Nutritional Requirements for Psittacines (Parrots) by Jeannine Miesle

Red-Lored Amazon - FeedingNutritional Requirements for Psittacines (Parrots)
By Jeannine Miesle, MA, AFA FOA, CA Levels 1 & 2, PIJAC CAS Member, AFA, AAV



Academic researcher in the field of avian medicine. Member of the Association of Avian Veterinarians (AAV).




In the wild, birds in the parrot family (Psittacines, of the Order Psittaciformes) have a huge variety of foods from which to choose—fruits, seeds, insects, and vegetation. With these choices, they are able to meet their daily nutritional requirements through foraging. The physiology of a particular species determines its nutritional requirements, and these are determined for basal, maintenance, and total physiological states. Their nutritional intake varies over time, depending on the season and availability.

Nutrients are foods that supply the energy to maintain life and provide the precursors (a substance from which another is formed through metabolic reaction) for the synthesis of the structural and functional molecules. These include lipids (fats), proteins, carbohydrates, water, vitamins and minerals, and they are required for optimal health. 





Most psittacine illnesses seen by clinicians are related to nutritional imbalances. Many diseases have multiple etiologies; nonetheless, poor nutrition is often responsible for at least part of the ailment. Clinicians are at a disadvantage when considering differential diagnoses since comprehensive nutritional values for many psittacine nutrients have not yet been established. Many published requirements are still based on those established for domestic fowl, mostly chickens, since those values are well known and similar to those of Psittacines.

Malnutrition may cause specific illnesses. Sometimes an ailment, such as gastrointestinal (GI), kidney, or liver disease, can be directly traced to a nutritional imbalance. An illness can increase nutritional requirements, making a normally good diet inadequate for the unhealthy bird. The energy content of the food is insufficient to meet the demands of ongoing metabolic processes.


When malnutrition leads to poor growth and low body weight, the causes are:

  • Insufficient quantity of food, infrequent feeding, or too-early weaning to solid foods.
  • Inappropriate diet and unfamiliar food items.
  • Medical issues resulting in loss of appetite, maldigestion, or poor assimilation of food.



Malnutrition may be the cause of:

  • Poor feather condition, accompanied by dull, ragged feathers, hyperkeratosis (thickened, scaly skin), feather picking, the interruption of the normal molting process, and stress bars on the wings and tail, especially in neonatal birds.
  • Beak abnormalities in which the beak becomes soft, flaky, and more susceptible to injury.  In growing cockatiels, malnutrition causes narrowing of the beak.
  • Anorexia, as a result of Vitamins A, D, and E deficiencies and intestinal distress due to lactose and excessive amounts of green vegetables.

Other variables play a role in malnutrition: the bird’s age, sex, mental and physiological state. Also, the required nutrients and clinical signs of malnutrition vary among species. While one species may require more of one nutrient, another may need more of a different nutrient.

Sometimes the causes of nutritional deficiencies are other pathogens, such as parasites, bacterial infections, mycotoxins (fungal diseases) and pancreatic disease. These may interfere with the absorption of nutrients from the digestive tract.

Unless there is a medical cause, low body weight or poor weight gain can be improved by providing a high-energy diet along with digestive enzymes and fiber hemicellulose to increase the digestibility and absorbability of the nutrients.




In just the past few years, clinicians who had previously seen patients for illnesses caused by nutritional deficiencies are now also treating birds for ailments attributed to nutritional toxicities.  Hypervitaminosis is becoming increasingly problematic as birds converted to formulated diets are given additional supplementation with vitamin products by their owners.  Over 90% of the vitamins are stored in the liver; therefore, over-supplementation due to excess vitamin, mineral, fat, or protein consumption can lead to significant hepatic (liver) disease.

A vast number of papers have been written by avian veterinarians and pellet manufacturers on the benefits of total conversion to formulated diets. Pellets are readily available, easy to use, cost-effective, and they take the guesswork out of feeding the birds. Also, they claim that most companion birds, when given the freedom to select their own foods, will not make good choices most of the time. Adding pellets to the diet has resulted in improved health for many birds.


However, there are drawbacks to converting birds to a totally pelleted diet:

  • Pelleted diets do not provide the variety needed for species that often have a huge selection of food items in the wild.
  • Pelleted diets offer no opportunity for birds to display their innate foraging behavior.
  • Pelleted diets are extremely limiting and lead to boredom, which in turn may lead to behavioral issues.


As beneficial as they may be, pelleted diets have brought about a new set of complications for the practitioner and his clients.  Toxicities caused by over-supplementation have resulted in maladies involving the liver and kidneys. As new research studies emerge concerning the effects of formulated diets, veterinarians are now reconsidering their use, realizing that their clients must provide a more balanced diet for their psittacine companions. Formulated diets cannot provide all the nutrients that the birds need, nor can they provide the needed natural foods that birds enjoy. After all, the happiness of the bird, not just his health, must be considered.  Recent studies are verifying that a bird’s general, reproductive, and mental health will be improved if the birds are provided with a balanced diet which includes both formulated food and fresh fruits and vegetables. While seeds may be a part of the overall diet, offering a quality, seed-based diet alone is not sufficient, even if it is supplemented with fruits and vegetables, since those are 85-90% water.




Obesity has become a common and severe problem as seen in the avian practice. Birds eat to meet their daily metabolic requirements, and they often consume foods which are higher in energy content than they require. Fats provide a concentrated, immediate source of energy, and some birds, such as wild birds and extremely active companion birds, need this additional energy. However, most companion birds are sedentary and get very little exercise, so the addition of fats to their diets leads to obesity.

Over-consumption is secondary to high-fat diets; the bird overeats to obtain nutrients not found in his diet. Many birds are fed excess quantities of improper foods as well, such as sweets, nuts, peanuts, and sunflower and safflower seeds. Captive birds do not spend time foraging like their wild counterparts, so boredom sets in, and obesity and behavioral issues result.


Conditions resulting from high-fat, high-cholesterol diets:

  • Atherosclerosis, which is hardening of the arteries due to plaque formation.
  • Hepatic lipidosis (Fatty liver disease), a result of high fat foods or B-vitamin deficiencies.
  • Hepatophathies (liver dysfunction), which can be resolved by adding millet to the diet, giving multivitamin injections, and using lactulose. This is a synthetic, non-digestible sugar used to treat constipation. It is broken down in the colon into products that pull water out from the body and into the colon.
  • Hepatic encephalopathy, a complication of liver disease. This loss of brain function occurs when the liver is unable to remove toxins from the blood.
  • Pancreatitis, hypothyroidism (lack of iodine), self-mutilation, necrotic (dead tissue) crop infection and death.
  • Diarrhea, caused by low-fiber, high-fat intake, and poor calcium uptake in the intestines.
  • Xanthomas, lipoma, liposarcoma or fatty growths, and lipidosis (fat accumulation).



Carbohydrates are a quick source of energy for birds since they are readily converted into fats in the liver; however, when they are the main part of their diets, sedentary birds tend to develop hepatic lipidosis. These birds should be on a high-energy diet, including dextrose, and a variety of fresh fruits and vegetables. These easily digestible carbs are needed since liver disease decreases the absorption and storage of Vitamins A and D and inhibits the synthesis of Vitamin C. The diet should be low in protein and free of high-fat foods, such as sunflower and safflower seeds and nuts. The protein foods should possess high biologic value, such as hard-cooked eggs and cooked chicken.

Glucagon, not insulin, is the principal director of carbohydrate metabolism in birds. Small companion birds may collapse from hypoglycemia (low blood sugar) if deprived of food for even short periods. Hypoglycemia is a result of a poor nutrition and is resolved by converting to a high-energy, high-protein, glucose diet. Excess glucagon in the bloodstream results in avian diabetes mellitus.



Vitamins are organic compounds that are necessary for many of the body’s metabolic processes. Vitamins A, B, C, and E are vital to immune responses; thus, deficiencies in these compounds may increase the severity of infectious diseases. A balanced diet, along with the correct vitamin supplementation, is required for optimal health and must be monitored carefully. Even with adequate dietary intake, the excess of one vitamin can diminish the uptake and bioavailability (ability of the body to absorb a nutrient) of another. Birds receiving antibiotics may suffer from vitamin deficiencies since antibiotics can interfere with normal intestinal microflora. These birds should receive multivitamin supplementation.



Vitamin A affects every system in the body. The most active form is retinol, and it supports growth, testosterone synthesis, and tissue differentiation. Vitamin A is a fat-soluble vitamin formed in the liver through the conversion of beta carotenes. It belongs to a group of retinoids with similar biological activity and is an essential micronutrient. The dietary requirements for Vitamin A are not specifically known for Psittacines, and some species are more vulnerable to Hypovitaminosis A (Vitamin A deficiency) than others. This deficiency is caused by providing an all-seed diet. Seeds, especially sunflower and safflower seeds, are low in Vitamin A, and they can result in pan-systemic disease.


Vitamin A is required for:

  • The formation and integrity of normal mucous membranes and the maintenance of epithelial cells which line the surfaces of the body’s organs and tissues.
  • A healthy immune system and Bursa of Fabricus (a lymph organ in the cloaca) integrity.
  • Oral, respiratory, urogenital, gastrointestinal (GI), cardiovascular, and renal (kidney) health.
  • Brain development, behavior, vision, and a healthy Central Nervous System (CNS).
  • Skeletal development and growth and the production of hormones.
  • Reproduction, embryogenesis, and testosterone synthesis.
  • Healthy skin and feathers and the formation of pigments in feathers and resulting colors.


Hypovitaminosis A can lead to:

  • Oral candidiasis (fungal disease) with raised, crusty lesions at the commissures (soft sides of mouth where the upper and lower beaks meet) that bleed if disturbed.
  • Mycotic (fungal) infection leading to necrotic lesions on the beak.
  • Dermatomycosis (fungal skin infection). The fungi damage keratinized layers of the epidermis and produce inflammation, leading to massive destruction of the feather follicles; this is rare, and it is caused by poor hygiene and husbandry.
  • Aspergillus, a mycotic pathogen isolated from the plumage. It results in severe pruritus (inflamed, itching skin).
  • Squamous metaplasia (scaly-looking, abnormal tissue) or hyperkaratinization (excessive keratin) of mucous epithelial cells which line the cloaca, ureters and collecting ducts, Bursa of Fabricus  and conjunctiva of the eye. The respiratory, reproductive and digestive tracts undergo structural changes which render them unable to secrete the mucous which prevents invasion from pathogens. These pathogens then penetrate the mucous membrane barrier and invade the tissues. 
  • Hyperkeratosis and hypertrophy (enlargement) of epithelial cells, leading to obstruction of the respiratory airways.
  • Diseases of the oropharynx (the mouth and back of the throat).
  • Gross lesions are initially found in the esophagus and pharynx. The mucus glands and ducts appear as small, yellowish nodules which often coalesce with one another.
  • Keratinization of epithelial cells occurs, causing squamous metaplasia (benign change in the surface of cells that line the organs) of the mucous membranes and the glands of the oropharynx, leading to hyperkeratosis (production of too much keratin). The metaplasia blocks the ducts of the salivary and mucus glands, causing submandibular swelling involving abscesses filled with a yellowish, caseous exudate and blunting of the choanal papillae (small protuberances on the roof of the mouth). Ptyalism (excessive salivation) occurs and sinusitis is common.
  • White or pale swellings in the inter-ramular (the movable hinge joints in the jaw) region, beneath the tongue or elsewhere in the oropharynx, plaques in the mouth, or occlusion and swelling of the salivary gland ducts.
  • Abscesses that distort the glottis (opening of windpipe), causing labored breathing and eventual mechanical suffocation. Abscesses can grow large enough to block the choanal slit (an opening in the roof of the mouth). The result is profuse nasal discharge and obvious swelling around the eyes. The pain from these pockets of infection will cause a bird to starve. Microorganisms then spread throughout the bird’s body and will cause eventual death.
  • Sinus infections, caused by thickening of the sinus lining. Mucus flow, which washes the debris from the sinuses, is reduced. Bacterial growth then leads to infection.
  • Blockage of the uropygial gland (preen gland) with a keratin plug occurs, causing the gland to enlarge. It may become infected or burst if the gland is not expressed.
  • Anorexia. Treatment includes Vitamin A, D, and E injectables in birds with calcium deficiency. B-complex vitamins are given orally, intramuscularly (IM), or subcutaneously.
  • Urolithiasis, the formation of uric acid crystals leading to liths (hardened masses).
  • Renal damage and water retention with renal uric acid deposits, leading to:
    • Visceral gout, caused by keratinization of the kidneys. Instead of being excreted, the urates (white part of droppings) are deposited in the internal organs.
    • Articular gout, caused by the keratinization of the kidneys. The urates are deposited in the joints of the limbs, particularly the feet and legs, causing painful crippling. The tophi (nodules) show up as whitish swellings along the bare areas of the legs, ankles and toes. Treatment includes a low-protein diet, fruits and vegetables, and Vitamin A supplementation.
    • Polydipsia (excessive thirst) and polyuria (excessive urination) in mild cases, leading to squamous metaplasia. This causes partial or complete occlusion (obstruction) of the ureters, which leads to gout.
  • Foot damage and bone malformations, such as:
    • Hyperkeratosis of the plantar skin on the metatarsal and digital pads of the bottom of the feet. Normal papillary scale structure is lost, and the cornium is thickened, resulting in focal hyperkeratosis (corns) on the metatarsal pads.
    • Pododermatitis (bumblefoot). There are lesions on the plantar surface of the phalanges and tarsometatarsus (toes and back of foot) requiring supplementation of a multivitamin/mineral/amino acid preparation. Pododermatitis and plantar corns are associated with biotin and Vitamin A deficiencies, particularlyin obese birds.

  • Giardia and coccidiosis. Protozoan infections interfere with the absorption of vitamins from the intestinal tract. Treatment includes improved nutrition and supportive treatment, including Vitamins A, D3, E and B-complex, and selenium supplementation. Malabsorption of fat-soluble vitamins is possibly a mechanism of giardiasis.
  • Sub-optimal immune response, caused by both toxicity and deficiency. Deficiencies may not impact immunocompetence for as long as 18 months after withdrawal of Vitamin A in cockatiels. Deficiency in chicks leads to rapid loss of lymphocytes (white blood cells which are important to the immune system), diarrhea, and pneumonia.
  • Reproductive disorders. Birds may experience reduced egg production, increased time between clutches, egg binding, poorly formed egg shells, decreased testes size, decline in sexual activity in males, decreased sperm counts and sperm motility, abnormal sperm, reduced hatchability, increased embryonic mortality, and decreased survival time of the young. Treatment includes Vitamin A supplementation.
  • Poor feathering on the head, neck and breast and facial dermatitis with rough, scaly skin.
  • Dry eyes, thickened nictitating membranes (third eyelids), poor vision, and blindness.
  • Neurological signs, such as weakness, incoordination, and ataxia (poor muscle coordination.) Treatment includes Vitamin A supplementation.


Vitamin A Toxicity

Hypervitaminosis A has been reported in birds on formulated diets who receive high supplemental levels. Pellets already contain high levels of many vitamins and minerals, and the addition of supplements creates toxicosis. Toxicity is greater in adults than young birds.


Vitamin A Toxicity may cause:

  • Epithelial damage and keratinization of squamous cells leading to conjunctivitis.
  • Changes in vocalization patterns and more intense stress calls in cockatiels.
  • Behavioral difficulties.
  • Iron storage disease and splenic hemosiderosis (excess iron stored in spleen).
  • Digestive conditions, including enteritis, diabetes, and pancreatitis in cockatiels.
  • Skeletal abnormalities and bone deformities, including disruption of long-bone growth plates, fractures and slow growth.
  • Reproductive disorders, such as compromised fertility, hatchability, and survivability of chicks caused by excessive Vitamin A interfering with the body’s uptake of Vitamin E.
  • Feather defects. Hyperkeratosis often exists along with parakeratosis (dry, scaly skin). Both result in persistent feather sheaths, scaliness of unfeathered skin, pruritus, poor feather development, and feather-picking due to dry, flaky, pruritic skin.


Treatments include

  • Vitamin A and Retinol (from liver and fish oils) administered orally or parenterally and corrected diet.


Foods high in Vitamin A:

  • Fish liver, fat, oils, egg yolk
  • Dark leafy greens, such as spinach, lettuce, broccoli leaves and flowers.
  • Citrus fruit, cantaloupe, mango, papaya, apricot, tomato, peaches, plums.
  • Yellow and orange vegetables, pureed carrots, green peppers, fresh and dried red chili peppers, sweet corn, sweet potatoes, and pumpkin


Foods low in Vitamin A

  • Corn, white potatoes, summer squash, grapes, iceberg lettuce, bananas, apples, oranges



The B-Complex vitamins are necessary for immune system integrity. Adequate levels of both B complex and Vitamin E improve the body’s response to pathogens. The B-complex vitamins have been shown to improve some cases of CNS signs. The B-vitamins cannot be stored in the body and must be replenished daily.

Vitamin B1 (Thiamine) is found in yeast, whole grains, beans, peas, nuts and meat. It is needed for nervous system health, muscle function, digestion, and carbohydrate metabolism. Severe thiamine deficiency may lead to diseases in the nervous and digestive systems, brain, muscles, and heart. Hypovitaminosis B1 is uncommon in seed-eaters, since seeds and grains generally contain sufficient thiamine. Deficiency levels have not been elucidated for Psittacines.


Hypovitaminosis B1 can cause:

  • Anorexia, ascending paralysis, and opisthotonos (head tilted back and back arched).
  • Polyneuritis with myelin degeneration, a nerve infection with destruction of the myelin (protein) sheath around the nerves.
  • Adrenal hypertrophy (enlarged adrenal glands), skin edema (fluid buildup), torticollis (wry neck), in which the head is held in an abnormal position.
  • Seizures, poor physical condition, and a ruffled appearance. These  have responded to the use of B vitamins, particularly if endoparasites are present



Vitamin B2(Riboflavin)

Vitamin B2 supports energy production by aiding in the metabolizing of fats, carbohydrates, and proteins. It is also required for red blood cell formation, respiration, antibody production, and for regulating growth and reproduction. It is essential for healthy skin, nails, growth and general health, including regulating thyroid activity. Treatment for B1 and B2 deficiency includes the addition of dietary sources such as grains and leafy green plant material to the diet and supplementation.


Hypovitaminosis B2 can cause:

  • Curled toe paralysis (walking on hocks with toes curled inward) in poultry and nesting budgerigars; chronic cases have resulted in irreversible damage.
  • Weakness, muscle atrophy, diarrhea, and emaciation, despite good appetite.
  • Demyelinating peripheral neuritis with nerve edema (peripheral nerves lose myelin sheaths and are surrounded with fluid), leading to nerve damage in chronic cases.
  • Fatty liver disease and decrease in white blood cells counts.
  • Decreased hatchability and embryo mortality.
  • Excessively long primary wing feathers and pigment alterations in primary feathers


Vitamin B3

Vitamin B3 (Niacin/Nicotinic Acid) is found in meat, greens, poultry, fish, and egg. It may lower the risk of cataracts, osteoarthritis, diabetes, and atherosclerosis and improve CNS integrity. Requirements have not been elucidated for Psittaciformes.


Vitamin B3 deficiency can cause:

  • Poor feathering, nervousness, diarrhea, stomatitis (inflammation of the mouth) in poultry.


Vitamin B5 (Pantothenic Acid)

Vitamin B5 is found in meat, alfalfa, fish solutions, peanut meal, molasses, mushrooms, rice, wheat bran, vegetables, cereal grains, legumes, eggs, and yeasts. It is an antioxidant and lowers cholesterol levels.


Vitamin B5 deficiency can cause:

  • Poor feather growth and early death in chicks, retarded growth, skin lesions.


Vitamin B6 (Pyridoxine)

Vitamin B6 is involved in amino acid metabolism and breakdown of proteins fats and carbohydrates. Requirement  levels have not been elucidated for Psittacines.


B6 deficiency causes:

  • Jerky, nervous walking, running, falling, and flapping the wings, leading to death.
  • Scoliosis (abnormal curvature of the spine). This is caused by serum melatonin deficiency through continuous light exposure and deficiencies of copper and manganese.
  • Depressed appetite, poor growth, spasmodic convulsions, and decreased white blood cell counts in chicks


Vitamin B7 (Biotin)

Vitamin B7 is found in meats, egg yolks, nuts, beans, and fish. It aids in treating skin conditions, heart disease, neurological disorders and wound healing. Mycotoxins (toxic mold) interfere with biotin uptake.


Hypovitaminosis B7 may cause:

  • Exfoliative dermatitis or erythroderma: The signs are excessive scaling and throwing off of skin tissue on face, feet, and legs and swelling and ulceration of foot pad. Treatment is with multivitamins to compensate for nutritional deficiencies.
  • Perosis, in young birds. This is a deformity of the leg bones with enlargement of the hock, twisted metatarsi, and slipped tendons.  It is caused by deficiencies in biotin, manganese, and choline.
  • Ataxia, poor growth, and poor feathering, including white streaks and feather breakage.


Vitamin B9 (Folic Acid)

Folic acid is important for the synthesis of amino acids and protein and is essential for cell growth and metabolism, particularly Omega 3 fatty acid metabolism


Causes of deficiency:

  • High levels of fat and low levels of methionine, choline, and Vitamin B12 in the food.
  • Absence of animal source ingredients in the food and intestinal bacterial overgrowth.
  • Exocrine pancreatic insufficiency (insufficient fluid secretion through the pancreatic duct).


Folic acid deficiency in poultry can cause:

  • Embryonic mortality, poor growth, and anemia.
  • Deformation of the upper mandible, bending of leg bones, and perosis.



Cobalimin is required for normal brain and nervous system functions and blood formation. Toxicity causes change of urine or urate color from white to yellow, brown, or orange/pink. Toxicity is rare. It is found in fish, meat (especially liver), eggs, and poultry.


VITAMIN C (Ascorbic Acid)

Ascorbic acid is present naturally in foods such as citrus fruit, tomatoes, broccoli, green peppers, potatoes, and leafy vegetables. It is important for bones, connective tissues, muscles, and blood vessels, and it also aids in iron absorption and red blood cell production. Vitamin C is synthesized in the liver and/or kidneys in seed-eating birds. Birds under stress require increased amounts of Vitamin C. Deficiency levels have not been elucidated for Psittaciformes.


Deficiencies can result in:

  • Heat stress, poor growth, eggshell strength, and egg production.


Excesses can result in:

  • Growth deficiencies and hemochromatosis (iron storage disease).
  • Aortic rupture and decreased elastin content of the aorta with diets deficient in copper.



Vitamin D3 stimulates gastrointestinal absorption and resorption of calcium and regulates the hormones controlling calcium and phosphorus (P) excretion in the kidneys. The sources are sunlight and UV full-spectrum lighting to activate D3 synthesis in the skin. D3 precursors in the uropygial gland may be spread on the feathers, activated by UV light, and then consumed during preening activities. Although supplementation with D3 may be necessary for indoor birds, the owner should be careful about over-supplementation. Requirements for Psittacines have yet to be established, but many formulated foods exceed the levels suggested.


Hypovitaminosis D3 leads to:

  • Skeletal/muscular disorders. Ca/P/D3  imbalances or magnesium deficiencies cause demineralized, bent bones and pathological fractures, including:
    • Rickets. This is the inadequate calcification (hardening) of bones in growing birds. It occurs mainly in hand-reared birds whose mineral intake is deficient or unbalanced.
    • Splayed-leg syndrome. The hip joints and intertarsal joints are deformed as a result of low Ca/D3 and high protein intake. It results in too-rapid growth and obesity without the strong skeletal structures to support it. The bird suffers leg weakness due to bone fractures, as well as thoracic and spinal deformities.
    • Osteomalacia. This is the softening and demineralization of bone.
    • Easily broken bones in juveniles and neonates. Leg bones may be bent into grossly distorted positions, the sternum may be bent laterally or indented, and the spinal column may undergo lordosis (inward curvature of the lumbar spine) or fracture easily, causing pressure on the nerves, leading to paralysis.
  • Thin- or soft-shelled eggs, poor egg production and hatchability, failure to pip, inadequate maternal transfer of Vitamin D3, poor beak development, and embryonic death.
  • Seizures


Hypervitaminosis D3 may cause.

  • Renal nephrosis with calcification of the renal tubules and arteries.
  • Widespread calcification of soft tissue and visceral calcinosis (formation of calcium deposits in soft tissue), resulting in renal constipation (deposits of uric acid in the ureters).
  • Visceral and articular gout.
  • Abnormalities in chick development.



Vitamin E is the collective name for a group of fat-soluble compounds with distinctive antioxidant properties. It is needed for strong immunity and healthy skin and eyes. The two most recognizable compounds are ?-Tocopherol and ?-Tocopherol. They can be found in corn oil, soybean oil, margarine, green plants, and dressings with wheat germ oil, sunflower oil, or safflower oil. Nuts have insufficient Vitamin E, and the positive effects of Vitamin E are negated by polyunsaturated fatty acids.  It is one of the least-toxic vitamins.


Hypovitaminosis E is associated with:

  • Muscular and skeletal dystrophy. These are common in lutino cockatiels. Muscle fibrosis results in the loss of wing movement and marked clamping of the wings to the underlying sternum, bringing the wings together at the front of the body.
  • Persistent feather sheaths. The sheaths remain on the feather and don’t detach.
  • Parakeratosis. This is caused by Vitamins E and B5 deficiencies. It is an abnormality of the horny layer of the uppermost layer of skin and prevents the formation of keratin.  It responds to Vitamin B therapy and the elimination of any endoparasites.
  • Excessive biological oxidation at the cellular level. This leads to brown, fatty pigment accumulation in liver cells.
  • Encephalomalacia (softening of the brain). It is caused by deficiencies in Vitamin E and selenium, mostly in young birds.
  • Exudative diathesis. This is an oozing condition in which the bird is susceptive to disease. It is found mostly in hatchling budgerigars.
  • Feigned polyphagia (excessive hunger).  It is caused by Vitamin E and selenium deficiencies. The bird hulls the seeds and appears to be eating, but the crop remains empty. This may be seen in very weak birds or those offered inappropriate foods.
  • Oral paralysis in cockatiels related to Vitamin E and selenium deficiencies. It is a malabsorption syndrome secondary to giardiasis.
  • Malabsorption or maldigestion. They are a result of Vitamin E and selenium deficiencies secondary to giardiasis. The causes are excess oil in the diet and dehydration.
  • Edema of subcutaneous tissues. It is a result of Vitamin E and selenium deficiencies.
  • Poor immune response. B complex vitamins and vitamin E improve this condition.
  • Muscular dystrophy of the heart and ventriculus. Degeneration of ventricular musculature is associated with Vitamin E and selenium deficiencies.
  • Seizures and localized paralysis. These are due to salt toxicity and low levels of thiamine, calcium, and Vitamin E.
  • Exertional rhabdomyolysis (spraddle legs). It is due to Vitamin E and selenium deficiencies.
  • Pododermatitis.
  • Hypothyroidism.  This leads to obesity, goiter, and retarded healing.
  • Reproductive disorders. These include infertility, poor hatchability, egg binding, degeneration of the pipping muscle in neonates, and nestling deaths. It is caused by calcium, Vitamin E, and selenium deficiencies.



Hypervitaminosis E may lead to:

  • Calcinosis, crop liths, and impaired bone mineralization.
  • Decreased absorption of Vitamins A, D, K, resulting in reduced hepatic and egg yolk storage of Vitamin A.
  • Coagulopathies (poor blood clotting).
  • Impaired neuromuscular, vascular and reproductive systems.


VITAMIN K (Phylloquinone, Phytomenadione, or Phytonadione)

Vitamin K1 is synthesized by plants and is found in apple peel, spinach leaves, and green leafy vegetables. Bacterial flora in the intestine are its natural source. K1 is required for synthesis of prothrombin (a protein required for blood clotting) and is one of the treatments used to manage anticoagulant rodenticide intoxications. Deficiency results in delayed blood clotting. Without it, birds may experience excessive bleeding and exsanguinate (bleed out) from minor injuries. Toxicities result in kidney tubule degeneration.



Minerals are needed by the body for building bones, making hormones and regulating the heartbeat. Some minerals, although important, are common in most foods, and deficiencies are rare in Psittacines. Potassium is required for glucose and protein metabolism. Arginine deficiency causes wing feathers to curl upward and is associated with a lack of contour feathers.


Sodium and chloride. In Psittacines, deficiency may cause:

  • Self-mutilation, soft bones and corneal keratinization.
  • Hemoconcentration, an increase in the concentration of blood cells resulting from blood loss and a decrease in cardiac output.
  • Reduced utilization of protein and carbohydrates.
  • Gonadal inactivity and adrenal hypertrophy.

Sodium and chloride toxicity result in polydipsia, convulsions, muscle weakness, and demineralized bone formation.



Calcium is essential in the Psittacine diet, and most of it is stored in the skeletal system. It is absorbed in the small intestine through diffusion. A bird’s calcium intake may be adequate, but its uptake can be negated by supplementation or high phosphorus content in the diet. It is the most predominant mineral in a bird’s body, making up 1.5% of its body weight. It is important in new bone growth and for maintaining bone strength. High-fat diets may interfere with calcium uptake from the intestine.


Calcium is required for:

  • Myofibril (muscle fiber) contraction and transmission of nerve impulses.
  • Normal metabolism, mineralization and the permeability (capacity for transmitting a fluid) and excitability of cell membranes, blood coagulation and bone formation.
  • Activation of enzyme systems, glandular secretions, and fertility.


The calcium-to-phosphorus (Ca:P) ratio and diet

The dietary ratio of Ca:P should range from 1:1 to 2:1. To accomplish this, high-phosphorus foods such as meat, Brazil nuts, peanuts, pumpkin seeds, safflower seeds and sunflower seeds should be minimized in the diet. Foods low in calcium include sweet corn, pumpkin, muscle meat, milo, oats, safflower and sunflower seeds, millet, peanuts, and pine nuts. Most seeds, fruits, and vegetables are low in calcium, resulting in an unbalanced Ca:P ratio. Foods with a correct ratio include blackberries and citrus fruits. Pellets and a Ca/D3 supplement should be included in the diet.


Calcium deficiency (Hypocalcemia) can cause:


  • Orthopedic disorders and diseases.
  • Metabolic bone diseases such as rickets, which occurs in growing animals, and osteomalacia, which occurs in mature birds. They are caused by an inadequate dietary intake of calcium, phosphorous, and Vitamin D3 (Ca/P/D3).
  • Tibiotarsal bone fractures, brittle bones, and bone distortion due to Ca/P/D3 imbalance. Deficiencies in Ca or D3 or excesses of phosphorus lead to bone conditions since Ca absorption is dependent on the presence of D3.
  • Leg deformities, toe malposition, and leg paralysis in neonates. These are associated with calcium, chloride or riboflavin deficiencies.
  • Decreased bone mineralization and abnormalities of the long bones and the vertebral column, particularly in growing birds.
  • Skeletal abnormalities, such as dyschondroplasia, (a defect of the growth plates) in poultry. There are abnormal cartilage masses under the growth plates of the long bones and enlarged, painful joints. It is similar to osteoporosis; the bones become weak and porous until the weight of the bird or pull of the muscles creates bone deformities or fractures.
  • Beak demineralization, caused by insufficient Ca/D3 and methionine leading to hyperparathyroidism (overactive parathyroid glands).
  • Rapid growth, due to excessive levels of protein and energy, and Ca:P imbalance.
  • “Angel wing,” “straw wing,” or “flip wing.” Imbalances of Ca/P/D3 along with high protein levels in young waterfowl lead to rotation of the distal wing tip. This is due to growth that is too rapid and heavy, blood-filled, developing flight feathers being supported by non-rigid, inadequately mineralized bones. The primary fight feathers fan out perpendicularly at the elbow joint when the wings are folded against the body, rendering the bird flightless. It is a result of a valgus deformity of the growing carpometacarpal bones which rotate laterally 180 degrees. It occurs in some Psittacines species also.
  • Beak overgrowth, resulting in soft and flaky beak tissue.
  • Hyperexcitability and seizures due to a decrease in electrical resistance and an increase in the membrane permeability of nerve tissue to sodium and potassium.
  • Feather and skin abnormalities such as:
    • Dull, discolored, fragile plumage. The feathers lack sheen.
    • Asymmetric feather loss with poor molting and stress bars on the feathers.
    • Non-uniform growth of the plumage, often related to egg-laying.  
  • Hyperparathyroidism, caused by high serum phosphorus levels which interfere with blood calcium levels. Only part of the calcium from the diet is absorbed, leading to an increase in the size of the parathyroid gland as it attempts to maintain normal blood calcium levels. A high phosphorous-to-Vitamin D ratio exacerbates the condition.
  • Hypocalcemic tetany, mostly in African greys whose diet is also deficient in D3.
  • GI disorders, including increased thirst, loss of appetite, and regurgitation. Calcium gluconate or calcium borogluconate injections, improved diet, and balanced Ca/D3 supplementation are part of the treatment.
  • Dyspnea (extended neck) and wheezing associated with goiter and obstruction of respiratory passages or sinusitis.


Calcium deficiency and the reproductive system


During the reproductive cycle, a bird’s calcium and phosphorus needs change. The calcium levels need to be increased so that the bird does not draw calcium from her own bones for egg formation. Calcium levels fluctuate prior to and during egg-laying, and Ca is needed for the calcification of eggshells and uterine contractions during egg-laying. Ca deficiency and imbalance are caused by chronic egg-laying, which drains calcium stores, and gross obesity.

Rising estrogen levels promote increased intake of calcium supplements like cuttlefish bone and calcium-rich foods. However, dietary sources are usually insufficient for the massive deposition of calcium required for eggshell calcification. For eggshell calcification when dietary Ca levels are low, mobilization of calcium from the medullary bones, in the marrow cavity of long bones, is needed. This process is known as “osteomyelosclerosis.” This usually occurs overnight.


Calcium deficiency may lead to these reproductive disorders:
  • Embryonic death. If the embryo has not received enough Ca/D3 in the egg for proper mobilization of eggshell calcium, it will die.
  • Hatching difficulties. The Ca/D3-deficient hen may lay soft- or thin-shelled eggs which may crack during incubation. She may also suffer from delaying or decreased egg-laying due to reduced oviduct muscle activity.


Calcium and Vitamin D3 deficiency may lead to these nervous system disorders


  • Hyperesthesia (greater response to sensory stimulation), opisthotonos, ataxia, episodic convulsions, head twitching or flicking, weakness, and muscle cramps.
  • Diet supplementation with Ca/D3 or natural, unfiltered day sunlight or UV lighting using full-spectrum bulbs is needed to correct these conditions.


Calcium toxicity leads to:

  • Articular gout, due to excess Ca/protein/Vitamin A deficiency. Firm, white swellings (tophi) form over the joints of the limbs and feet. Improved diet, Vitamin A supplementation, and perch adjustment are needed to resolve this issue.
  • Renal disease and dehydration, leading to nephrosis and soft-tissue mineralization.
  • Decreased iron absorption and feather color mutations in chicks.
  • Lipemia (fat in the blood) associated with ovulation. This can falsely elevate blood calcium levels during the female reproductive cycle.
  • Bone tumors from osteolysis (resorption of bone by the body).




Phosphorus is needed for bone formation, maintenance of acid-base balance, fat and carbohydrate metabolism, and calcium transport in egg formation. Phosphorus deficiency results in decreased egg production, poor eggshell quality, and rickets. Deficiencies are rare since it is common in most food items. Excess phosphorus leads to increased renal elimination of calcium.



Selenium and Vitamin E function synergistically as antioxidants, affecting whole blood levels. Selenium is needed for growth, reproductive success, and for the production of thyroid hormones. These conditions may sometimes be seen in Psittacines, but the link with selenium deficiency has not been established.


In poultry, selenium deficiency may cause:

  • Alopecia (feather loss), poor feathering, and dermatitis.
  • Impaired fat digestion, exocrine pancreatic malfunction, and pancreatic atrophy.
  • Abnormal skeletal formation and muscle disease.
  • Diminished immune function along with a reduction in immune response.
  • Ventricular myopathy, alterations to cell division, and delayed sexual development.
  • Early embryonic death, fetal abnormalities, weak chicks, and retarded growth.



Selenium toxicity may result in:

  • Decreased hatchability, deformed embryos, emaciation, and liver lesions



Zinc is needed for the formation of insulin, the proper functioning of Vitamin A, enzyme metabolism, cell replication, growth, the development of cartilage and bone, feathering, molting, and appetite regulation. Supplemental zinc is used to induce molt in chickens.


Zinc deficiency results in:

  • Short, thickened long bones and enlargement of the hock in poultry.
  • Dermatitis, pododermatitis and sepsis.
  • Impaired T-cell function. (T-cells are part of the immune system.)


Zinc toxicity

Zinc toxicity sually arises from ingestion of zinc-coated aviary wire or metallic foreign bodies, often from new cages containing galvanized wire or hardware. Toxicity results in:

  • Nerve dystrophy and neurological signs.
  • Perosis, due to additional deficiencies in manganese, biotin, pantothenic or folic acid.
  • Pancreatic cell necrosis and feather-damaging behavior.


Clinical signs of toxicity include:

  • Anorexia, ataxia, paresis (partial loss of movement) and lethargy.
  • Acute gastroenteritis; yellow, bright green, or dark feces; diarrhea, vomiting and passing blood in the feces.
  • Extreme loss of plumage and pallor of the oropharynx.
  • Hepatomegaly (enlarged liver), pancreatic cell necrosis and sudden death.
  • Treatment includes increased exercise and a low-mineral diet, or possibly surgery.



Iron is needed for the production of hemoglobin and many enzymes, and proper feather pigmentation. It carries oxygen from the lungs to the rest of the body. It is present in fruits, vegetables, whole grains, lean meats, fish, beans, eggs, nuts. Birds require very little iron.


Iron deficiency result in:

  • Anemia, due to low levels of red blood cells and hemoglobin.



Iron toxicity results in:

  • Hemochromatosis, which is an abnormal accumulation of iron in the liver, leading to liver toxicity due to the body’s inability to eliminate excess iron. It is caused by foods rich in iron and Vitamins C and A, or over-supplementation.
  • Ascites (excess fluid in the abdominal cavity). This is associated with excessive dietary levels of iron in birds that are susceptible to hemochromatosis.



Manganese is required for normal bone and egg-shell formation, growth, and reproduction. It is found in nuts, legumes, seeds, tea, whole grains, and leafy green vegetables.

Manganese deficiency and may result in:

  • Ataxia, or poor muscle coordination. Growth is retarded.
  • Perosis. The birds are crippled and usually die of starvation. In poultry, young birds develop short, thickened limbs, a parrot beak, and a protruding abdomen.
  • Luxation (dislocation) of the tarsometatarsal joints. Manganese deficiency may be due to an excess of calcium and deficiencies of choline, biotin, and zinc in the diet. The deficiency causes rotation of the intertarsal joints (bones in the foot) and prevents normal use of the limb.
  • Seed diets are deficient in manganese. Requirements for Psittacines have not been established.



Copper is needed for heme (iron compound) synthesis and healthy blood vessels, bones, and connective tissue. It is an important component of several enzymes. It is stored in the bones, and very little is required.


Copper deficiency could result in:

  • Impaired feather pigmentation. Deficiency interferes with melanin production and causes dark-colored feathers to become lighter.
  • Deficiencies in essential amino acids, which form keratin.
  • Aortic rupture and bone fragility.
  • Egg production and shell abnormalities in poultry.
  • Requirements for Psittacines have not been established.



Magnesium is present naturally in many foods and may be given as a supplement.  It is needed for bone formation, heart health, carbohydrate metabolism, and the activation of many enzymes.
Magnesium deficiencies in poultry result in poor growth, lethargy, convulsions, and death.
Toxicity causes diarrhea, irritability, decreased egg production and thin-shelled eggs. Requirements for Psittacines have not been established.



Iodine is used to treat thyroid hyperplasia (enlargement of the thyroid gland or goiter) particularly in budgerigars. Deficiency is a result of insufficient thyroxine production by the thyroid gland. The treatment is iodine supplementation.

Iodine deficiency may cause:

  • Hypothyroidism, which leads to obesity, thyroid hypertrophy, goiter, lipoma formation, depressed growth rates, and CNS signs.
  • Elongated down feathers, which extend out from the body as they grow longer than the other feathers, and changes in molting and feather structure.


The Use of Grit

Grit is finely ground stone or shells. This mineral is needed by some birds to aid in digestion. However, these birds eat their seeds whole and have special organs to deal with the grit. Psittacines shell their seeds before eating them, so they do not require grit; in fact, impactions of the crop, ventriculus and proventriculus in Psittacines may be caused by the consumption of grit. The charcoal in grit interferes with absorption of Vitamins A, B2 and K, and it leads to hepatopathy (liver disease), pancreatitis (inflammation of the pancreas), renal dysfunction and general malnutrition. Grit should never be given to birds in the parrot family.





Proteins are composed of nitrogen-containing molecules and amino acids. Since feathers are formed from protein, they comprise approximately 20% of the total body protein requirements in Psittacines. In general, the larger the species, the higher the protein requirements.

The molting process requires increased energy, so birds need additional protein during this time. Extra protein provides more insulation to maintain warmth when it has fewer feathers. It takes 8-10 months for captive Psittacines to renew all their plumage since they molt continuously, and malnourished birds take even longer to molt. Anemic birds need a diet high in energy and protein, supplemented with B complex vitamins.


Protein deficiency may cause:

  • Fatty liver disease, as a result of the liver’s inability to produce lipoproteins, the transport form of hepatic lipid. Malnutrition and choline deficiency inhibit the transport of protein. This forces the liver to retain the fat that it manufactures.
  • Stunting, poor growth and development, and high mortality in chicks. Birds on decreased protein levels increase their food intake in order to attempt, unsuccessfully, to compensate for protein deficiency; as a result, they gain weight from excessive body fat.


High serum protein levels (hyperproteinemia) may cause:

  • Regurgitation, rejection of food, and weight loss, particularly in cockatiels.
  • Neurological signs, behavioral changes, including aggressiveness, biting, nervousness.
  • Poor growth rates, overgrowth of beak and nails, and increased susceptibility to disease.
  • Renal dysfunction, nephritis (inflamed kidneys) and dehydration.
  • Gout, caused by high levels of protein/Ca/D3. Although there is no empirical evidence that high-protein diets cause gout, sudden increases to a high-protein diet appear to lead to it. Psittacines excrete uric acid as the chief component of nitrogenous waste (the urates), so excessive intake of proteins or nucleic acids may lead to hyperuricemia (excess uric acid in the blood), which interferes with the kidneys’ ability to excrete the uric acid (renal constipation). Excess uric acid is then stored in the viscera or joints.
  • Liver lesions.
  • Treatment consists of feeding a low-protein diet to decrease the workload of the kidneys. This should include formulated foods, fruits and vegetables, and energy sources other than protein. Ca/P/D3, magnesium, and sodium levels should be reduced to avoid renal mineralization. Vitamin A should be provided for proper function of the mucous membranes lining the ureters, and increased B vitamins are needed to compensate for the loss of body fluids.



Choline deficiency causes poor growth, fatty liver disease, perosis in poultry, and unpigmented wing and tail feathers in Psittacines.



Amino acids combine to form protein, and protein is broken down into component amino acids before being absorbed by the intestines. Most hand-rearing mixes for Psittacines lack sufficient quantities of the sulphur amino acids (methionine and cysteine), which leads to stunted feather growth. Cysteine is abundant in the epidermal structure and feather barbs. Methionine deficiencies result in dark, horizontal stress lines on feathers, while excesses are correlated with soft, weak feathers. Deficiencies in the sulphur amino acids cause pronounced curvature and periodic restriction of the rachis (feather shaft), abnormal persistence of the basal sheath, and misshapen vanes. Adequate dietary lysine is an amino acid linked to feather strength.



Essential Fatty Acides are required by humans and animals for optimal health, but the body cannot synthesize them. The term "Essential Fatty Acid" refers to fatty acids required for biological processes and does not include the fats that only act as fuel. Lipids supply energy and essential fatty acids, are precursors of many hormones, and facilitate the absorption of fat-soluble vitamins. EFA’s are needed to form cells and membranes, to regulate cell functions, and to aid in mediating inflammation. Soybean oil is a good source of EFA’s.


Deficiency in EFA’s (particularly linoleic acid) is associated with:

  • Reproduction difficulties, such as embryonic death, poor hatchability, and poor growth.
  • Hepatomegaly, due to an accumulation of liver fats, leading to fatty liver disease.
  • Obesity, decreases in metabolic efficiency, and reduced resistance to disease.
  • Diarrhea and poor absorption of other nutrients such as calcium.
  • Oily feather textures.


Omega-3 and Omega-6 Fatty Acids (N-3, N-6 FA)

There are several N-3 and N-6 Omega fatty acids, and they have anti-inflammatory, lipid-stabilizing, anti-neoplastic, and renal-protective properties. They also possess antibacterial, antifungal, and antiviral properties to ward off pathogens. Omega fatty acids are polyunsaturated and rich in linoleic acid, an Omega-6 fatty acid. Flax seed is an important, stable source of fatty acids since it is high in linoleic acid. Omega fatty acids reduce mortality rate in chickens and allow birds to maintain their body weight. Birds cannot manufacture Omega-3 and 6 FA’s; they must ingest them from their diets or supplementation. When they discuss EFA’s, most veterinary medical sources refer to the Omega-3 fatty acids.


Deficiencies in Omega-3 Fatty Acids may lead to:

  • Changes in feather color. The quality of the feathers is an indication of nutritional status.
  • Atherosclerosis, caused by high-fat, high-cholesterol diets, lack of exercise, age, species susceptibility, and exposure to some infectious agents. The result is long-term, chronic inflammation. The type of dietary fat eaten affects the development of atherosclerosis more than the total amount of fat consumed. Atherosclerosis leads to stroke, heart attack, and vascular disease and is seen in parrots with increasing frequency. The clinical signs for birds include circulatory conditions, lethargy, dyspnea, fainting, sudden falling, nervous symptoms due to blood loss in areas of the body, and sudden death. Diets high in N-3 FA’s protect against atherosclerosis in parrots.


Supplementation with Omega-3 Fatty Acids has been shown to improve:

  • Bone health in poultry. No studies have been released on Psittacines.
  • Neurological development in poultry. Increased cognitive ability and higher concentration were found in chicks whose parents were fed high amounts.
  • The risk of cancer. Research shows a lower risk of cancer and increased survival time in poultry. The group supplemented with flax seed maintained their weight and had better overall health than those not fed flaxseed. No studies have been done on Psittacines.
  • Renal function. In studies with mammals, N-3 FA supplementation improves renal function and decreases progression of some kidney diseases. No studies have been done on Psittacines.
  • The risk of obesity. Supplemental N-3 FA’s have been shown to substantially affect fat deposition in poultry. In studies, birds had lower fat-pad masses and reduced overall body-fat mass. No studies have been done on Psittacines.
  • The Immune System. N-3 FA supplements increase antibody responses in chickens.




In a normal companion bird’s environment, his diet is his primary link to health and longevity. It is imperative that the care-giver pay very close attention to the quantity and quality of the food he or she provides. Although many seed mixes claim to contain daily requirements for most vitamins and minerals, most are deficient, and some formulated diets contain more than the required amounts. Bird owners should be aware of the consequences of both over- and under-supplementation and be watchful for any signs of deficiency or toxicity.






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Information contained on this website is provided as general reference only. For application to specific circumstances, professional advice should be sought.