Quote from Dr. Garrett Smith on April 5, 2019, 3:57 pm

Nutrition I - Avian Medicine

Vitamin A Toxicity

In the wild, noncarnivorous birds are rarely exposed to dietary excess of vitamin A.

Let me make that more clear.  In the wild, a bird that eats NO meat would NEVER come across any retinoids ("animal Vitamin A", what the author calls just Vitamin A) in their food AT ALL.  There's a reason it is called "animal Vitamin A", and that's because it isn't ever found in plants!

These birds probably depend on the conversion of carotenoids to biologically active vitamin A. Toxicities are avoided because the efficiency of conversion of vitamin A from ß-carotene decreases with higher levels of intake. Conversion efficiency in the chicken drops from a ratio of 2:1 to 5:1.46

Here's what really happens.  As an animal (this includes birds and humans) becomes more toxic with retinoid Poison/"Vitamin A", their bodies slow down the cleavage/conversion/"cutting" of carotenoids into retinoids.  It is a SAFETY/DEFENSE mechanism!

"Toxicities are avoided", do you understand the implication of that statement?  The body is PROTECTING itself.

Studies of Japanese quail also indicate a saturation of the retinol-transporting system, as birds supplemented with ß-carotene do not develop increased levels of retinyl palmitate.60

Saturation of retinol-binding protein (RBP) implies Poison/"Vitamin A" toxicity levels have absolutely been reached.  RBP is one of the main things your body uses to protect you from Poison/"Vitamin A" while it is detoxifying it.  When it can't hold any more ("saturated" means full to the brim), then the free/unbound retinol that has no RBP to bind to causes even MORE damage.

Cockatiels at maintenance are more susceptible to vitamin A toxicity than deficiency.30 Perhaps ß-carotene would be a superior source of vitamin A in some psittacine diets; however, ß-carotene may not be appropriate for hand-rearing mixes because chicks may not efficiently convert ß-carotene to vitamin A.

This is a ludicrous statement and assumes that birds in the wild could have never survived on their natural diets, and they somehow were designed to need human veterinary scientists to custom-make their diets.  Noncarnivorous birds in the wild would have eaten plants, and plant-eaters of all things don't need any "animal Vitamin A" in their diet!

Toxicities have been reported in cockatiels maintained at 10,000 IU/kg of vitamin A. Many commercial diets exceed this level.30 Some hand-rearing diets have levels in excess of 47,000 IU/kg.85

Maybe these veterinary nutrition "experts" need to have some serious conversations with the commercial feed makers...but then again, poisoned/sick birds come into the vet's offices more often and make everyone involved (except the paying owner) more money, right???

In lorikeets, commercial diets high in vitamin A and deficient in vitamin E are correlated with high rates of infertility, decreased hatching and survivability of chicks.42

Do Westernized countries have problems with infertility?  (Yes.)
Do Westernized countries have problems with infant mortality?  (Yes.)

The author hypothesizes similar levels may contribute to the increased incidence of iron storage disease in these birds. Vitamin A toxicity causes epithelial damage and keratinization of squamous cells.33 Epithelial damage results from penetration of retinol into the lipid portion of the membrane, causing it to expand. Weakening of the membrane results from the inelastic protein portion of the membrane resisting expansion and increases access to pathogens and infection.

Let me summarize what Vitamin A toxicity is known to do in birds, from the above:

• Iron overload disease
• Skin (epithelial) problems
• Increased infections

Clinical signs of Vitamin A toxicity include:

Vocalization Patterns
Cockatiels maintained on excess dietary vitamin A exhibit frequent stress calls of greater intensity and duration.30 Vitamin A toxicities may contribute to behavioral problems in companion birds. Vocalization changes were observed in psittacines maintained on diets that contained recommended levels of vitamin A.47,75

Maybe you are dealing with, or know others who are unable to tolerate stress well, have anxiety, and/or have behavioral problems (look at America's youth!!!)?

Iron Storage Disease
See Section II Nutritional Disorders for the potential contribution of excess vitamin A to iron storage disease. Splenic hemosiderosis has been correlated with excess vitamin A in cockatiels.30

More evidence that non-genetic-related iron overload is caused by Poison/"Vitamin A" toxicity!  Anemia is also a well-known side effect of Poison/"Vitamin A" toxicity too.  Different bodies can very much react differently to the same poison/stressor.

Here is the Section II Nutritional Disorders part related to Poison/"Vitamin A" and iron storage disease that is mentioned above:

The syndrome of excessive iron overload in mynahs shares most of the important histopathologic characteristics with idiopathic hemochromatosis in human beings. Iron storage disease has been correlated with immunological stress,25,36 as well as crowded conditions.53 Reduced peristalsis or neuropathic gastric dilatation may increase iron absorption.36 Stress increases lipid peroxidation and diminishes vitamin E levels, resulting in a lower level of antioxidant activity. Iron and vitamin E are involved in electron transfer in reduction/oxidation cycles; a dietary surplus of either iron or vitamin A decreases the α-tocopherol concentration. Therefore, any impact on vitamin E levels may reduce the protection of biological membranes against oxidation. In addition, diets high in saturated fats increase iron absorption.79

Poison/"Vitamin A" depletes Vitamin E.  Vitamin E is protective against Poison/"Vitamin A" damage.  Too much A, not enough E, equals health disaster.

Pancreatitis
Pancreatitis was diagnosed in cockatiels fed excessively high levels of vitamin A.33 Hypervitaminosis A increases the activity of sucrase and eliminates the duodenum’s ability to regulate this enzyme in the small intestine 71 which may lead to diabetes and digestive difficulties.

Pancreatitis and DIABETES and digestive problems!  Can you say "Western chronic disease patterns"!?!?  It really doesn't get any more clear-cut than this.

Iron Storage Disease
See Section II Nutritional Disorders for the potential contribution of excess vitamin A to iron storage disease. Splenic hemosiderosis has been correlated with excess vitamin A in cockatiels.30

Here is the Section II Nutritional Disorders part related to Poison/"Vitamin A" and iron storage disease that is mentioned above:

The syndrome of excessive iron overload in mynahs shares most of the important histopathologic characteristics with idiopathic hemochromatosis in human beings. Iron storage disease has been correlated with immunological stress,25,36 as well as crowded conditions.53 Reduced peristalsis or neuropathic gastric dilatation may increase iron absorption.36 Stress increases lipid peroxidation and diminishes vitamin E levels, resulting in a lower level of antioxidant activity. Iron and vitamin E are involved in electron transfer in reduction/oxidation cycles; a dietary surplus of either iron or vitamin A decreases the α-tocopherol concentration. Therefore, any impact on vitamin E levels may reduce the protection of biological membranes against oxidation. In addition, diets high in saturated fats increase iron absorption.79

Poison/"Vitamin A" depletes Vitamin E.  Vitamin E is protective against Poison/"Vitamin A" damage.  Too much A, not enough E, equals health disaster.

Pancreatitis
Pancreatitis was diagnosed in cockatiels fed excessively high levels of vitamin A.33 Hypervitaminosis A increases the activity of sucrase and eliminates the duodenum’s ability to regulate this enzyme in the small intestine 71 which may lead to diabetes and digestive difficulties.

Pancreatitis and DIABETES and digestive problems!  Can you say "Western chronic disease patterns"!?!?  It really doesn't get any more clear-cut than this.