1 How Dietary Deficiency Studies Have Illuminated the Many Roles …
3
(NCBI/PubMed). The primary conclusion of all of this work is the well-established
tenet that vitamin A deficiency leads to biochemical and physiological dysfunction
in almost every organ system in all vertebrate animals, including amphibians, birds,
rodents, and humans, from conception to death. This chapter provides an overview of
representative studies that have used a dietary vitamin A deficiency animal research
model to advance our understanding of the role this essential factor plays in prenatal
and postnatal development and well-being.
History
In Pursuit of an Unknown Factor
Stepp… found that food mixtures after extraction with lipoid solvents could not maintain
life in mice. The total material extracted by the solvents when added to the diet made the
food efficient once more; but Stepp was unable to obtain this result by adding any known
lipoid (Hopkins 1912).
…42 rats upon the artificial dietary were compared with 52 taking similar food with a small
addendum of milk. In every individual case in which the conditions were at all comparable,
the rats taking the milk grew much faster than those without it, and the latter, if purity of diet
was secured, always ceased to grow altogether after comparatively short periods (Hopkins
1912).
The earliest vitamin A deficiency experiments were carried out to work out the biological role of this previously unknown, essential, dietary factor and as an assay to
help determine the chemical identity of the fat-soluble vitamin. In retrospect, relying
solely on vitamin A deficiency feeding and re-feeding experiments to establish the
presence or identity of vitamin A in a ration was problematic for several reasons.
First, mishandling the vitamin A used to supplement diets could have inactivated it.
Second, dietary supplements may have contained impurities that could compromise
interpretation. Third, dietary supplements may have lacked important factors that
synergize with vitamin A to elicit growth. Fourth, the vitamin A status of animals
in different (and sometimes, the same) studies would have assuredly been different
depending on when and how long the deficiency diet was fed to the animals. Nonetheless, the foundational results obtained in these early studies successfully established
the presence of a non-proteinaceous growth factor and initiated the quest that led to
its chemical identification.
Although ancient societies were aware of differences in the nutritional, medicinal,
and toxicologic properties of different food sources, it was not until the late 1800s that
a chemical understanding of these properties began to develop. Studies conducted by
Gustav von Bunge and his students from 1881 to 1891 demonstrated that protein, fats,
and carbohydrates were insufficient to sustain the life of laboratory mice (references
in (Rosenfeld 1997). In 1901, Paul Knapp published that rats fed a diet of protein,
carbohydrate, fats and minerals developed conjunctivitis and corneal ulceration prior
3
(NCBI/PubMed). The primary conclusion of all of this work is the well-established
tenet that vitamin A deficiency leads to biochemical and physiological dysfunction
in almost every organ system in all vertebrate animals, including amphibians, birds,
rodents, and humans, from conception to death. This chapter provides an overview of
representative studies that have used a dietary vitamin A deficiency animal research
model to advance our understanding of the role this essential factor plays in prenatal
and postnatal development and well-being.
History
In Pursuit of an Unknown Factor
Stepp… found that food mixtures after extraction with lipoid solvents could not maintain
life in mice. The total material extracted by the solvents when added to the diet made the
food efficient once more; but Stepp was unable to obtain this result by adding any known
lipoid (Hopkins 1912).
…42 rats upon the artificial dietary were compared with 52 taking similar food with a small
addendum of milk. In every individual case in which the conditions were at all comparable,
the rats taking the milk grew much faster than those without it, and the latter, if purity of diet
was secured, always ceased to grow altogether after comparatively short periods (Hopkins
1912).
The earliest vitamin A deficiency experiments were carried out to work out the biological role of this previously unknown, essential, dietary factor and as an assay to
help determine the chemical identity of the fat-soluble vitamin. In retrospect, relying
solely on vitamin A deficiency feeding and re-feeding experiments to establish the
presence or identity of vitamin A in a ration was problematic for several reasons.
First, mishandling the vitamin A used to supplement diets could have inactivated it.
Second, dietary supplements may have contained impurities that could compromise
interpretation. Third, dietary supplements may have lacked important factors that
synergize with vitamin A to elicit growth. Fourth, the vitamin A status of animals
in different (and sometimes, the same) studies would have assuredly been different
depending on when and how long the deficiency diet was fed to the animals. Nonetheless, the foundational results obtained in these early studies successfully established
the presence of a non-proteinaceous growth factor and initiated the quest that led to
its chemical identification.
Although ancient societies were aware of differences in the nutritional, medicinal,
and toxicologic properties of different food sources, it was not until the late 1800s that
a chemical understanding of these properties began to develop. Studies conducted by
Gustav von Bunge and his students from 1881 to 1891 demonstrated that protein, fats,
and carbohydrates were insufficient to sustain the life of laboratory mice (references
in (Rosenfeld 1997). In 1901, Paul Knapp published that rats fed a diet of protein,
carbohydrate, fats and minerals developed conjunctivitis and corneal ulceration prior