Review: Phosphorus in Fish Nutrition

freshwater fish Labeo rohita (Rora) with diets containing vitamin D 2 (550, 1,100, 1,650 IU/kg) and vitamin D 3
(1,100, 1,650 IU/kg). The growth, feed efficiency, mortality, carcass protein, fat, Ca and P contents did not differ
between vitamin D-defici ent fish and fish fed any forms of the vitamin at any doses. Vielma & Lall (1998b) found
that hepatic cholecal ci ferol content of Atlantic salmon was 58.5 ng/g when fish were fed for 15 weeks with a
low-P-low-Ca diet (3.1 g P, 1.3 g Ca /kg), and 9-10 ng/g when they were fed diets supplemented with either Ca or P.
Vielma et al. (1999) reported that growth and feed effi ciency of rainbow trout (initial wt 12.4 g) were not influenced
by dietary cholecal ci ferol and P levels in a 20 week feeding trial. Liver cholecalci ferol concentration was higher
(4.9 vs 9 ng/g) when fish were fed diet containing 2600 IU of cholecalci ferol /kg diet than when they were fed 100
IU/kg, but dietary P had no effect on the hepatic concentration of the vitamin. A high dietary P level increased
urinary P concentration, whereas dietary cholecalci ferol level had no effect. In mammals, dietary P restriction
increas es 1,25(OH)D3 or calcitriol, but in trout, Coloso et al. (2001) did not see any such change based on
radioimmunoassay. Coloso et al. (2003) reported that 1,25(OH) 2D and 25(OH)D concentrations in plasma of
rainbow tourt (bw 73 g) did not respond to 31d of dietary P restriction (0.3-0.6% total P in semi-purified diet).
Mellanby's Toxamin Theory
May Mellanby (1918) published a paper that contained a section entitled "Harmful nature of modern dietary in
regard to the teeth", in which she wrote, "Our diet, particularly that of the poor, is now more than ever made up of
specially prepared cereals, such as wheat, rice, oats, &c. . . . There is no doubt that our modern dietary is harmful as
far as the teeth are concerned." Edward Mellanby (1918), May Mellanby's husband, first developed standard diets
that produced rickets on puppies (such diets contained bread or cereals), and then added to the standard diets a test
substance in order to determine their effect on the development of rickets. Mellanby (1919) wrote, "Since the
dietetic problem is one of balance, foodstuffs which contain no anti-rachitic factor cannot be considered as neutral,
but as positively rickets-producing, for the more of them that is eaten the greater is the necessity for foods
containing the factor. Since there is a limit to what a child can eat, the inference is obvious. It is probable that
bread is the worst offender, and to allow bread to form too large a part of an infant's dietary seems to me to be
courting disaster. The same statement may apply to other cereals, but this has not been worked out to any extent."
Subsequently, Mellanby (1922) showed that rickets-producing power vari ed greatly among the kinds of cereals---
oatmeal the worst followed in order by brown flour, barley, rice, and white flour. Mellanby (1925) reported that
oatmeal and maize had a powerful rachitogenic effect. He wrote, ". . . the amount of Ca and P in the food is of but
secondary importance in the control of the deposition of these elements in growing bone. In view of the evidence
of interaction and balance among food constituents provided by this investigation, the value of the expression
‘optimum Ca content of a diet’, so commonly used nowadays, must be doubted. The optimum varies every time
the other elements of diet are changed." Mellanby (1926) found that a powerful anticalci fying cereal like oats
lost some of its action after cert ain simple forms of chemical treatment, namely, 1) boiling with acid, and 2) malting
followed by heating. This crude experiment showed that cereals contained a definite anticalci fying substance
whose action could now be modified in two entirely different ways, 1) by adding vitamin D and to a lesser extent by
adding Ca salts, and 2) by destroying the hypothetical toxic substance by boiling with acid or by malting.
Mellanby (1926) named this unidentified harm ful substance(s) in cereals 'Toxamins', which was later (1934)
identified as phytic acid. The toxamin prevented utilization of Ca, and this toxic action was antagonized by the
anti-rachitic vitamin. In fact, Holst (1927) also wrote, "If oatmeal is extracted with hydrochloric acid and the
extract is given in addition to the starch, the animals develop rickets. The rickets-producing factor of oatmeal must
therefore be ascribed to some toxic substance. Evidence is given to show that this substance can pass through
parchment -paper and that it can be precipitated with alcohol. Rickets produced by feeding with cereals can be
prevented by the administration of calcium-s alts, whereas phosphates have no such effect." However, back to
Mellanby (1919) paper, he also wrote, "It was found that adding orange juice did not prevent rickets. Further, that
the addition of 5g. calcium phosphate, or doubling the separated milk and so increasing the calcium intake in this
form was without preventive action on the development of the disease." Green & Mellanby (1928) showed that
oatmeal could be boiled with water or heated in the dry state at 120°C for 18 hours without correction of its
anticalci fyig properties. If, however, it were boiled with 1% HCl for 1.5 hours and then neutralized, the product
was found to have lost its anticalci fying effect.
Steenbock, Black & Thomas (1930) drew attention to the possibility that cereals contain a form of P less
available to rats than inorganic P. Templin & Steenbock (1933b) showed that the disappearance of rachitogenic
effect after boiling with acid was accompanied by a change of organic P to inorganic P in the cereal, and suggested
that the organic P might be less available than inorganic P. Then, Bruce & Callow (1934) showed that phytic acid
forms an insoluble Ca salt and interferes with the absorption of Ca in rats. Lowe & Steenbock (1936a,b) and
© 2000, 2005. Shozo H. Sugiura. All rights reserved.
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