copper is vitally involved in hemoglobin and blood chemistry in mammals. Copper is necessary of the synthesis of hemoglobin and red blood cell maturation. A copper deficiency can induce an iron deficiency anemia. The metalloprotein ,ceruloplasmin, functions in iron absorption.

Copper is a part of several metalloenzymes. Cytochrome oxidase is essential for cellular respiration (exchange of oxygen across the cell membranes). And lysyl oxidase is important to connective tissue formation and the cross linking of collagen fibers. If copper deficiency occurs, bone collagen and cartilage may be defective and skeletal malformations may occur. (And that could include teeth problems !)

The other copper deficiency problem that could really affect the pelt industries is the graying (achromotrichia) of black hair (or fur). Copper is an essential component of tyrosinase, the enzyme involved in the conversion of tyrosine, an amino acid to melanin- the black pigment of hair(fur and wool). Mink fed extra copper had darker fur color than the control minks did. This is something that should investigated in chinchilla fur.

For a trace mineral, copper is very important. You just don’t need large amounts of it in the diet. Copper deficiencies is a wide spread problem in many areas of the United States and Canada. The symptoms of copper deficiency includes-anemia(both copper and iron induced anemia), reduced growth( poor skeletons poor growth), depigmentation and changes in the growth and physical appearance of hair, wool or fur, cardiac failure, easily fractured bones, diarrhea and low reproduction with delayed or depressed estrus. Just a few major problems that could destroy a herd ‘s production efficiency.

Copper has an antagonistic relationship with molybdenum and sulfur. Molybdate and sulfide interact to form thiomolybdates and the addition of copper creates an insoluble complex in ruminants but not in rabbits. High concentration of iron and zinc may also reduce the availability of copper. Since water can be contaminated with parts per million levels of iron sulfides and still be drinkable, water analysis might not be a bad idea.

Alfalfa fiber may bind copper and if the feed ration is already a low copper diet-a deficiency could occur.Copper supplements in poultry and swine promote growth. The trials on copper as a growth promoter had mixed results. The death rate of a control group of rabbits was 25% from gastroenteritis and only 4% in the copper supplemented groups. That is significant difference.

Copper can be supplemented as copper sulfate, copper carbonate or copper oxide forms. Copper sulfate (yes, the same stuff you use as a fungicide, for a dormant spray on roses and peaches and for water treatment) is the best choice for cost/ bioavailability. The organic forms of copper (copper lysine, copper glycinate or copper EDTA) are equal if not more bioavailable than copper sulfate. However the organic copper does cost more.

Copper toxicity does happen. Sheep are susceptible to copper toxicity.There are some breeds of dogs that are prone to copper toxicity. It seems to be a particular problem of the terrier group. The copper is accumulated in the liver. When a hemolytic crisis occurs, the liver releases copper which causes hemolysis(destruction of red blood cells), methemoglobinea , hemoglobinea, jaundice, icterus ,widespread necrosis and death.

The North Ronaldsay sheep breed evolved the ability to eat seaweed that washes ashore on its remote Scottish island. Seaweed is low in copper and this breed developed mechanisms to retain copper. So when fed a normal sheep ration, the North Ronalday develop copper toxicity symptoms; A perfect example of the weird little differences between breeds.

Iodine

Iodine is an essential component of the thyroid hormones ,thyroxin(T4) (tetraiodothyronine) and triiodothyronine (T3) which regulate the energy metabolism in the body. Yes, cats(hyperthyroidism),dogs and horses (hypothyroidism) can have thyroid disorders. Thyroid or iodine deficiencies can have subtle symptoms which could cause serious medical and certainly financial problems for breeders.

Thyroid or iodine deficiencies attack the breeding performance of an animal. Babies are born hairless, weak or dead. Males have poor libido and poor semen quality. Females will exhibit irregular cycling, low conception rate, and retained placenta. Interesting item is when people come in for fertility counseling, a complete endocrine panel is done checking on thyroid levels and other hormones that are stimulated by the thyroid hormones.

There are plant materials that are goitrogenic(thyroid inhibiting). The cyanogenetic goitrogenics from white clover are thiocyanate while kale, cabbage, turnips, mustards and rapeseed/oil(canola) contain glucosinolate. From the feed point of view, cottonseed meal and soybean meal contain compounds that are goitrogenic Plant breeders have been trying to reduce the amount of goitrogenic compounds in feed /forage plants. Thyroid deficient human patients need to select their vegetables and salad materials very carefully. A tasty dish of coleslaw could have some serious side effects.

The classic symptom of a thyroid problem is the enlargement of the thyroid. However problems in energy (therefore feed conversion and growth) and breeding performance can occur long before the “goiter” is visible. Both thyroid deficiency and thyroid excess can have goiter. There really is no excuse for an iodine deficiency -all you need is free choice iodized salt available for the animal or the addition of iodized salt to the feed ration. Yes, there are iodine deficient soils in the United States and the world but it is so easy and cost efficient to add the iodine to the salt. Diseases of the thyroid and the resulting hypothyroidism or hyperthyroidism are a medical/veterinary problem and must be treated as such.

Sea salt – rich in iodine, calcium iodinate or ethylenediamine dihydroiodide(EDDI)-an organic from of iodine are the usual choices for iodine supplement. EDDI is fed to prevent footrot in cattle-an interesting idea-to feed the preventive “medicine” rather than dip the infected foot.

There are people who are allergic to iodine in its many forms. They have to avoid sea salt, iodized table salt ,sea food, Betadine disinfectants, and several imaging/contrast media products used for x-rays . Since salt is usually labeled as “salt” on food labels, imagine the problems these people have trying to find “sea salt” free products.

Iron

Tired blood? Try Geritol. Yes, iron is very essential for life. Without iron, your blood doesn’t transport oxygen. Iron is a major part of several respiratory pigments-hemoglobin, myoglobin and cytochromes and enzymes such as catalase and peroxidase. Hemoglobin is the blood pigment that transport oxygen. Myoglobin is the muscle pigment that takes up the oxygen. Myoglobin is the major cause of loss in the meat industry. All that discolored dark meat from stressed – out animals must be discarded as unfit for consumption. It is excess levels of myoglobin in the muscles that discolor the meat. Cytochrome is involved the oxidation reactions and the production of ATP, water and hydrogen in the cells. Catalase ia an oxidizing enzyme that occurs in both plant and animal cells. It breaks down hydrogen peroxide that forms in living cells. Commercially catalase is used in food preservation (removes oxygen in packaged foods) and decomposes residual hydrogen peroxide in bleaching and oxidizing processes (hair coloring and perms). So look for its name on packaged foods and hair coloring /bleaching products. Peroxidase is also an enzyme found in most plant cells and some animal cells. Its function is to oxidize phenols, aromatic amines , etc. by means of hydrogen peroxide. I bet you didn’t know we, animals had those kinds of chemicals inside our body !

Ok, now you have had a brief biochemistry lesson, you have to admit iron is rather important to living. Anemia(hypo chromic microcytic) is the primary effect of an iron deficiency. The anemia is caused by impaired hemoglobin formation ( remember Sickle Cell Anemia or Hairy Cell Anemia). The erythrocytes or red blood cells (RBC) are made in the bone marrow and iron is incorporated into the hemoglobin molecule. Remember back in the copper section-if you have a copper deficiency-you can have an induced iron deficiency which causes anemia.

Iron deficiency can occur on an all-milk diets. Baby pigs are routinely given iron injections at birth to prevent anemia. Iron deficiency produces anemia, listlessness, reduced feed intake , reduced weight gain, pale mucus membranes and atrophy of the papillae of the tongue. Iron toxicity causes diarrhea, metabolic acidosis, hypothermia, reduced gain and reduced feed intake.

If animals are supplemented with free-choice loose trace mineral salt/ block or have access to dirt (yes DIRT), an iron deficiency should not occur.

In humans, cooking a couple of times a week in a cast-iron pan will keep iron deficiency-induced anemia away. Most commercial feedstuffs contain more than adequate levels of iron.

Manganese

This metal’s deficiency seems to cause a universal set of symptoms and then depending on the species an additional problem affecting reproduction. Manganese is an essential component of pyruvate carboxylase, arginase, superoxide dismutase enzymes . It is absolutely required for the galactotransferase enzyme. Manganese activates a number of other enzymes -hydrolases, kinases, transferases and decarboxylases.

The one universal problem with a manganese deficiency is skeletal abnormalities- stiffness, twisted limbs, enlarged joints and weak bone strength. Interesting in cattle, reproduction problems occur. However cattle on a manganese deficient diet will have depressed or irregular estrus, low conception rate, abortion, stillbirths and low birth weights. Rabbits don’t have any reproductive problems. I wonder where chinchillas fit in- the ruminant model or the rabbit model ?

Manganese can be supplemented with manganese sulfate(best choice), manganese oxide(worst choice), or organic forms such as manganese methionine, manganese proteinate, manganese polysaccharide complex or a manganese amino acid chelate. The organic forms are the most digestible but also the most expensive.

Molybdenum

In most practical situations of livestock production ,molybdenum should never be deficient in a feed ration. However the presence of copper and sulfur in the wrong amounts can screw everything up Copper and sulfur are antagonistic to molybdenum. So most symptoms of a molybdenum deficiency or toxicity are actually copper or sulfur deficiencies or toxicity.

There are enzymes that need molybdenum- xanthine oxidase, sulfite oxidase and aldehyde oxidase. Xanthine is a component in something very familiar to coffee, cocoa and tea drinkers and chocolate eaters. Theophylline and theobromine are dimethylxanthines and caffeine is trimethylxanthine.( I managed another quick chemistry lesson there !)

Selenium

Selenium is perhaps the most misunderstood mineral in mammal nutrition. For many years, it was considered a “bad guy” as the safety margin between deficiency and toxicity is very narrow ! Substitute Vitamin E instead of selenium ! Now the current thinking is that we can’t live without it. Pre- 1957, the entire focus had been on the toxicity problems. Selenium is the toxic factor in alkali disease and blind staggers in livestock. But in 1957, selenium started to become a “good guy” when it was discovered to be an essential nutrient. Without selenium, rats develop degenerative liver disease; calves and lambs (and other species) develop white muscle disease, nutritional muscular dystrophy or stiff lamb disease. Humans on a selenium deficient diet have a lower resistance to viral diseases and cancer cells.

In 1973, the first selenium based enzyme was identified. Glutathione peroxidase catalyzes the reduction of hydrogen peroxide and lipid hydroperoxides which prevents oxidative damage to body tissues. In 1990, the second enzyme was identified -iodothyronine 5’-deiodinase. This enzyme catalyzes the deiodination of thyroxine (T4) to the more metabolically active triiodothyronine(T3) in the tissues. So selenium is essential for a healthy level of thyroid hormones !

The function of Vitamin E and selenium are inter-related. That much all researchers agree on but the relationship varies from species to species. Rats and swine develop liver necrosis and chickens gets exudative diathesis. ( Will somebody tell me what exudative diathesis is ?) Rabbits will develop nutriaitonal muscular dystrophy if on a Vitamin E deficient diet and the addition of selenium has no effect. But rats and swine will respond to either Vitamin E or selenium in the diet. What about the chinchillas’ requirement?

White muscle disease, stiff lamb disease or nutritional muscular dystrophy are clasic descriptions of a selenium-Vitamin E deficiency problems. There is a degeneration and necrosis in both sketelal and cardiac muscles. The affected animals may demonstrate stiffness, lameness and cardiac failure. There are other symptoms that may be related to the thyroid hormones- unthriftiness with weight loss and diarrhea. And the lack of glutathione peroxidase could have caused the reduced immune response, heinz body anemia and liver necrosis.

Yet a tiny amount of too much selenium and terrible toxicity problems occur. The toxicity is well studied in hoofed animals- alkali disease and blind staggers.

Chronic toxicity results in lameness, anorexia, emaciation, loss of vitality, sore feet, cracked and deformed hooves, liver cirrhosis, nephritis and loos of hair from tail and manes. Acute toxicity symptoms include labored breathing, diarrhea, ataxia, abnormal posture and eventually death from respiratory failure.As you see from this article that nutrition can affect animal production and efficiency. The swine, poultry and dairy industries have pourer millions of dollars into nutritional research in the attempt to produce peak performance of their herds. There are areas of research that can be carried out at the chinchilla ranch level. We don’t need universities or the USDA to do some good basic research. It would be nice to have the weight of the USDA and a university behind our chinchilla research but that takes MONEY.

A good feed anaylsis on your hay and concentrates is a must. The addition of free-choice mineralized salt blocks to cages is an easy way to increase birth weights and weaning weights- the Hungarian chinchilla ranchers have already proven that and published it in SCIENTIFUR. The addition of the three sulfur bearing amino acids in the ration will cost a bit more but they are a proven solution for increasing mink / fox fur and sheep wool values.

Take a good long look at the nutritional research done in the wool and fur industries and then think about chinchilla nutrition.

Do you have any questions?