Emanuel M. Josephson's Nutritional Theory of Myopia

MYOPIA -- ITS CAUSE AND PREVENTION

Near-sightedness, or myopia, owes its origin to the same type of disturbance in the fluid exchange of the eye as does glaucoma. This concept of the origin of myopia differs from that generally accepted; but the large mass of supporting data forces its acceptance and compels the abandonment of the older explanations.

In myopia the eyeball is too long. Parallel rays of light, coming from a distance, are brought to a focus, consequently, before they reach the retina. The victim sees only an out-of focus blur when he looks at a distance. Concave glasses cause the light rays to diverge before entering the eye and serve to bring them ot a focuson the myopic retina, correcting the near-sightedness.

The abnormally long, myopic eyeball is filled with a larger volume of fluid than the normal eye. In the more advanced cases the volume of fluid may be so great as to cause a change in the fluidity of the vitreous humor and a disruption of its structure; and may even go so far as to stretch and rupture the eyeball.

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There is no dearth of clinical evidence that myopia and glaucoma are manifestations of the same underlying disease process. Most rapidly advancing cases of myopia have symptoms during the active stages of progress, similar to those of glaucoma--headaches, pain in the eye, vertigo, halo vision and others. But in the average case of myopia there generally is absent the effects of sustained pressure on the optic nerve which give rise to cupping and attendant loss of field of vision in glaucoma. This difference results from the elasticity and yield of the eyeball in myopia.

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In the myopic eye, the ocular tension, as measured by a tonometer, may be very low. Even during the period of active advance of the myopia, when the amount of fluid in the eye is steadily increasing, the eye is stretching, and symptomes are acute, the tension may be in the range of low normal. Nevertheless, the stretchng of the eyeball is clear evidence that the intraocular pressure exceeds the limit of resistance of the eyeball.

The tissues of the myopic eyeball are weak and distensible, and stretch under the pressure of the circulation of intra-ocular fluids. For the same reason the cornea stretches and dents deeply under the weight of the tonometer. The tonometer reading in a case of myopia is not an accurate guage of intra-ocular fluid pressure. The situation regarding tension in these cases is the same as in the glaucoma cases which never show a rise of tension above normal levels.

The injury sustained by the tissues of the eye in myopia and glaucoma shows differences in character which reflect the difference of stretch of the eyeball. Because of the slight stretch in glaucoma, the optic nerve and other structures in the eye are compressed. In myopia, however, the stretch of the entire eyeball does not result in any such concentration of the damage, except during the periods when the eyeball resists further stretch. The greatest damage to the optic nerve and the most acute symptoms occur at these periods, which are often terminated only by actual interstitial tearing of the tissues in the eye.

THE CAUSES OF NEARSIGHTEDNESS

The usual cause of organic near-sightedness is lengthening of the eyeball caused by increased volume of fluid in the eye. The distrubance of the exchange of water in the body that causes the near-sightedness is not limited to the eyes, but involves all parts of the body. For water constitutes over eighty percent of the weight of all the tissues, and a sdisturbance of its distribution vitally affects every part of the body. Signs of this disturbance can be recognized in every part of the body by the skilled observer.

The mechanism of control of water-exchange in the body is an extremely complicated problem concerning which much is not known. It is known that the glands of internal secretion and the autonomic nervous system play a paramount role in this mechanism. The most significant role, from the viewpoint of near-sightedness, is played by the outer part of the adrenal gland, the adrenal cortex.

The adrenal cortex influences the water exchange of the body by causing retention of salt in the blood. The determining force in the exchange of water between the blood and the organs is their relative salt content. When the salt of the blood is reduced in quantity, water seeps, or osmoses, out of the blood into the organs. Insufficient secretion of the adrenal cortex causes such a disturbance and results in the increased flow of fluid into the eye. Thus is near-sightedness caused.

The eyes have no mechanism for controlling the amount of fluid which flows into them from the blood. They therefore succumb to every disturbance which cases increased seepage of fluid into them. As a result, there deveops stretching and near-sightedness, or increased pressure and glaucoma, or other defects.

THE PREVENTION OF NEARSIGHTEDNESS

The prevention of near-sightedness hinges largely on the prevention of disturbances of the water-salt metabolism of the body. Such disturbances occur most frequently in infacncy, in childhood, and at puberty. As a consequence, the prevention of near-sightedness is best begun in infancy, or even before the birth by the care of the health and diet of the expectant mother.

Malnutrition and defective diets play a large role in causing glandular disorders and the other disturbances which give rise to nearsightedness. A diet which is high in carbohydrates, starches and sugars, and low in proteins and fats, favors the development of near-sightedness. It is probable that such diets are apt to be deficient in vitamins; and that vitamin deficiency aggravates their effects.

Absence of sufficient vitamin A in the diet directly affects the status of the eye tissues. It also serves to destroy vision by depriving it of the light-sensitive visual purple upon which depends the registering of light stimuli.

Absence of the vitamin B factors from the diet, or a deficiency, results, in its extreme form, in a profound disturbance of the water-salt exchange of the body known as beri-beri. Even milder forms of this deficiency may exert profound influence on the optic nerve and vision. It also causes an increased inflo of fluid into the eye which induces either glaucoma, nearsightedness or other eye defects of this group.

Deficiency of any of a whole range of food elements influences the general health and the development of near-sightedness. The inclusion of meat or other proteins, liver, fresh green vegetables, citrus fruit and sufficient table salt, help to protect the child against the development of near-sightedness.

These facts are borne out by a survey of the dietary habits of peoples among whom nearsightedness is most widely prevalent. Port-Ricans who often live largely on a diet of rice and beans show a high incidence of near-sightedness and of other eye defects. The Germans, who present so much near-sightedness, make potatoes rather than protein-containing bread the staple of their diet.

One of the most clear-cut illustrations of the influence of diet on near-sightedness that has come under my observation was the enormous rise in the incidence among the school-children of New York City during the depression. In 1925, it was reported that 25% of the school-childreen attending a group of clinics in New York were afflicted with near-sightedness. With the advent of the depression, the figure rose steadily from over 40% in 1932 to 72% in 1935. Reflecting re-employment and improved nutrition in 1936, the percentage incidence of near-sightedness dropped to about 51%. In 1937, the figure dropped to 42%.

At the same time, I noted and reported a high incidence of day and night blindness among the school-children due to vitamin A deficiency, which previously was supposed to exist only in countries such as China, which suffered from chronic malnutrition. So rare had the disease been regarded by the American authorities that my report, when published in 1934, aroused considerable scepticism until it was amply confirmed by other workers.

In some cases, dietary measures are alone sufficient to prevent the development or to arrest the advance of near-sightedness. Dietary deficiencies arise, however, even in persons who have adequate diets but fail to assimilate essential food factors. This is illustrated by the case of retinitis pigmentosa.

Retinitis pigmentosa has been a blinding disease for which there was no hope. It is characterized by the early development of night-blindness which is followed by progressive and total degeneration of the retina and finally blindness. In the past, it has meant hopeless blindness. Study of the condition led me to feel that the similarity of the night-blindness to that found in vitamin A deficiency showed conclusively that retinities pigmentosa is also a vitamin A deficiency disease. But the feeding of vitamin A brought about absoluetly no improvement in these cases. Nevertheless, I felt certain that my "hunch" was correct. Finally it dawned on me that the vitamin A might not be assimilated when taken by mouth in these cases. To overcome this possible obstacle, I resorted to injection of the vitamin and its precursors into the body muscles. Improvement was startling. Vision was restored to the vitims of retinitis pigmentosa, and another hopelessly blinding disease was conquered. (/Nature/, Jan. 23, 1937)

Reliance, therefore, cannot be placed in the mere presence of vitamins and of other requisite elements in the diet. If near-sightedness and other deficiency-caused defects are to be averted, it must be made certain that the body is properly utilizing those elements.

A word of comment is in order on the denaturing of food by our modern methods of processing. This plays as large a role in the production of near-sightedness as in other diseases.