Rickets and a Deficiency of the Fat-Soluable A-Vitamin



The discovery
of the indispensability of the fat-soluble vitamin for the growth of rats,
together with the well-known curative action upon rickets of cod-liver oil,
milk, butter and eggs, food-stuffs rich in this vitamin, gave rise to the
theory that rickets might be connected with an insufficiency of this factor in
the food. Both Hopkins and Funk suggested that rickets, like beri-beri and
scurvy, was the result of a specific deficiency in the diet. Hopkins
first acquired a bias in favour of a dietetic factor in the causation of
rickets by observing in Venice
that this disease was most frequent in families who never used dairy products
of any kind. This view is strengthened by the conclusion of Drs. Cheadle and
Poynton from their clinical experience with rickets. Before the conception of
accessory food factors wasi formulated, they wrote :1

" Rickets is produced as Wtainly by a rachitic diet as scurvy by a scorbutic diet. Children of
well-to-do parents,
under hygienic
conditions so far as air, light, cleanliness and
warmth are concerned, get rickets if the diet is at fault. Such cases are cured in fact by an antjrachitic diet as
certainly as scurvy by an antiscorbutic diet. The fault is of quality, not
A child may be reduced by starvation to the last stage of atrophy and yet not
be rickety. Conversely, it may be over-fed,
fat and gross and yet be extremely rickety."

The known facts concerning the disease of rickets can now be reviewed in
a new light, and it will be seen how they fit in with the theory that rickets
is the result of a diet containing an insufficiency of the A-vitamin in a form
available for the use of the infant.

1 In Allbutt and Rolleston's System of Medicine. 72


Fig. i 6.—Front View.

Fig. 17.—Side View.

of Child's Skull in Rickets.

Reproduced by kind permission of Dr. E. Cautley from Diseases of Children, edited by A. E. Garrod,
F. E. Batten and J. H. ThursEeld.  
Edward Arnold & Co.

RICKETS                                73      «

The havoc caused by rickets is more widespread than is generally
realised. The cases with obvious bone deformity are only a small proportion of
all those affected. The statistical figures of Lawson Dick in London
and of Schmorl in Germany
are appalling. Schmorl, from microscopical examination of the bones and of
other organs of children dying under four years of age, found that 90 per cent,
had rickets. Lawson Dick found that 80 per cent, of the children in some London
County Council schools were affected. Another set of figures is very striking.
The infant death-rate in the west of Ireland
is only 30 per thousand, but in poor urban districts in Great Britain from 100 to 300 per thousand;
rickets in the west of Ireland
is practically unknown, but in the slums of English and Scottish towns it is
very prevalent.

Symptoms.—Rickets is not merely a disease of
the bones; the health, growth and development of the whole body is affected. It
is seldom observed before the child is six months old, and is most active between
the ninth and twenty-fourth months. A child, previously thriving and often
growing particularly fast, becomes whining and restless, is disinclined for any
exertion, and in severe cases may make no attempt to sit, walk or stand. The
head enlarges and becomes flat and square on top with bulging sides as shown in
Figs. 16 and 17. Only about 20 per cent, of these children look badly
nourished; more often they are flabbily fat. The bones grow irregularly and
remain soft and cartilaginous, leading in bad cases to permanent distortions
and deformities, such as bow legs and knock knees. At the junction between the
bones and carti­lages of the ribs there is a thickening which gives rise to the
condition known as the rickety rosary or beading of the ribs (cf. Scurvy, p.
36). The ends of the long bones enlarge, most obviously at the wrists and
ankles. As the disease progresses the chest wall is distorted; it becomes
narrow and depressed under the arm-pits, greatly reducing the chest cavity.
Lung and heart troubles are caused by the pressure of the mis­shapen chest. The
muscles are wasted and ligaments are soft and lax; the child seems "
double-jointed " and is able to place the limbs in queer positions. The
limbs are not tender to touch, and if there is appreciable tenderness a
complication with scurvy should be suspected. Rounding of the spine is produced
by muscular weakness; if placed in a


sitting position the child may sink in a heap. The
state of the whole
body has its effect upon the nervous system;
various forms of spasm and convulsion (tetany) are
easily excited. Digestive troubles frequently, but not invariably,
accompany rickets and the abdomen is distended.
of the head is often observed.

Although generally associated with infancy and early childhood, rickets
has been observed at a much later age. Late rickets, as it is called in older
children, was a rare disease, but since the War it has become quite common in
Central Europe, especially in Vienna.
Late rickets does not respond to treatment with cod-liver oil so quickly as in

Central Europe is now afflicted with rickets to a greater extent and in severer forms
than ever before experienced in breast-fed and artificially fed infants. In one
Austrian community rickets was diagnosed in ioo per cent, of the infants of
nine months. It occurs in infants at a much earlier age than usual, and amongst
older children there is much dwarfism and deformity. In Germany since
1917 there has been a marked increase of rickets showing all grades of
deformity; 10 per cent, of the children of three to five years of age cannot
walk, and it is likely that a considerable proportion of these children will
eventually become a burden upon the State.

Rickets is seldom directly fatal, but children suffering from this
disease are more easily attacked by broncho-pneumonia, tuberculosis and other
infectious diseases. Whooping-cough, measles and bronchitis are far more grave
if the child is rickety. Either sex is equally affected, but the consequences
are far more serious for the female, as the contracted pelvis, a frequent
result of rickets, makes childbirth difficult. The rachitic child also carries
a stigma throughout life in the form of de­fective teeth. These children suffer
more frequently from adenoids and enlarged tonsils. Lawson Dick found 66 per
cent, had both adenoids and enlarged tonsils; 14 per cent, had enlarged tonsils
alone; and 20 per cent. had adenoids alone.



Since Glisson first described this disease in his famous Treatise on
the Rickets
nearly 300 years ago, it has con­tinually increased in spite of
numerous theories and investigations as to its cause. It is now generally
agreed that the prevention of rickets is fundamentally a dietetic problem. Dr.
Still has classified the diets associated with the development of rickets :


Very starchy food, such
as bread, potato, biscuits, or cornflour with little milk.


Excessively diluted
cow's milk, whether fresh, condensed, or dried.


Patent cereal foods.


Breast milk supplemented
by starchy food.


Breast milk alone.

If one particular fault in the food is the cause of rickets it must be
common to all these diets.

Excess of carbohydrate cannot be the essential factor, since diluted
cow's milk and poor human milk without any added carbohydrate are included
amongst the diets associated with rickets.

Insufficient protein is not the cause, since rickets occurs on diets 2,
4, and 5, which are not necessarily deficient in protein, for cow's milk
diluted with an equal volume of water contains as much protein as human milk.
Again, experiences at the London Zoological Gardens have proved that
insufficient protein is not the cause; lion cubs weaned early and fed on a high
protein diet of raw, lean meat became so rickety that they could not be reared.

An insufficient quantity of fat is common to diets 1, 2 and 3, and
possibly to 4 and 5, but in rare cases rickets occurs if cream, making 6 to 7
per cent, of fat, is added to a milk mixture; after gaining well for a time
such infants eventually suffer from disordered digestion, the fat is not
assimilated and rickets occurs.

To whatever defect in diet or
hygiene rickets is ascribed,


is one cure which is so generally successful that it may be regarded as a
specific, namely cod-liver oil.1 The value of cod-liver oil in the
treatment of this disease in infants has long been known, and at the suggestion
of Bland-Sutton the rickety lion cubs at the Zoo were treated and cured by
cod-liver oil. Other substances which have proved of value both in prevention
and cure, but to a lesser degree, are butter, cream, eggs and milk. All these
substances are fatty foods rich in A-vitamin (pp. 49, 62). This particular
constituent of the fat is lacking in those diets associated with rickets except
in the special case of over-feeding with fat.

A study of the social and economic factors in the causation of rickets,
carried out in the city of Glasgow
by Miss Ferguson, also showed the connection of rickets with a shortage of
A-factor in the food, although this point was overlooked by Miss Ferguson. The
non-rickety families had more milk, meat, margarine, fish, eggs and cheese than
the rickety families, who used more flour, potatoes, sugar and oatmeal.

Fresh cases of rickets occur most frequently in the spring. In the United States twice as many occur from January
to June as in the other half of the year; similar reports come from Great Britain and Germany. This seasonal variation in
the incidence corresponds with the seasonal variation of cow's milk in respect
to its content of A-vitamin. It has been shown by Drummond that the milk from a
grass-fed cow is richer in A-factor than the milk from the same cow after
several weeks of winter feeding. A-factor is of vegetable origin and is formed
in the green parts of the plant. The feeding of cows in winter on straw and
turnips, as is done in some districts,

1 The value of cod-liver oil in A-vitamin
is reduced by refining to remove the fishy taste, or by emulsification and
admixture with other ingredients to make it more palatable. The crude oil has
also been found to be the best in the treatment of rickets. A sample of
cod-liver oil exhibited at a recent Sanitary Congress (1921) was described as
" tasting like warmed-up pSche Melba "; the efficiency of such a
pleasant preparation would probably be very slight, and it might have to be
given in large quantities which would upset the digestion.



likely to produce a milk very poor in this vitamin, as the green parts of the
turnip are not eaten.

The antirachitic value of milk thus depends on the diet of the animal.
In the same way breast-fed babies may receive milk lacking in A-vitamin if the
mother's diet is poor in this respect. This fact is illustrated by statistics
from New York:
in a certain poor quarter 90 to 100 per cent, of the negro babies suffer from
rickets, though almost all are breast-fed; the mother's food was found to be
lacking in good fats and in green vegetables. A generation earlier the parents
of these negroes lived in the West Indies on
an entirely different diet of fresh natural food-stuffs; rickets amongst them
was unknown.

Cheadle and Poynton only observed rickets to occur on a diet containing
plenty of milk if loss of food had been caused by vomiting or diarrhoea. The
rare cases occurring on an apparently ideal diet are traceable to the same
cause; digestive disturbance, though not always obvious, may prevent the
assimilation of A-factor as contained in butter or milk fat. All these cases
respond to treatment with cod-liver oil, probably because oily fats like cod-liver
oil are better assimilated than a hard fat like butter fat, and also because
cod-liver oil has been estimated as being approximately 250 times richer than
butter fat in A-vitamin. A-factor given in spinach has no power to alleviate
rickets in infants because it passes through the intestine practically
unaltered even when given in a finely-sieved form. The A-vitamin is of no use
to the infant if offered in a medium which it cannot digest. Scurvy and rickets
are frequently associated in the same child. It is now clear that the lack of
either B-factor or C-factor or good protein in the food causes digestive
trouble. A diet deficient in any of these ways, either singly or collectively,
is therefore likely to prevent the assimilation of fat. Rickets in such cases
may be of secondary origin; that is, not the direct result of food lacking in
A-factor, but inability to utilise the good fats supplied.   Feeding experiments on birds by Plimmer and


Rosedale indicated that
A-factor, given as cod-liver oil, was only effective if the food contained a
good supply of B-factor; increasing the amount of cod-liver oil without
simultaneously increasing the amount of B-f actor actually caused loss of
weight. For normal growth and the prevention of rickets the diet must therefore
be properly balanced. An infant over-fed with cream on a diet deficient in
other factors may thus get rickets. Con­versely, it has been shown by Hess and
Unger, that on a well-balanced diet containing a relatively small amount of
A-vitamin slow-growing children did not develop rickets. The requirements of
slow-growing children for this vitamin are apparently less than those of
fast-growing children, and the diet used by Hess would probably not have
prevented rickets in children growing at a normal rate. Rickets must be
regarded as a disease accompanying growth and is not seen in atrophic

poorly calcined bones of rickety children led to a belief that rickets is
caused by the absence of calcium salts in the food, and that it can be cured or
prevented by the use of lime water. An insufficiency of lime salts in the food
of a growing child or animal certainly produces soft bones, but the condition
is not identical with true rickets. There is seldom a shortage of calcium salts
in the usual rachitic diets, for even diluted cow's milk contains sufficient.
Lime salts in cow's milk are chiefly present as acid calcium phosphate, which
becomes insoluble in alkaline digestive juices, and will therefore pass through
the body unchanged and be of no use. The assimilation of calcium as calcium phosphate depends upon the presence of
hydrochloric acid in the gastric juice, which converts the calcium phosphate
into calcium chloride and phos­phoric acid, two soluble substances, probably
separately assimilated in the intestine. For the proper calcification of
growing bones two conditions are necessary : sufficient calcium salts must be
assimilated; the calcium salts after assimilation must be deposited in the
bone.   True rickets

RICKETS                                79

independently of the supply of available calcium; it is caused by an inability
to retain the calcium salts in the body. There may even be a negative calcium
balance; that is, more calcium salts are excreted in the urine than are
assimilated from the food. The adminis­tration of cod-liver oil, egg, butter,
etc., enables the body, by some means not yet understood, to retain and deposit
in the growing bones and teeth the assimilated lime salts and to use them for
the general purposes of the body. Sufficient calcium must, of course, be
present in the food, and a deficiency of calcium is only likely to occur on a
largely cereal diet. True rickets develops independently of the supply of lime
salts in the food and cannot be prevented or cured by the simple addition of
lime salts.


Professor E. Mellanby has shown that the production of rickets in
growing puppies can be controlled by the kind of fat in the food. His
experiments were upon newly weaned puppies, five to eight weeks old, and con­tinued
to the age of six months. The animals were constantly examined by X-rays to
detect imperfect calcification or malformation of the bones. The results of
these experiments are capable of extension to the treatment of children. A
basal diet was selected which was consistent with fairly good health and
growth, and yet soon produced rickets.  
The diet consisted of—

250 to 350 c.c. separated milk.

Unlimited white bread.

5 to 10 grms. of yeast (for

3 c.c. orange-juice (for G-factor).

1 to 2 grms. of common salt.

10 c.c.
linseed oil.

The separated milk contains calcium salts and sufficient protein to
supplement the poor protein of white bread.


contains B- and C-. factors and chlorides and is really only deficient in the
A-vitamin. The development of rickets could be controlled by simply
substituting other fats for linseed oil. Experiments were also made to
determine the effect of extra lime salts, which were increased by doubling the
quantity of separated milk or by adding pure lime salts. In neither case was
the development of rickets prevented.

Mellanby found that he could roughly
classify food­stuffs according to their power of preventing rickets :

Preventing Rickets. Cod-liver
oil. Whole milk. Butter.

Slight Preventive Action. Olive
oil Peanut oil. Lard.

Cotton-seed oil. Lean meat.

No Preventive Action. White
wheat bread. Oatmeal. Rice.

Separated milk. Yeast.

Orange juice. Linseed oil. Vegetable
margarine. Calcium phosphate

lime salt). Sodium chloride. Milk protein.

The fats preventing rickets correspond to the good fats, and the fats
not preventing rickets to the bad fats for A-vitamin (see p. 49).

Rickets developed soonest in the fastest growing puppies, and sometimes
disappeared as the puppies grew older without any change in the diet. These
observa­tions accord with the history of rickets in children; the disease is
rare amongst wasted infants; it tends to accompany rapid growth; and may
disappear spontane­ously during the third year of life. The symptoms of rickets
in puppies and children are alike. The puppies' bones are improperly calcified,
the long bones are bent and the ends enlarged (see Figs. 18 and 19). The
rickety puppy is lethargic and seldom barks or plays, just as the rickety child
does not shout or play. Rickety puppies are more easily affected by distemper,
broncho-pneumonia and mange than puppies on a normal diet.

Fig. 18.—Severe
rickets in puppy (Mellanby).

Fig. 19.—X-ray photograph of
wrist-joint of

same puppy (Mellanby). Reproduced by kind permission from the Lancet, 1920,
i, 860.

RICKETS                                    81

Exercise was found to delay the onset of rickets in poorly-fed puppies.
Puppies kept in confinement on a " good " fat diet showed no signs of
the disease. Con­finement or lack of
exercise are therefore only of secondary
importance, contrary to the
belief of Paton and Findlay of Glasgow, who still believe that any child or
animal kept without exercise will develop rickets, however good the diet. As
Mellanby has pointed out, if lack of exercise were the cause of rickets how
easy it would be to stamp out the disease. It would be absurd to attribute the widespread epidemic of rickets in Central Europe following the War to any want of
exercise; neither has there been any deterioration in the general hygienic
conditions to account for this increase. The exercise of a healthy infant
consists of a number of small movements carried out continually during waking
hours; it could only be restricted in the infant by binding it hand and foot.

rickets were produced by confinement in stuffy and insanitary rooms, the disease
should be very prevalent in the island
of Lewis in the Hebrides,
where many of the people live in what are called " black houses,"
built with very thick walls of turf and stones with thatched roofs. There is
often neither chimney nor window; the smoke from a continually burning peat
fire has no outlet except by the door, which may open directly into the
cow.byre,; chickens have the run of the house and get on the beds,' dressers
and tables. The babies are seldom or never carried out, and remain in this atmosphere
until they can run out by themselves. Yet the infant death-rate in Lewis is
extraordinarily low, only about 40 per thousand as compared with 100 to 300 in
large towns. Rickets is practically unknown in Lewis, and the inhabitants in
general have perfect teeth, though presumably tooth­brushes are not in daily
use. The common food-stuffs are fish, oatmeal and egg; the oily liver of the
fish is a favourite dish mixed with oatmeal and milk and cooked in cod's heads,
one head for each member of the family. The diet is thus rich in food
containing A-vitamin.



During the course of Mellanby's experiments upon puppies, Mrs. Mellanby
made a parallel series of observa­tions on the effect of the various kinds of
fat upon the development and health of the teeth. The animals had the basal
diet already described (p. 79).

On the diet containing cod-liver oil, at the termination of the
experiment (age about six months), all the " milk " teeth were
changed and the permanent teeth developed in perfect condition.

On the diet containing butter, the results were not quite so good; at
the end of six months some milk teeth still remained in the jaw, all the
permanent teeth had not erupted and their enamel was slightly defective.

On the diet containing linseed oil, the change of teeth was still
further delayed and the enamel was dark brown in colour.

It may be noted that in all cases the food was of a pappy consistency. The softness of our food is commonly
as the cause of defective teeth, but from these experiments the
texture of the food appears to be of no importance. The conclusion was that
good teeth were formed if the food contained cod-liver oil or butter, but that
if the diet contained only food-stuffs poor in the antirachitic factor, there,
was delay in the shedding of the first teeth and in the formation of the
permanent teeth. The diet affects the structure of the teeth from within, and
they are then easily infected from the outside later.

Stefansson, the Arctic explorer, has stated that dental caries (decay)
was practically unknown in Iceland
before 1850. The diet then consisted chiefly of milk, mutton, fish, fowl, eggs
of wild birds, carrageen moss and occa­sionally turnips and potatoes. Cereals
and sugar (foods deficient in the A-factor) were introduced later, and since
they have been in general use decayed teeth have become common. A similar
deterioration was observed in the teeth of the Eskimos in Alaska when their original diet of meat and
fat was replaced by cereals and canned foods.

RICKETS                                  83

We are almost forced to conclude that malnutrition in respect to the
kind of fat is probably the primary cause of rickets and decayed teeth, and
that the antirachitic property of certain fats is due to some still unknown
chemical substance associated with them. There is evidence to suggest that the
antirachitic substance is identical with the A-factor, and this view has been
adopted by the Medical Research Committee in their Report, No. 38.

Rickets has been described in other species of animals. McCollum has
observed signs of the disease in rats kept on a diet containing fat poor in the
A-factor. Pigs are often said by farmers to be rickety; in some cases this
condition in pigs is undoubtedly scurvy and responds to antiscorbutic
treatment. An attempt by Golding, Drummond and Zilva to produce rickets in two
young pigs fed from birth on a rachitic diet failed to produce typical
symptoms. The animals did not grow normally; there was some beading of the
ribs; one animal declined and died; the other declined, but health and normal
growth were restored by the addition of cream to the diet.

Harden and Zilva kept three monkeys for several months on a diet poor in
A-factor. No signs of rickets were observed, but as the animals were about two
years old at the beginning of the experiment they were beyond the usual age for
the appearance of this disease; the monkeys declined and died unless returned
to a normal diet. Mackay fed kittens on a diet deficient only in A-factor. The
kittens became very emaciated and died; there were no definite symptoms of
rickets although there was some abnormality of bone formation at the rib
junctions. The symptoms resembled those of coeliac disease in children, a
condition in which there is a failure to digest fat, arrested growth,
emaciation, distended abdomen and a hankering for food.


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