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Food as Medicine: A New Perspective on Nutrition
P. Burgmann, BSc, DVM, Dip ABVP(Avian Practice)
"Whatsoever was the father of the disease, an ill diet was the mother" (Old Chinese proverb)
Proper nutrition is vital to any successful avicultural enterprise. The understanding that food is medicine is a key concept in the future development of sound avicultural practices, in that what a bird eats is so important to its health that it can be the single factor involved in a bird's death or in its ability to ward off disease. This paper illustrates this concept by discussing a few of the most commonly recognized nutritional deficiencies and excesses in pet birds, and makes suggestions on what to feed and why. How aviculturalists can be a vital part of future nutritional research is also addressed.
The understanding that food is medicine is one of the most profound developments in Western medical thought in the last fifty years. Similarly, the understanding that there is no more potent medication in the entire veterinary medical profession than a proper diet will also begin to be realized. Avian medicine can be at the forefront of this revolution in thought, since nutritional deficiencies and their role in disease are still a daily occurrence in pet bird practice. Irrespective of the disease process diagnosed in a pet bird, from sinusitis to polyomavirus, what the bird was fed was involved in the disease process, either directly due to obvious nutritional deficiencies, or more subtly by lowering the bird's resistance and thereby making it susceptible to illness. This concept will be illustrated by briefly discussing three of the more common nutritional deficiencies still seen daily in avian pet practice. The effects of nutritional excesses will also be addressed, as will suggestions of what should be fed. Aviculturists' role in the future of nutritional research is also discussed.
Vitamin A is necessary for normal mucoprotein synthesis, by helping a form of sulfur to combine with mucopolysaccharide, a building block of mucoprotein. Mucoproteins are jelly-like, slippery, or sticky substances that provide lubrication or act like cement in cells. A lack of vitamin A makes biological membranes unstable, especially those of lysosomes, mitochondria, and red blood cells. This lack also changes the structure of epithelial cells from a columnar (column-like) morphology to a stratified keratinizing epithelium (flat layers of cells full of keratin). Vitamin A's main function, then, is to protect the integrity of mucus membranes and epithelial tissues of the skin, intestine, kidney, respiratory tract, and reproductive tracts. It may also be necessary for maintaining the integrity of the adrenal cortical cells responsible for the synthesis of the hormones corticosterone, deoxycorticosterone and progesterone. It is also involved in the retinal pigment rhodopsin. Rhodopsin is made up of a protein, opsin, and vitamin A. Rhodopsin is broken down and resynthesized under the stimulus of light. When vitamin A is deficient, resynthesis is poor.
Vitamin A deficiency causes night blindness and xeropthalmia (a form of inflammation of the conjunctiva of the eye characterized by a dry and lusterless condition of the eyeball). It effects the respiratory tissues resulting in a swollen choanae, swollen blunted choanal papillae, pharyngitis, and the presence of sterile abscesses formed from squamous metaplasia, (abnormal proliferation of squamous cells). These changes predispose the respiratory tissues to inflammation and secondary bacterial infection causing sneezing, nasal discharge, and sinusitis. The digestive tract is involved with severe metaplastic changes in the salivary glands, and gizzard erosion. Hyperkeratosis causes rough scaly skin and corns on the feet. Hyperkeratosis of the kidney tubules leads to renal disease and gout. Hypovitaminosis A also interferes with the development of bones, normal sperm formation, and the maintenance of health of the fetus. Soft shelled eggs, weakness, and a poor feather coat may also be signs of vitamin A deficiency.
Vitamin A occurs in two forms. Retinol is the natural form of vitamin A found in animal fats and fish oils. Carotenes are the form found in foods of plant origin. Carotenes are provitamins, which are substances the body can use to manufacture vitamins. Beta-carotene is the most active form of carotene and is converted into vitamin A by enzymatic reactions in the intestinal mucosa and liver. One molecule of beta-carotene can be cleaved to produce two molecules of vitamin A in vitro, but biological tests have shown that it does not appear to be used as efficiently in the mammalian body. Pure vitamin A has twice the potency of beta-carotene on a weight-to-weight basis, thus one international unit of vitamin A has been set at 0.3 micrograms of retinol or 0.6 micrograms of beta carotene. Some evidence suggests, however, that the conversion of beta-carotene to vitamin A becomes greater in deficiency states, and that under optimum conditions and associated with optimum levels of vitamin E, beta-carotene may be converted to vitamin A with one hundred per cent efficiency. Some avian practitioners are of the opinion that the beta carotenes seem to be a superior source of vitamin A for birds, and may have other beneficial effects not yet recognized. I am of the same opinion. Although there is no published data yet in avian medicine to substantiate these impressions, the powerful antioxidant role of beta-carotene in human disease has been well documented, and no doubt will prove to be equally important in avian medicine.
All seeds, other than yellow corn, are notorious for their low vitamin A content, and large parrots on sunflower seed-only diets invariably suffer from vitamin A deficiency. In fact, it is one of the most commonly recognized vitamin deficiencies in pet birds. Vitamin A is also easily oxidized, and care must be taken in how foods containing these substances are processed.
Orange and yellow vegetables and fruits have high vitamin A values because of the beta-carotenes they contain. Some green, leafy vegetables also contain a lot of carotene, but their yellow color is masked by the green pigment chlorophyll. Thus carrots, yams, squash, corn, dandelion leaves, spinach, red peppers, cantaloupe, peaches and broccoli are all good sources of beta-carotene.
Liver is very high in pure vitamin A, however, many experts recommend that liver should not be fed more than once a month due to the toxic substances it contains. These toxic substances occur as a result of exposure of an animal to environmental pollutants, since the liver is the organ responsible for detoxifying substances. The longer an animal is alive, the greater its exposure to environmental toxins, therefore the liver of a calf, for example, should be less toxic than the liver of a full-grown cow. Fish oils, egg yolks and cheese are also high in vitamin A.
The supplementation of cod liver oil in the diet of psittacines was a common practice among aviculturists, and one can see that this practice probably arose in an effort to counteract vitamin A deficiency. However, cod liver oil may not only supply excess vitamin A, but may also contribute to the destruction of vitamin E, exacerbating vitamin A deficiency.
Excess vitamin A can cause feather loss, joint pain, nausea, bone and muscle soreness, headaches, dry and flaky skin, diarrhea, rashes, enlarged liver and spleen, stunted growth, and interfere with fertility. Excess carotene in the diet may cause yellowing of the skin on the soles of the feet, but appears to be less harmful than excess ingestion of vitamin A.
Vitamin D: Cholecalciferol
Vitamin D generally refers to two chemically similar compounds; vitamin D2, or calciferol, and vitamin D3, or cholecalciferol. Vitamin D2 and D3 have about the same potency for most mammals, but vitamin D3 is 30 to 100 times as effective as vitamin D2 in birds. Several other compounds also have vitamin D-like activity, but we will restrict this discussion to the most important element for birds, vitamin D3.
Vitamin D is a complex element. Not only must it be in the active form to be used in the body, which depends on the function of the liver, the kidney, the availability of direct sunlight, or the ingestion of the vitamin in its active form, but it is also influenced by calcium, phosphorus, strontium, and magnesium and the glands and hormones which control these minerals.
Vitamin D is ingested and absorbed from the intestine where it is transported to the liver. In the liver it is converted to relatively inactive excretion products called vitamin D esters, and into an important compound called 25-hydroxycholecalciferol. Under the stimulus of low serum calcium, this substance is transported via the blood stream to the kidney, where it undergoes another chemical process called hydroxylation to yield two different dihydroxycholecalciferol compounds. When calcium is needed the kidney produces 1,25-dihydroxycholecalciferol, which is the active form of vitamin D3. If calcium is not needed, the other form is produced. The active form of vitamin D, 1,25-dihydroxycholecalciferol, enhances the absorption of calcium from the intestine by inducing a calcium-binding protein which actively transports calcium. This calcium-binding protein has been found in the intestines, kidney, shell gland of laying hens, and in chick brain tissue. There is also evidence that vitamin D mobilizes bone mineral to help maintain serum levels of calcium and phosphorus, and plays a role in the deposition of calcium salts into the cartilagenous matrix of bone. It also effects mitochondrial metabolism.
Several other factors also influence vitamin D metabolism. If vitamin D3 is not supplied in the diet, the ultraviolet rays of direct sunlight are required to convert the precursor of vitamin D (7-dehydrocholesterol), which is present in the skin, to activated 7-dehydrocholesterol, or cholecalciferol. (The equivalent wavelengths of ultraviolet light can be supplied by some fluorescent tubes such as Vitalites, which is why these light sources should be provided for pet birds). Dietary strontium inhibits the synthesis of 1,25-dihydroxycholecalciferol by interfering with the kidney hydroxylase system. Vitamin D may also play a direct role in phosphorus metabolism by being involved in a vitamin D-dependent active phosphate pump. There also appears to be an inverse relationship between dietary vitamin D levels and serum magnesium levels.
The clinical signs of vitamin D deficiency relate to its effects on calcium and phosphorus metabolism. Rickets is the term applied to the clinical signs of vitamin D deficiency in young animals. It is characterized by a decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. Growth may be stunted; the beak may be soft; long bones may have curving defects and pathological fractures; the ends of long bones may be enlarged and may be so soft that they can be cut with a knife. "Rachitic rosary" refers to the swelling and appearance of "beading" of the rib heads, which is a common feature of the disease.
In adults, the condition is called osteomalacia. Since cartilage growth has ceased, the disease is characterized by a decreased concentration of calcium and phosphorus in the bone matrix only. The cortices of the bone are thickened, but are composed of fragile fibrous connective tissue which fractures easily. The sternum and rib cage are soft, and the sternum may actually curve. Soft-shelled eggs, egg-binding, and a decrease in hatchability can also occur.
Few foods naturally contain significant amounts of vitamin D, which is why this substance must often be supplemented in the avian diet. Fish oils are the exception, another reason why cod liver oil has been used as a supplement in the past. However, as with vitamin A, overdosage of vitamin D3 can have severe metabolic effects. At first calcification of bone may be accelerated, but in later stages bone resorption is increased leading to a demineralized and weakened skeleton and hypercalcemia. Hypercalcemia results in calcium deposition in the kidneys, heart, joints, arteries and other tissues causing irreversible damage. Hypervitaminosis D in macaw chicks is a common disease. Clinical signs can include weight loss, poor crop emptying, regurgitation, dehydration, and calcium deposits in the skin and joints.
Calcium is the chief mineral constituent of the body. It is required in the diet in larger amounts than any other mineral. Calcium performs four key functions in the body. First, in conjunction with phosphorus, it forms an integral part of bone mineralization in the form of calcium-phosphorus salts. Second, it is an integral part of cell membranes, where it functions in maintaining cell membrane integrity and normal permeability. Third, it forms the link between excitation and contraction in all forms of muscle, and plays a similar role in the excitation and secretion of the glands of the body. Fourth, it acts throughout the body as a regulator, activator, or inhibitor of key enzymes, such as blood clotting. Thus, virtually all key processes in the body are dependent on the availability of calcium.
Calcium deficiency results in a myriad of health problems related to its various functions within the body. Contrary to popular opinion that bone, once formed, doesn't change, bone is a very dynamic organ. It continually undergoes remodelling throughout life. Calcium, and phosphorus, are essential to this process. If insufficient amounts of calcium are absorbed from the intestine, the mineralization process of bone cannot keep pace with the synthesis of organic bone matrix. When this occurs, the typical signs of rickets or osteomalacia appear.
Most, (about 99%), of the calcium found in the body is in the bones, however, a small, but extremely important, portion of calcium is found in the blood plasma and interstitial fluid. Because it is such an important mineral, its concentration in the blood plasma is very closely regulated by a number of substances. The role of vitamin D has already been discussed. Phosphorus is also very important, in that the proper ratio of calcium to phosphorus must exist in order for these minerals to function optimally. Parathyroid hormone, produced by the parathyroid gland, and calcitonin, secreted by the thyroid gland, also play an essential role.
The maintenance of serum calcium levels is at the expense of bone; in other words, the body would rather weaken the skeleton than give up the calcium needed for all its other functions. When the body needs to withdraw calcium from the bone, the process is called demineralization. Too much demineralization, (losses of one-third or higher amounts of calcium), results in spontaneous fractures, soft bones, and locomotor disturbances. Paralysis, weakness, and central nervous system disturbances in the form of seizures, are signs of deficiency related to its role in nerve impulse transmission. Since calcium also stimulates the secretion of hormones, prolonged calcium deficiency results in a reduction in the secretion of gonadotrophic hormones, resulting in decreased egg production and body weight. Eggshell is almost entirely formed of calcium, in the form of calcium carbonate. The calcium required for eggshell production is derived from intestinal absorption and/or bone resorption. The medullary (inner) bone is the most important source of calcium for eggshell formation, but when these reserves are gone, the cortical (outer) bone will also be used. Many causes of egg-binding have been postulated over the years, but the truth is that calcium deficiency is the primary cause of this condition. Soft-shelled eggs are also a sign of calcium deficiency.
Calcium deficiency is an extremely common problem in pet birds. Not only are seeds themselves notoriously deficient in calcium, but also the fatty acids present in the oils of seeds such as sunflower and safflower seeds combine with calcium to form insoluble soaps, even further decreasing its absorption. Phytic acid, a substance found in whole grains, also binds with calcium and other minerals and prevents their absorption. This is of significance in seed-eating birds, which consume large quantities of whole grains. Muscle meats are also low in calcium, but are high in phosphorus, causing an imbalance in the calcium:phosphorus ratio as well as a deficiency of calcium itself. Oxalic acid, present in some vegetables, combines with calcium and prevents its absorption. Because of this, some people have advised that feeding some foods such as broccoli or spinach may be harmful. It is very important to note, however, that spinach, broccoli, kale, and chard are extremely good sources of calcium themselves and that only a small amount of calcium is bound up by the oxalic acid. Rhubarb leaves, however, do concentrate oxalic acid and should not be fed.
Calcium carbonate is an ideal source of calcium for birds. Oyster shells and cuttlebone are composed primarily of calcium carbonate, which is why they have long been recommended as a supplement for pet birds. However, not all birds will consume oyster shell or cuttlebone, even when it is provided, or, even if they do eat it, may not be in sufficient quantities to compensate for a diet high in phosphorus such as a seed-only diet provides. For this reason it is essential to achieve a proper calcium:phosphorus ratio in the diet. In poultry, a calcium:phosphorus ratio of 3:2 is considered optimum. Therefore, the diet for egg-laying chickens generally contains 1% calcium and 0.7% phosphorus, depending on the energy level of the diet. In psittacine nutrition, however, the optimum value has not yet been determined, and there is some variation in the ratios recommended by various avian practitioners and food manufacturers. Tom Roudybush, who has done work on nutrition in cockatiels, feels that 0.1% of the diet is sufficient for maintenance, and 0.9% for breeding. Greg Harrison feels that 0.36% is required for maintenance and 0.9% is required for breeders. Mark Hagen (Hagen) and Randy Brue (Kaytee) among others have been active on a committee to establish minimum standards in pet bird nutrition. Their recommendation is a minimum of 0.6% to 1.2% calcium to 0.3% phosphorus. It may be found that the requirement for calcium during egg production may indeed be 1.0%, especially as we breed these birds more intensively and increase our egg yields. Nonetheless, it should be noted that these high levels of calcium are required for egg production, and not for maintenance; one of the reasons why breeding rations should not be fed year-round, even to breeding birds.
Aside from oyster shell and cuttlebone, good dietary sources of calcium include yogurt, salmon, navy beans, broccoli, cheese, turnip greens, kale, and tofu.
Given the importance of calcium to the body and the incidence of calcium deficiency, a temptation arises to oversupplement with calcium. As with the other elements mentioned, oversupplementation can be just as harmful. Turkey pullets fed high calcium diets exhibited nephrosis syndrome with kidney failure and resultant visceral urate deposition (gout complex). Heavy calcium diets without a concurrent increase in manganese and zinc levels will interfere with absorption of these trace elements and lead to perosis, a type of bone disease.
What to Feed
Hopefully, the previous examples have given you a fresh perspective on nutrition; food can cure or kill just as potently as any disease. But how much is too much, and how little is too little? Surely if one just provides the birds with a little bit of everything, pellets, seeds, soft food, fruits and vegetables they'll pick out what they need and no harm can be done. And in fact that approach might work, if they ate every bite of everything offered, and given that everything has been provided in the right proportions. Unfortunately, that's not what happens.
There have been two studies done on this very subject, one by Ullrey in 1991 using Timneh African Greys, and another just recently at the Metro Toronto Zoo with a pair of Major Mitchell's cockatoos. Details of the two studies are beyond the scope of this paper, but the end result of both studies was that when pellets and vegetables were offered, pellets were consumed in adequate amounts, but when seeds were offered as well, the consumption of pellets dropped dramatically, and contrary to popular opinion that birds know what's best for them, the resulting diet the birds consumed was demonstrably deficient in calcium, available phosphorus, sodium, manganese, zinc, iron, iodine, selenium, vitamins A,D,E,K, riboflavin, pantothenic acid, niacin, B12, and choline. Ullrey also found that when eight psittacines species previously fed seeds, fruits and vegetables for two years were fed a pelleted ration, fruits and vegetables but no seeds for one year, fledgling percentage increased from 66 to 90%, a 24% per cent increase in fledglings in ONE YEAR. (Wouldn't you like to increase your production rate by that much?)
Granted that those two studies are right and we can't trust the birds to pick out what's best for them, why do they do okay in the wild? The answer is, Mother Nature has had millennia of experience in diet formulation, and the birds in their various natural habitats have evolved to fit the diets available to them in the wild. In the wild seasons change, availability changes, and one generation teaches the next what to eat. In captivity they are entirely dependent on what we supply them with, which usually has absolutely no resemblance to what they have evolved to eat. For example, budgies in the wild eat a diet consisting primarily of grass seed heads which have quite a low fat content. Hyacinth macaws by contrast eat a diet consisting mostly of palm nuts or palm fruit, which have been shown to have a fat content of 53% to 67% fat. In fact, many macaws have higher fat or caloric density requirements than other bird species, which is why there is such a high incidence of "stunting" in macaw chicks, (although "stunting" can occur in any species for a number of reasons which are beyond the scope of this paper.) On the other hand, a diet too high in fat in cockatiels, budgies, amazon parrots, and Rose-breasted Cockatoos not only leads to obesity, but is also part of the disease complex known as fatty liver syndrome, where an excessive amount of fat builds up in the liver leading to liver failure.
So what, then, should we feed? Unfortunately, the answer at this time is not as clear as one would hope. We do know that birds in captivity definitely do better on pelleted diets than on seeds. What we don't yet know for certain is what levels of each nutrient is required for each species for optimum health, longevity, and productivity.
In my own opinion, at this point in time, for maintenance of most of the common species of mature pet birds, a diet consisting of 85% to 90% maintenance parrot pellets, 10% dark leafy green vegetables or yellow vegetables high in beta carotene, and no more than 5% fruit is the best alternative available. It is also essential that this needs to be the proportions they actually eat, not just the proportions offered. Which brand of pellets depends on the birds' preference and on the pellets' composition, particularly with respect to its caloric density; for example, choose a higher fat content for macaws than for amazons.
Why do I recommend feeding a proportion of fresh foods when some of the pellet manufacturers say you shouldn't? I believe the main reason they say you shouldn't is because they're afraid that the birds won't eat the correct proportion of pellets, and the pellets will be blamed for being inadequate when in fact it's the overconsumption of fruits or vegetables that are really at fault. Why risk feeding fresh foods? Because there is tremendous things being discovered in human nutrition that haven't even begun to be dealt with in aviculture.
To quote from Jean Carper's excellent book, "Food-Your Miracle Medicine":
"Many of our health misfortunes are due to a perversity of oxygen. Yes, the very stuff that gives life can also help take it away. It's a remarkable propositionthat our cells are perpetually besieged by toxic forms of oxygen, our existence wiped out, a molecule at a time, by the element's fierce destructive powers. Attacks by continual bursts from oxygen reactions help clog our arteries, turn our cells cancerous, make our joints give out and our nervous systems malfunction. In fact, this new theory about oxygen has revolutionized the way scientists look at the genesis of disease and its prevention. It is the single most significant line of inquiry behind science's strong new belief in the power of food to thwart bodily deterioration. So far, scientists have linked destructive oxygen reactions to at least sixty different chronic diseases, as well as to aging itself.....One of the great revelations of the last few years...is that you may be able to eat your way out of this dilemma...You can supply your cells with antioxidant food compounds that strike down, intercept and extinguish rampaging oxygen molecules and even repair some of their damage. Foods, notably plant foodvegetables and fruitsare packed with a variety of ferocious antioxidants....Nothing you can do for your health and survival is more important than consistently eating foods packed with disease fighting antioxidants."
Let's illustrate this point with some specific examples. Lycopene, a pigment that gives tomatoes their red colour, is twice as powerful as beta carotene at stopping "singlet oxygen" a toxic oxygen molecule that can trigger cancer in cells. Tomatoes are the major source of lycopene in the food supply, and that includes all tomato products like cooked or canned tomatoes and sauces, tomato paste and ketchup. It's also highly concentrated in watermelon. Dark green vegetables such as spinach, kale and broccoli are loaded with antioxidants, including beta carotene, folic acid, and lutein, a little-known antioxidant scientists think may be just as potent as beta carotene.
Diet can have a direct effect on a disease process. Capsaicin, contained in hot peppers, has been shown to bring blood to the surface of tissue, increase mucus secretion, and may boost immunity. A study on broiler chickens fed 5 to 20 ppm of capsaicin showed a significantly lower rate of susceptibility to Salmonella enteritidis than control counterparts, with no adverse effects. Does feeding hot peppers to parrots have a similar disease fighting effect?
Another fascinating example of how diet can have a direct effect on a disease process relates to the herpes virus. People who get cold sores, canker sores (ulcers inside the mouth), genital blisters, shingles, or infectious mononucleosis are all victims of the herpes virus. And, although the virus lies dormant in 90% of us, diet may well determine whether the virus is reactivated or not. Apparently, if you feed the herpesvirus enough of the right stuff, it grows ferociously, prodding the body to manifest the disease. One substance that acts like a potent fertilizer to the herpes virus is an excessive amount of the amino acid arginine. When arginine was added to cell cultures of herpesvirus growth accelerated dramatically. But when a different amino acid, lysine, was added to the cell cultures, it stopped the growth and spread of herpes virus in the cells.
In one study patients were given a diet high in arginine (500mg) and low in lysine. Three out of five subjects quickly (overnight) developed such severe herpes outbreaks they had to stop the study. How much would one have to eat to get 500 mg of arginine? Just two ounces of nuts or chocolate. At the same time, eating enough lysine-rich foods like milk or soybeans can override the effects of the arginine and prevent the herpes outbreak.
How does this example apply to aviculture? Consider that there are thirteen different avian herpesvirus types known, causing everything from Marek's disease in chickens, to amazon tracheitis, to Pacheco's disease, to cauliflower-like growths on the feet of cockatoos. To use Pacheco's disease as an example, although there is a vaccine against Pacheco's disease which is effective, and acyclovir in the drinking water prior to the development of clinical signs helps, you can't vaccinate in the face of an outbreak and acyclovir tends to settle out in the water and is a potent nephrotoxin. If the birds are on pellets, which often contain soybean meal, this information may not be of benefit. But what if the birds are always offered nuts, like Brazil nuts, walnuts or almonds, which are known to be high in arginine? Would witholding nuts, and increasing the consumption of lysine by offering soybeans during an outbreak be beneficial? Would it, in conjunction with other natural foodstuffs known to boost the immune system, be able to slow down or stop the spread of this otherwise fatal disease? The answer isn't known, but isn't it worth considering?
The examples and implications are endless. Carrots, for example, are loaded with beta carotene. A carrot a day slashed stroke rates in women by 68% and cut the risk of lung cancer in half, even among formerly heavy smokers. Carrots reduce the risk of degenerative eye diseases like cataracts, as well as depressing blood cholesterol. The implications in terms of health improvement in an overweight, sunflower-eating amazon parrot with hypovitaminosis A eating as little as 1/8 of a carrot a day are obvious.
Spirulina, a blue-green algae found in warm water alkaline volcanic lakes, has recently gained attention. Preliminary studies indicate that it may possess potent anti-viral activity by inhibiting viral replication. It may also improve immune system function, help protect against certain cancers, and enhance the body's ability to produce new red blood cells.
Being a part of the future
In the next ten years, no research facility in the world will be able to produce the research data that aviculturalists can by working together openly and scientifically doing some real control studies using their own flocks and starting with the premise that food is medicine.
To be a part of this future:
1) Start with what you're currently doing; start keeping careful records of what you're feeding and what the birds are actually eating. Keep careful records of your production rates and the incidence of disease in your flocks. Always have a full post mortem done on any dead bird.
2) Research your species. Read reference texts first to get a clear idea of what you need to know and to get a true appreciation of how complex the subject is. Find out what your birds actually eat in the wild, and the nutrient content of that diet. Use research libraries and get on the Internet and start talking to each other about who's feeding what and compare notes on production rates, growth rates, when your chicks' eyes open, etc. Take what you read on the Internet with a grain of salt; there are a lot of people out there posing as experts who aren't, and remember that what you're doing is experimenting with the most potent medicine known. If in doubt, talk to your avian veterinarian and get their opinion on what you're reading.
3) Once you've researched it and have come up with an idea of something you feel you should change from what you're currently doing, change over 1/3 to 1/2 of your flock to the new regime, not all of them, and don't change too many things at once. Record all your results, and then compare them with the numbers you recorded before. Even if you notice an improvement, resist the temptation to change over the second half of the birds until you've completed your study time frame, which should be a minimum of two months, and may even be as long as six months or more.
4) If it's working, pass the information on with exact details of what you've done so the next person can duplicate it and verify your findings.
If each of you participated in this nutritional revolution, in ten years we wouldn't still be guessing what species needs what; we would know. And we'd have a healthy avicultural industry with healthier birds producing more chicks than any one can imagine at this time.
P. Burgmann, BSc, DVM, Dip ABVP(Avian Practice)
Dr. Burgmann received her Bachelor of Science and Doctor of Veterinary Medicine degrees from the University of Guelph, and has been practising exotic pet medicine since 1984. She is the author of "Feeding Your Pet Bird", as well as numerous articles in avian and exotic pet medicine. She is the owner of The High Park Animal Clinic, and is the veterinary consultant for the Ontario Science Centre. She was the first Canadian to be board certified in Avian Practice.