Nutritional Diseases

It should be clear to everybody that too little food will result in starvation and that in most cases too much food will cause obesity, and also that both of these conditions are menaces to health. It is still a matter of argument as to whether or not obesity should be called a disease. In this book we shall consider it as such, because it paves the way for many other more serious dis­eases and because even without any other disease it often causes discomfort and reduces physical efficiency.

Nearly all nutritional diseases, how­ever, are deficiency diseases not nec­essarily from a limited total quantity of food, but from a shortage of certain food constituepts, usually vitamins, sometimes minerals, occasionally pro­teins. On the other hand, a harmful excess of either minerals .r vitamins, though uncommon, could cause nutri­tional disorders.

For instance, large doses of vitamin D sometimes pre­scribed in medical treatment have in some cases seriously upset calcium me­tabolism in the body. Excessive vita­min A has also proved harmful.

Vitamin deficiency diseases are col­lectively called avitaminoses. Discus­sions of avitaminoses will comprise the bulk of this chapter, but a few other diseases with a nutritional basis will be included. Then, in the latter half of the chapter, problems aid diseases of metabolism will be discussed, the term metabolism including the several proc­esses by which the body assimilates nutrients.

Avitaminoses
VITAMIN A DEFICIENCY.
A mild deficiency of vitamin A tends to produce roughness and dryness of the skin. A greater degree of deficiency increases this tendency and causes damage to the epithelial tissues of the body, which become more susceptible to infection.

In later stages, severe in­fections of the mouth, the genitourinary tract, the respiratory organs, and the eyes are likely to occur. The eye infection often develops into, or in connection with, a serious condition called xerophthalmia, which may lead to blindness. Another common effect on the eyes is a loss of ability to see in dim light, a condition called night blindness.

What to Do
1. Include more vitamin A in the diet. It may be convenient to take some oil rich in vitamin A, such as cod-liver oil or halibut-liver oil. Vi­tamin A is also available in purified form and may be taken as such.
2. It is best to consult a physician, especially if eye symptoms are trou­blesome. He can advise as to what to take, how much, and how long to continue the treatment; and he can give, or arrange for giving, such spe­cial treatments as the eyes may need.

VITAMIN B DEFICIENCIES.
The so-called vitamin B complex consists of four separate vitamins: thia­mine (vitamin B1), riboflavin (vitamin B2), niacin or nicotinic acid, and vita­min B12. Likewise, there are four sepa­rate nutritional problems in this area, each associated with a deficiency of one of these vitamins. There are two other B vitamins, folic acid and pyro­doxine, each with its associated nutri­tional problems.

A. Thiamine (Vitamin B1) Defi­ciency. The disease beriberi is the most common manifestation of serious thia­mine deficiency. It is characterized by an inflammation and degeneration of nerve trunks, producing disturbances of both motion and sensation. There is loss of appetite. The patient becomes weak, especially in the legs. His mus­cles tend to waste away. Partial paraly­sis and a tendency to dropsy are com­mon. The nerves controlling the heart action may be badly affected, and heart failure and sudden death may result.

Beriberi occurs most frequently among people whose diet consists mostly of polished rice, but anybody who lives chiefly on highly refined starchy or sugary foods may get it. It may develop in infants, especially those nursed by mothers who have the dis­ease. If the disease is not far advanced, correction of the diet usually will bring about rapid and complete recovery. If the neuritis has continued until the nerve trunks have degenerated, how­ever, normal motion, sensation, and heart action can never be restored.

Wernicke's syndrome is also a condi­tion caused by a deficiency of thiamine. It occurs most commonly among heavy users of alcohol. It is characterized by a clouded mental state, weakness of the muscles which move the eyes, unsteadi­ness, and deterioration of many of the nerves (peripheral neuritis) .

What to Do
Correct the diet. No other remedy or treatment can do much good. Thi­amine abounds in the outer layers of the grains of rice, wheat, and other cereals. Fresh milk, eggs, brewer's yeast, concentrated yeast extracts, and malt extract also contain gener­ous amounts of thiamine. Fresh fruits and vegetables are helpful. Among flesh foods, liver is best.

B. Riboflavin (Vitamin B2) Defi­ciency. Riboflavin deficiency is likely to cause visual disturbances, eye pain in bright light, an overflow of tears, and redness of the eyes. Perhaps the commonest signs are wrinkling, moist­ness, and fissures of the skin at the an­gles of the mouth. The tongue tends to be unnaturally red. Loss of weight and vigor are common. B2 deficiency is often associated with B1 deficiency, giving a somewhat confusing picture. When either deficiency seems to be present, look for signs of the other.

What to Do
1. See that the diet contains ade­quate milk each day, and plenty of eggs and green vegetables.
2. In severe cases consult a physi­cian. He will probably prescribe liver extract or tablets of riboflavin, among other things.
C. Niacin Deficiency (Pellagra) . One characteristic sign of pellagra is a pe­culiar skin eruption. The eruption looks much like a bad case of sunburn, with considerable cracking, crusting, and scaling, and occasionally some small blisters. It usually appears on the ex­posed areas of the skin, such as the backs of the hands and wrists, the face, and the neck, less frequently on the legs and ankles, and occasionally on the external genitals. The upper edge of the eruption usually has a- well-de­fined border, giving rise to the descrip­tive term "glove-like" when it occurs on the hands and wrists. Exposure of the skin to sunlight is believed to stim­ulate the appearance of the eruption.

People with pellagra usually have capricious appetites and frequently di­gestive disturbances. Diarrhea is com­mon. A victim's tongue usually looks abnormally smooth and deep red. Pa­tients are often addicted to alcohol, and about one in fifty of them will probably eventually have mental disturbances severe enough to amount to true de­mentia.

Many of them are troubled with such nervous symptoms as weak­ness, dizziness, insomnia, and distur­bances of the sense of touch.A correct diet will cure most cases of pellagra, but a pellagrin who continues to drink alcoholic liquor will be hard to cure. The cure is usually complete, ex­cept in those cases that have resulted in insanity; and even in them the mental condition is often much improved.

What to Do
1. In the acute stage of the disease there should be bed rest. The diet should consist of milk, vegetable pu­rees, tomato juice, and soft-boiled or poached eggs. Yeast extract broths can be given with benefit.
2. If diarrhea is troublesome, give a teaspoonful of bismuth subcarbo­nate in water every three or four hours.
3. Lanolin to which 5 percent of boric acid powder has been added will help soothe the skin eruption.
4. When the acute stage of the dis­ease is past, the chief remedy is still the diet. It should include a quart of milk a day and plenty of eggs and green leafy vegetables. Lean meat is allowable, but fat meat is valueless. The milk may be fresh, dried, canned, or buttermilk. Brewer's yeast or some concentrated yeast ex­tract will prove helpful.

The following foods are all low in or almost devoid of niacin: corn and all products made from it, molasses, potatoes, carrots, yellow turnips, rice, ripe onions, most animal fats, cotton­seed oil, and gelatin. In parts of the country where people live wholly or chiefly on foods in this list, pellagra is common.

5. Alcoholic beverages should be left alone.
6. In severe cases the services of a physician are advisable.

D. Vitamin B12 Deficiency. A de­ficiency of B12 is the cause of perni­cious anemia. This problem is discussed in detail in the consideration of blood diseases in chapter 10 of this volume.
Persons who eliminate all animal products from their diet, including dairy products, are particularly likely to de­velop a deficiency of vitamin B12 with symptoms of pernicious anemia. Treat­ment consists of including milk and eggs in the diet and using vitamin B12 supplements.

E. Folic Acid Deficiency (Megalo­blastic Anemia of Infancy and of Preg­nancy) . Folic acid, one of the group of B vitamins, is an important and widely distributed vitamin which occurs abun­dantly in many vegetables. Long-con­tinued cooking of food is progressively destructive to folic acid.
Deficiency of folic acid occurs com­monly among persons who are mal­nourished and produces a form of anemia very similar to pernicious ane­mia. The megaloblastic anemia resulting from a deficiency of folic acid is most likely to occur under conditions in which the body requirement for folic acid is greater than usual: in infancy and during pregnancy.

The megaloblastic anemia of infancy typically occurs between five and eleven months of age, a period of rapid growth. Infants who were born pre­maturely and those who have had re­peated infections of the gastrointesti­nal organs are particularly susceptible. The condition may be easily confused with that caused by a deficiency of vi­tamin B12. It is important to avoid such confusion, for the cure of this condition depends specifically on the administra­tion of folic acid.

Megaloblastic anemia of pregnancy (pernicious anemia of pregnancy) ap­pears in about one percent of preg­nancies during the last three months, at a time when the personal require­ments for folic acid are increased be­cause of the rapid growth of the un­born child.
The administration of tablets of folic acid, under a physician's direction, brings about a dramatic cure in almost all cases.

F. Pyridoxine (Vitamin Bs) Defi­ciency. Pyridoxine is another member of the vitamin B group. Symptoms of this deficiency are particularly impor­tant in infancy and early childhood, when they consist of convulsions. They develop in infants who have received formulas in which the milk or the ce­real has been "over processed," pro­longed processing having depleted the vitamin.

What to Do
There is an adequate quantity of pyridoxine in human milk, also in cow's milk and in cereals if these lat­ter are not over processed.
For the immediate treatment of convulsions due to a deficiency, an intramuscular injection of pyridox­ine gives prompt relief. For in­fants who seem to be in danger of this deficiency, the physician will ar­range for small doses of the vitamin to be added to the diet.


VITAMIN C DEFICIENCY (SCURVY).
A person with scurvy tends to be­come weak and anemic, to have spongy gums and loosening teeth, and to be subject to hemorrhages, especially about the joints and beneath the skin. The joint hemorrhages cause severe pain and sometimes lead to a mistaken diagnosis of arthritis or rheumatism.

The spongy gums may bleed easily, be­come ulcerated, or become the seat of infection. In case the patient suffers a wound, the wound heals slowly.
A baby that is developing scurvy will be pale and stop gaining weight. The slightest bruise of its skin will result in a black-and-blue spot. Its gums will not make much trouble until the teeth begin to come through. The pain and swelling of the joints will likely be se­vere and cause the child to be irritable and to cry a great deal.

In scurvy, either in babies or in older people, correction of the diet brings about almost miraculous improvement. Pain may disappear within a day or two, and all other symptoms within a week or two. The same diet that will cure scurvy will prevent it. A person who takes a properly balanced diet will never have this disease.

What to Do
1. For a baby with scurvy, give fruit juice. Orange juice is good, but lemon, grapefruit, or tomato juice may be used instead. Fruits and green vegetables should be added to the baby's diet as soon as it can take them.

2. For an older child or an adult, be sure there are plenty of green vegetables and fruit in the diet. Ad­ditional fruit juice may be helpful. Some very good sources of vitamin C are citrus fruits, strawberries, canta­loupes, tomatoes, green peppers, and raw cabbage (especially green cabbage).

VITAMIN D DEFICIENCY (OSTEOMALACIA, RICKETS).
Rickets develops almost exclusively among young children, though its ef­fects may persist throughout life. Os­teomalacia is a similar condition some­times seen in adults. Rickets is most common between the ages of six months and eighteen months.

It can be caused by a deficiency of calcium, phosphorus, or vitamin D in the diet. The vitamin D deficiency, however, is more common than the mineral defi­ciency. Calcium and phosphorus are the chief mineral elements in the framework of the body. Vitamin D is necessary for the work of building these elements into bones and teeth, and vitamin C helps it in this work.

The earliest symptoms of rickets are restlessness, irritability, and sweating of the head. Then the joints between bone and cartilage at the front end of the ribs begin to enlarge, forming two rows of hard nodules, one row begin­ning a short distance from each side of the upper end of the breastbone and running obliquely downward and side­ways to the lower border of the ribs. These nodules can be easily seen in thin children with rickets, and they may be felt in those who appear to be well nourished.

The child's head gradually takes on a somewhat square shape. The fonta­nels, or "soft spots," in the top of the skull may remain open long after they should be closed. The bones that form the wrist joints, and often other joints, are softer and larger than they should be. The child with rickets is fre­quently bowlegged, though sometimes knock-kneed, and becomes even more so when he begins to walk.

His abdo­men may protrude markedly and his bowels be constipated. If his blood is tested, it will be found below normal in phosphorus or in calcium, but not necessarily in both. X rays of the joints of his limbs will show a characteristic lack of development near the ends of his long bones. Pelvic deformity due to rickets in a girl may persist until ma­ture years, making normal childbirth difficult.

Since skeletal deformity resulting from advanced rickets is in so many cases an incurable condition, preven­tion is of prime importance. If it is not entirely prevented, but detected early, however, a satisfactory cure is not diffi­cult. It is usually easy to obtain a diet containing sufficient calcium and phos­phorus, especially if an ample quantity of milk is available.

Milk is a good source of calcium, contains a consider­able amount of phosphorus, and is a good source of vitamin D if whole milk is used, especially if the cows giving the milk spend a large part of their time out in the sunshine. Egg yolks also furnish good amounts of both phos­phorus and vitamin D.

What to Do
1. Give a child who shows any signs of possible rickets at least a quart of whole milk a day. Milk fortified with vitamin D is now com­mon.

2. From the age of five or six months onward, one egg yolk a day will be helpful.

3. Daily sunbaths are also help­ful. Exposure to sunlight, within reasonable limits, causes the skin to produce a certain amount of vitamin D.

4. Give the child cod-liver oil or some other good source of vitamin D. Begin at three or four weeks of age, giving half a teaspoonful twice a day, and increase gradually to one and a half teaspoonfuls twice a day at the age of three or four months and thereafter. A few drops of hali­but-liver oil or of viosterol may be used instead of cod-liver oil, and this is better for babies who tend to be fat. It is well also to see that the baby's diet is not short of vitamin C. (See above.)

5. Properly graduated quartz-light treatments may take the place of sunbaths.

VITAMIN E DEFICIENCY.
Vitamin E is apparently conducive to health in several rather indefinite ways, but whether or not a deficiency of it will cause disease in human beings has not yet been conclusively proved. Fur­thermore, almost any otherwise well-balanced diet will contain sufficient vitamin E.
VITAMIN K DEFICIENCY.

Vitamin K occurs in sufficient abun­dance in most green leafy vegetables to make any serious deficiency of this vi­tamin rather uncommon. When an insufficient amount of it is eaten or ab­sorbed, however, an increased tendency to hemorrhage develops; and laboratory studies have shown that this tendency is associated with a less­ened amount of prothrombin in the blood.

Hemorrhages due to this condi­tion can often be prevented or checked by injections of vitamin K.
Vitamin K deficiency exists most com­monly in newborn infants or in people with jaundice and whose intestinal ab­sorption of digested food is poor.

At­tention to the diet is usually not enough to correct such a condition in people past infancy because dietary deficiency is rarely the sole cause. Ensuring that a prospective mother's diet contains an abundance of vitamin K is the best way to prevent a deficiency of this vitamin in her newborn baby. If her diet is possibly inadequate in this respect, she should have injections of vitamin K during the last month or two of her pregnancy.

What to Do
If a newborn baby shows tenden­cies to hemorrhage, have a physician take charge of the case immediately. There may be other reasons for the tendency, but injections of vitamin K may prove to be the most helpful remedy.

Other Nutritional Diseases
NONTOXIC GOITER.
NUTRITIONAL EDEMA (FAMINE EDEMA, WAR EDEMA).
Nutritional edema results from long-continued deprivation of protein that is biologically complete. It usually oc­curs in famine areas. The first step in its development is a general weight loss. Later there is water retention, which appears to check the loss of weight but leads to a pitting edema, appearing first in the legs but later spreading upward and sometimes in­volving the entire body.

A variety of nutritional edema fairly prevalent among babies and young children in parts of Africa, Asia, south­ern Europe, and Central and South America, where low protein foods are fed and milk is not available, has been called kwashiorkor. In this disease the liver is enlarged and the pancreatic tis­sue more or less degenerated.

In addi­tion to showing edema, the young vic­tims do not grow well and are irritable and apathetic. Their appetite is poor, and they are troubled with vomiting and diarrhea. They are likely to have skin rashes, irregularity of pigmenta­tion of skin and hair, and ulceration or inflammation about the mouth and eyes. If not treated early and properly, more than half of the victims of kwa­shiorkor die.

What to Do
Provide an abundant diet, other­wise well-balanced, but containing an abundance of protein, a consider­able proportion of which should or­dinarily come from non vegetable sources. The amount needed to cure an adult who has developed nutri­tional edema is from 120 to 150 grams per day. For babies and young children, the most important dietary treatment is to give an abundance of milk and eggs.

Since the disease usually attacks poor people, the expense of provid­ing suitable dietary protein may be an obstacle to effective treatment. In some places a mixture of vegetable proteins has worked well. This should be easier where soybeans are grown or otherwise available, be­cause soybeans are the best known vegetable source of complete pro­tein.

OBESITY.
Obesity is nearly always due to over­eating. There are a few cases—usually in childhood or early youth—in which glandular imbalance plays an impor­tant part. Obesity is objectionable chiefly because it is apparently a pre­lude to many cases of diabetes and heart disease. It makes arthritis of the hips and knees worse because of the abnormally great pressure it puts on the joints and articular cartilages. Dif­ferent people may have other reasons for not wanting to be overweight, but very few have anything reasonable to say in its favor.

What to Do
1. If there is any question about the cause of the obesity, have a phy­sician study the case.
2. If it is clear that overeating is the chief or only cause, reduce the weight to normal.
PERNICIOUS ANEMIA.
SPRUE.
Inborn Errors of Metabolism
A person's characteristics are deter­mined in part by heredity and in part by environment. Heredity gives the in­dividual his start in life and determines physical and mental traits which pro­vide the gross outline of his body and of his personality. The influence of en­vironment is then superimposed on that of heredity to fill in the details.

With respect to disease, there is con­siderable variation in the relative im­portance of heredity and environment. In some diseases the influence of heredity seems to be the main factor, with environment playing the minor role. In others environment plays the major role, with the influence of hered­ity serving only to make the person more or less susceptible to the disease. Under this subhead, "Inborn Errors of Metabolism," we deal with certain faults of metabolism caused essentially by unique heredity rather than by what may have happened to the person since his birth.

DISORDERS IN PIGMENT METABOLISM.
The outstanding example here is the disease porphyria, in which there is a disturbance of the metabolic process by which the body uses the chemical substance known as porphyrin to help build its hemoglobin and some of its other pigments and enzymes. Heredity is blamed for most cases of porphyria. There are various forms of the disease, all resulting in an excess of porphyrin compounds in the urine.

In some forms of this disease there is a sensitivity of the skin to sunlight or to artificial ultraviolet light, with re­sulting skin lesions and abnormal pig­mentation. In one form the patient shows symptoms of abdominal pain, vomiting, and constipation, together with paralysis of certain of the mus­cles. Acute attacks are usually brought on by the use of alcohol, by certain drugs, or by infections.

The treatment consists largely of avoiding alcohol and drugs and of pro­tecting the skin from sunlight.

DISORDERS IN PROTEIN METABOLISM.
Here the example is the disease phe­nylketonuria, the cause of which is he­reditary. The laws of some states now require that tests be made on the blood or urine of newborn infants as a means of detecting this disease in time to pre­vent its tragic complications. The prob­lem occurs in about one child out of every 25,000.

The disease is caused by the lack of an enzyme necessary to the proper syn­thesis of tyrosine (one of the amino acids) within the body. As a result, phenylalanine (a precursor of tyro­sine) accumulates within the body's tissues and fluids and flows over into the urine. The complications of the full-blown disease include damage to the patient's brain with resulting abnor­mal movements and mental retarda­tion.

The treatment, which is quite effec­tive, consists of arranging a diet which contains a minimum of phenylalanine. Obviously, a child with this disease must be under the care of a physician.

DISORDERS IN CARBOHYDRATE METABOLISM.
In this category there are two impor­tant hereditary diseases. First is galac­tosemia. In this disease the infant's body is unable to convert one form of carbohydrate into another (galactose to glucose) because of the absence of the necessary enzyme. An infant with this disease appears normal at birth but after a few days develops difficulty in feeding and begins to vomit. If the dis­ease goes untreated, failure in growth and eventual death from malnutrition will result. Treatment is relatively sim­ple, consisting merely of eliminating from the diet all galactose-containing foods. This means that milk and milk products are strictly forbidden. Even though the patient is still an infant, it will do very well on a properly de­signed diet which provides all the nu­tritional essentials by foods other than milk.

The second disease is glycogen stor­age disease. It is usually fatal within the first year or two of life, for it in­volves an inability to convert glucose to glycogen (two forms of carbohydrate) and vice versa, with the result that ex­cesses of glycogen become deposited in various tissues of the body. Symptoms are fatigability and hypoglycemia (low blood sugar) with resulting shock and convulsions. In some cases the hypo­glycemia can be combated by frequent feedings. If the patient survives the period of early childhood, his condition may gradually improve.

DISORDERS IN LIPID (FAT) METABOLISM.
In hereditary disorders of lipid me­tabolism some patients suffer from an increase in the amount of lipids in the body fluids and tissues, and others from a decrease. Perhaps the most notable disease in this group is essential hyper­cholesteremia (xanthomatosis) .

Here the amount of cholesterol is increased more than the other lipids that nor­mally occur in the body, the amount in the blood serum being perhaps two or three times normal. Swellings pro­duced by accumulations of cholesterol-laden cells (foam cells) occur in the skin (xanthomas) ; in the subcutaneous areas at pressure points such as knees, elbows, and buttocks; in the heart; and in certain tendons. Conditions such as arteriosclerosis and coronary artery disease, which are associated with an increase in cholesterol, are, of course, more frequent than usual in cases of es­sential hypercholesteremia.

These cases are benefited by institut­ing measures which tend to lower the concentration of cholesterol in the blood serum. Of first importance is a diet regimen which excludes the sources of saturated fatty acids such as meat, dairy products, eggs, and the common cooking fats. In their stead the patient may use vegetables and un­saturated fats such as corn oil. In ex­treme cases the physician may pre­scribe one of the cholesterol-lowering drugs.

DISORDERS IN KIDNEY TRANSPORT.
Among the numerous functions which the kidneys have to perform is the recovery from the "glomerular fil­trate" of the chemical substances needed by the body's tissues.
As blood comes into the kidneys for renovation, the waste products to be eliminated from the body plus a great deal of water and such chemical molecules and radicals as glucose, carbo­nate, sodium, chloride, potassium, phosphate, calcium, and sulfate pass through the delicate membranes into the kidney tubules.

All this makes up the so-called glomerular filtrate. But many of these chemicals cannot prop­erly be spared, and so specialized cells which line the kidney tubules reach out and salvage what the body needs as the filtrate passes by.
In the hereditary disorders of kidney transport, the specialized cells of the kidney tubules are defective to the ex­tent that they permit certain molecules or radicals to pass on through into the
bladder.

A notable example of these diseases is called renal rickets. In this condition the cells of the kidney fail to recover as much phosphate as they should from the glomerular filtrate, with the result that the concentration of phosphate in the body's tissues and fluids falls to low levels. Symptoms similar to those of or­dinary rickets develop. But even though the symptoms are similar, this disease typically does not respond to the ad­ministration of vitamin D as ordinary rickets does. The disease usually pro­gresses to a fatal termination.

Diseases of Metabolism
In this group of diseases the metab­olism (transport, synthesis, breakdown, or excretion) of some normal chemical constituent of the body occurs in an ab­normal manner, and this abnormality of metabolism seems to be the primary cause of the illness. The various proc?
esses of metabolism are usually al­tered in other kinds of disease, but in these other instances the metabolic changes are the consequences of the disease rather than its cause.

CYSTIC FIBROSIS.
This is a serious disease of hereditary origin which affects that part of the pancreas which produces digestive enzymes, some of the salivary glands, glands of the respiratory tract, and sweat glands of the skin. The com cations are (1) malnutrition because the deficiency of the pancreatic dig five enzymes, (2) infections of the i piratory organs, and (3) a tendency heat exhaustion because of the ex( sive loss of sodium chloride throe the sweat. The disease typically be in childhood, and many children v~ this disorder do not live to adult With improved methods of treatment the prospective length of life has creased.

What to Do
1. The recommended diet is h in calories, high in protein, and m moderately low in fat.
2. Vitamin A in relative la doses is recommended.
3. Pancreatic extract to sups ment the reduced output of the j creas helps to allay the digest symptoms and improves the patie nutritional status.
4. The control of respiratory fections by the use of antibiotics; other medicinal agents is imports
GOUT.
Gout is mentioned here because fundamental cause is a defect in m, bolic processes with the result 1 deposits of uric acid occur in var: parts of the body, notably in cer joints and in the kidneys. This ca a very distressing type of arthritis. C as a disease is discussed in chapte of this volume.
DIABETES MELLITUS.
Of the two kinds of diabetes, betes mellitus and diabetes insip: diabetes mellitus is by far the common. When a person uses the "diabetes" without qualification, h feres to diabetes mellitus.


This is a disorder of carbohydrate metabolism, with obvious hereditary background in about 50 percent of cases, characterized by the production of large quantities of urine and by ex­cesses of glucose (blood sugar) in the blood and the urine.

It used to be assumed that the fun­damental cause of diabetes mellitus is a deterioration of the islets of Langer­hans in the pancreas, the cell groups which produce insulin. When the pan­creases of persons who have died from diabetes mellitus are examined, in many cases there is an obvious deteri­oration of the islets of Langerhans.

Strangely, however, in some cases no such deterioration can be detected. This observation together with other significant items of evidence has per­suaded medical scientists that the dis­ease is not always caused by difficulty in the pancreas itself. Other circum­stances within the body's tissues can also interfere with the metabolism of carbohydrate. For this reason our dis­cussion of diabetes mellitus is included here with diseases of metabolism rather than in the chapter on "Endocrine Gland Diseases."

Diabetes mellitus is not only a se­rious disease but a common one, oc­curring sometime during the lifetime of 4 percent of females and 2 percent of males in the United States. The onset may be at any age. Usually the disease first becomes apparent following some major demand on the body's resources such as severe injury, a serious infec­tion, or a circumstance of emotional stress. The incidence of diabetes melli­tus is higher in overweight persons than in people of normal weight.
In diabetes mellitus there is a defi­cit in the storage and release of glu­cose by the liver and an interference with the process by which the body's cells are able to use glucose as their source of energy. A person suffering from this disease must therefore derivemore of his energy from the metabo­lism of protein and fat than is normally the case.

Prior to the days of adequate treat­ment, the mortality rate for diabetes mellitus ran high. Even now for cases which begin in childhood it runs sig­nificantly higher than for those which begin in adult life. For a case in which the disease appeared first in adulthood, the life expectancy can be virtually as high as in a normal person, provided the treatment program is so carefully controlled at all times that the body processes proceed normally.

Symptoms the Patient Notices: When diabetes begins during childhood, the symptoms include excess production of urine, excessive thirst, a desire to void at night, bed-wetting, an increase in appetite in spite of a loss of body weight, weakness, and itching of the skin. For cases which begin during adulthood, the symptoms are excessive production of urine, increased thirst, weakness, and itching of the skin.

What the Physician Finds: When a physician examines a person with dia­betes, he finds sugar in the urine, a higher than normal concentration of glucose in the blood, and evidence (re­vealed by a "glucose tolerance test") that the individual is not using up his blood sugar as quickly, following a meal, as in a normal case. These evi­dences all indicate that the body is un­able to use glucose (the form in which carbohydrate appears in the circulating blood) in a normal manner. In other words, glucose accumulates in the blood and is eliminated by the way of the urine instead of being used in the body for the production of energy.

A tragic feature of diabetes mellitus is that when it goes untreated serious complications develop, thus reducing the patient's life expectancy. One of these is a tendency to early degenera­tion of the body's arteries with arterio­sclerosis developing throughout the body and with the coronary arteries of the heart being particularly involved. Abnormal conditions also tend to de­velop in the nervous system, such as peripheral neuritis, loss of the sense of vibration, and loss of normal control of the urinary bladder. Another compli­cation of inadequately treated diabetes is kidney disease.

A tendency to infec­tion of the skin and other body tissues is much greater than normal. Also ever-present is the danger of a loss of consciousness due to an imbalance be­tween the amounts of insulin and glu­cose in the patient's blood and tissues.

Two situations representing opposite conditions may cause unconsciousness in a case of diabetes. The first develops gradually, when for some reason the glucose in the blood reaches high levels and is not offset by an adequate amount of insulin. This condition is called dia­betic coma. The second may develop quite suddenly, when the patient has taken too much insulin or for some rea­son has depleted the supply of glucose in his blood and tissues so that his blood sugar runs dangerously low, not allowing enough to provide the energy food which his cells need. This condi­tion is called insulin coma or hypogly­cemic shock.
For the emergency treatment of these two conditions, "Handling Emergencies," under Unconsciousness, subsections B and C.

It is because of the lurking danger of insulin coma that a diabetic patient is advised to carry a wallet card or wear a bracelet stating that he is a diabetic, and that if he is found to be acting strangely or if he becomes unconscious, his doctor or an ambulance should be called at once.

The card should also give the follow­ing information: patient's name, ad­dress and telephone number; and phy­sician's name, address, and telephone number.
Diet is perhaps the most important factor in the treatment of diabetes. Many cases, particularly those that de­velop during adulthood, can be han­dled satisfactorily without the use of insulin or other medicines, provided the patient follows a consistent dietary program. A suitable diet for a diabetic patient is relatively normal, with the exception that it does not include the more rapidly absorbed carbohydrates except in small amounts. The special feature in administering the diet is that all portions must be carefully measured so that the patient eats neither too much nor too little. In other words, the various food elements in his diet must be very carefully regulated. It is when a diabetic patient becomes careless in following his diet, by eat­ing more or less of some particular item, that he encounters difficulty.

The second important factor in the treatment of diabetes is the administra­tion of insulin by hypodermic or of one of the newer "hypoglycemic agents" by mouth. Insulin (or its substitutes) is a necessary part of the treatment pro­gram for most juvenile diabetics and for adults who cannot control the con­dition by diet alone. Great advances have been made in the preparation of insulin for use by diabetic patients so that a physician can choose among var­ious products available as he adapts the program of treatment to the needs of the patient.
Once a case of diabetes has been di­agnosed, it is well for the patient to spend several days in the hospital un­der the direct supervision of the physi­cian and of the dietitian. Here he learns how to regulate and control his diet and also how to take his insulin or insu­lin substitutes if this is necessary. His ability to enjoy good health thereafter depends very definitely on his being consistent in following his treatment program. Also, periodic checkups are necessary as a means of measuring his progress and of modifying the treat­ment program to fit changes in his con­dition.

Certain circumstances requiring spe­cial provisions may occur in the ex­perience of a diabetic patient. During pregnancy, for instance, a diabetic pa­tient requires closer supervision than usual. Infant mortality is higher in a poorly controlled diabetic mother. When a diabetic patient must have sur­gery, it is necessary for his treatment program to be altered accordingly and to be regulated very closely, day by day, throughout the period of his sur­gery and recovery. In case an infection develops in the skin or in any other of the body's tissues, the treatment pro­gram must be altered accordingly.
The diabetic patient must regulate the amount of his physical exercise al­most as carefully as he regulates his diet. It is beneficial for him to have some physical exercise each day. Inas­much as the amount of exercise changes his requirements for energy food, the possible consequences of his taking ei­ther too little or too much exercise dur­ing a given period may be just as se­rious as taking too little or too much food.

HYPOGLYCEMIA (LOW BLOOD SUGAR).
Hypoglycemia is the condition in which the amount of glucose (blood sugar) drops below the level of 50 mg. of glucose per 100 ml. of blood. Hypo­glycemia is not a separate disease as such, for it may stem from any one of several causes.
The symptoms of hypoglycemia may follow two patterns, which can occur separately or in combination. First, cer­tain symptoms relate to the nervous system and result from the brain's be­ing deprived of sufficient glucose (en­ergy food) to maintain the normal ac­tivity of its cells. These symptoms may include mental confusion and anxiety,hallucinations, aimless activity, convul­sions, and eventual coma.

Second, other symptoms result from the body's automatic attempt to com­pensate for the lack of blood sugar by producing an emergency supply of epi­nephrine. These include sweating, pal­lor, chilliness, trembling, hunger, weak­ness, palpitation, and faintness.

1'he Causes of Hypoglycemia:
1. Hypoglycemia may result from an overdose of insulin. Insulin has the ef­fect of accelerating the body's use of blood sugar. An overdose of insulin, therefore, reduces the amount of blood sugar available in the blood.
2. A failure to eat the usual amount of food after taking insulin may cause hypoglycemia. In a diabetic patient, the amount of insulin must be carefully balanced against the amount of food the patient is expected to eat in order to maintain the level of blood sugar at its normal. When the patient does not eat this necessary amount of food after taking insulin, the effect is com­parable to that of an overdose of insu­lin, with the result that the blood sugar is reduced.
3. Hypoglycemia may result from excessive exercise by a person not con­ditioned for this overexertion. If the body's sources for replenishing the available supply of blood sugar thus used up are not momentarily adequate, hypoglycemia will result. A person with diabetes mellitus is particularly susceptible in this instance.
4. Hypoglycemia may result from an overproduction of insulin within the body, as in the particular type of tumor of the pancreas in which the insulin-producing tissue becomes overactive.
5. It may develop in cases of liver disease in which the blood sugar is not stored or released by the liver in a normal manner.
6. Hypoglycemia may occur in con­nection with diseases of certain endo­crine organs, as the adrenals and pituitary. Oddly, the "hypo" condition may occur early in the course of diabetes, before the usual "hyper" phase.


What to Do
1. The treatment of an acute at­tack of hypoglycemia will vary de­pending upon whether the patient is in the hospital or must be given emergency treatment elsewhere and on whether he is still able to swal­low or has already lost conscious­ness. When in the hospital, the ad­ministration by vein of 10 to 25 gms. of glucose will usually restore the patient, momentarily, to a rela­tively normal condition. Subsequent treatment is determined by the re­sults of laboratory tests indicating the level of the patient's blood sugar.

When the patient is not in the hospital but is still able to swallow, he should be given any sort of sweet­ened drink, such as orange juice, or its equivalent in candy or sugar. The symptoms of the immediate attack should improve within fifteen min­utes. Then he should eat bread or other food containing starch and protein to provide the necessary source from which his tissues can produce additional glucose.

When the patient is not able to swallow, he may be given sweetened fruit juice or a 5 percent solution of glucose by stomach tube. Prompt effort should be made to secure the services of a physician or to take the patient to the emergency room of a hospital.
2. For cases in which the cause of hypoglycemia may be organic dis­ease of the pancreas or liver, a physi­cian should study the case in order to determine the exact cause and ar­range the treatment accordingly. Sur­gery or other definitive treatment may need to be carried out promptly.
3. For cases of functional hypo­glycemia in which there is no actual disease of the liver or pancreas, an alteration in the patient's diet may correct the tendency to hypoglyce­mia. In such cases, the body's con­trol mechanisms may have become unusually sensitive to the taking of food containing carbohydrate to the extent that insulin is produced in ex­cessive amounts. A helpful proce­dure here is to adopt a diet which is low in carbohydrate and high in protein and fat, thus enabling the individual to derive the necessary amount of calories for his energy needs without overstimulating his own production of insulin.