Quote from Dr. Garrett Smith on January 2, 2019, 6:27 pm

If you had a child born with a cleft lip or cleft palate, I bet you never once heard from your obstetrician, pediatrician, or midwife that it was probably caused by Poison/"Vitamin A".  The research showing this goes back more than 50 YEARS.  I feel like my own medical school professors and nutrition teachers should be embarrassed that they didn't know this, and that I'm having to bring it back to people's attention now.  Below is evidence of this in mice, rats, rabbits, cats, and dogs...to assume the same wouldn't be true in humans is ludicrous.

Vitamin A induction of cleft palate.

Both retinoic acid and retinyl acetate, administered in high doses on days 13--15 of gestation, are capable of causing a 90 per cent incidence of cleft palate in Charles River rats. However, an attempt to develop as in vivo rabbit model system for the induction of clefts via hypervitaminosis A was unsuccessful. In the rat, the retinoic acid form of vitamin A is the more potent teratogen, inducing clefts at less than half the dose required to produce them with retinyl acetate. Histologic examination of fetal rat heads confirmed the biochemical evidence that retinoic acid is the more potent teratogen. Both forms of vitamin A prevented palatal shelf reorientation from occurring at the correct gestational age. The retinyl acetate treatment delayed the rotation for approximately 12 hours, the retinoic acid for at least 48 hours.

Hypervitaminosis A and reproductive disorders in rabbits.

Reproductive abnormalities in New Zealand White rabbits at a large commercial rabbitry were linked to an excess of dietary retinyl acetate. Fetal resorptions, abortions, and stillbirths were common in pregnant does. Examination of aborted and stillborn fetuses disclosed hydrocephalus, microencephaly, and cleft palate. Analysis of the commercially prepared feed disclosed a total vitamin A content of 102,278 IU/kg, of which 97,618 IU was retinyl acetate (recommended total vitamin A concentrations are 6,000 to 12,000 IU/kg). Levels of vitamin A in the plasma of does with reproductive disorders were 517 to 1,667 ng/ml (normal level is 300 ng/ml), and liver levels were 2,070 to 12,854 micrograms/g (normal range is 50 to 300 micrograms/g).

Morphological and autoradiographic studies of cleft palate induced in rat embryos by maternal hypervitaminosis A.

However, a carefully controlled treatment with hypervitaminosis A can produce a high incidence of cleft palate which is only rarely accompanied by other malformations (Giroud & Martinet, 1956).

Hypervitaminosis A induced teratogenesis.

In the past decade, the toxicology of reproduction has become increasingly important. This branch of toxicology focuses on mutagenic and embryotoxic effects. The study of embryotoxicity requires an extensive knowledge of the interaction of drugs and embryonic tissues, normal and abnormal developmental processes, and the susceptible stages during prenatal development. Hypervitaminosis A is one of the most extensively studied teratogens. It produces defects in almost all organ systems. Therefore, this article will first of all review the vitamin A-induced malformations in several organ systems. Moreover, it will discuss their morphogenesis and the susceptible developmental stages. Thus, the first ten chapters will cover the following subjects: malformations of the nervous system, ocular malformations, malformations of the ear, craniofacial malformations, cleft palate, defects of the circulatory system, defects of the respiratory systems, defects of the digestive tract, urogenital defects, skeletal malformations, and abnormal postnatal development. Since in general little is known about the mechanisms involved in the induction of congenital defects, we think it is of great value to review the knowledge and experience that have been gathered by the experimental work with hypervitaminosis A. Therefore, the next chapters will discuss the following subjects: teratogenic effects in different species, minimum effective dose, interaction with other agents, influence of chemical form, solvent, and route of administration, pathophysiology of vitamin A embryotoxicity, and hypervitaminosis A and human pregnancy.

Growth inhibition and occurrence of cleft palates due to hypervitaminosis A.

DNA synthesis in palatal processes obtained from fetal rats was 36% lower in the presence of excess vitamin A, but vitamin A-exposed maxillary explants showed only a modest decrease. Scanning electron micrographs of fetuses exposed to hypervitaminosis A in utero demonstrated both decreased head size and stunted palatal processes. The results suggest that cleft palates occur in this model system because the palatal processes are more sensitive to the actions of vitamin A than are the surrounding maxillary tissues.

Excess vitamin A intake during pregnancy as a possible cause of congenital cleft palate in puppies and kittens.

[Cleft palate in the rat embryo caused by maternal hypervitaminosis A].

[Hypervitaminosis A and cleft palate].

Effect of Cortisone on the Incidence of Cleft-palate Induced by Experimental Hypervitaminosis-A

Mouse palatal width growth rates as an "at risk" factor in the development of cleft palate induced by hypervitaminosis A.

Tritiated thymidine labelling of the palatal processes of rat embryos with cleft palate induced by hypervitaminosis A

Production of cleft palate with dexamethasone and hypervitaminosis A in rat embryos.