Medical Mystery of the Placebo

Medical Mystery of the Placebo

By NORMAN COUSINS with SUSAN SCHIEFELBEN

Not long ago, two patients on anti-depressant drugs were each given the same pill, described to them as a new promising preparation.  The first patient was told that the pill would sharply reduce her bleak feeling and help her general physical condition.  The second patient was told that the pill was still experimental, would probably have some adverse side effects, but was worth taking nonetheless.

Each patient reacted in line with the predicted expectations.  How could the same pill produce such different effects?  The pill wasn’t a drug at all, but a placebo—an innocent milk sugar capsule.

The study of this strange-sounding agent [pronounced plahase-bo, from the Latin verb “to please”] is opening vast areas of knowledge about the way in human body heals itself and about the mysterious ability of the brain to order biochemical changes that are essential for combating disease.  In the classical sense, a placebo is an imitation medicine—generally a nocuous milk-sugar tablet dressed up likes an authentic pill.  Today, it is used most often in the testing of new drugs.  Effects achieved by the preparation being tested are measured against those that follow the administration of a “dummy drug,” or placebo.

But today the once lowly placebo is receiving serious attention from medical scholars.  Investigators have found substantial evidence showing that the placebo can actually act like an authentic therapeutic agent.  While the way it works inside the body is still not completely understood, some researchers theorize that placebos activate the cerebral cortex, which in turn may switch on the endocrine system.  Whatever the precise pathways through the mind and body, enough evidence already exists to indicate that placebos can be as potent as—and sometimes more potent than—the active drugs they replace.

It is obviously absurd to say that doctors should never prescribe pharmacologically active drugs.  There are times when such medications are absolutely essential.  But the good doctor is always mindful of their power.  There is almost no drug that does not have some side effects.  And the more vaunted the prescription—antibiotics, cortisone, tranquilizers, anti-hypertensive compounds, anti-inflammatory agents, muscle relaxers—the greater the problem of adverse side effects.

Moreover, studies show that most patients who reach out for medical help are suffering from disorders well within the range of the body’s own healing powers.  The good physician tries to distinguish effectively between the large number of patients who can get well without heroic intervention and the much smaller number who can’t.  Such a physician loses no time in mobilizing all the scientific resources available when they are necessary, but he is careful not to slow up the natural recovery process of those who need his reassurance more than his drugs.  He may, for such people, prescribe a placebo—both because the patient feels more comfortable with a prescription in his hand and because the doctor knows that the placebo can actually serve a therapeutic purpose.

The placebo, then, is not so much a pill as a process.  The process works not because of any magic in the tablet but because the most successful prescriptions are those filled by the human body itself.  The placebo is powerful not because it “fools” the body but because it translates the will to live into a physical reality by triggering specific biochemical changes in the body.  Thus the placebo is proof that there is no real separation between mind and body.  Illness is always an interaction between both.  Attempts to treat most mental diseases as through they were completely free of physical causes and attempts to treat most bodily diseases as though the mind were in no way involved must be considered archaic in the light of new evidence about the way the human body functions.

Placebos will not work under all circumstances.  The chances of successful use are believed to be directly proportionate to the quality of a patient’s relationship with a doctor.  The doctor’s attitude toward the patient and his ability to convince the patient that he is not being taken lightly are vital factors in the treatment of illness in general.  In the absence of a strong relationship between doctor and patient, the use of placebos may have little point or prospect.  In this sense, the doctor himself is the most powerful placebo of all.

How much scientific laboratory data have been accumulated on placebo efficacy?  The medical literature in the past quarter century contains numerous impressive studies, including these three:

·      An anestheologist at Haward is considered the results of 15 students involving 1082 patients.  He discovered that 35 percent of the patients consistently experienced “satisfactory relief” when placebos were used instead of regular medication for a wide range of medical problems, including severe post-operative wound pain, seasickness, headaches, coughs and anxiety.

·      During a large study of mild mental depression, patients who bad been treated with anti-depressants were taken off the drugs and put on placebos.  The patients showed exactly the same improvement as they had gained from the drugs.

·      Eighty-eight arthritic patients were given placebos instead of aspirin or cortisone.  The number of patients who benefited from the placebos was approximately the same as the number of benefiting from the conventional anti-arthritic drugs

Inevitability, the use of the placebo involves built-in contradictions.  A good patient-doctor relationship is essential to the process.  But what happens to that relationship when one of the partners conceals important information from the other?  Is it ethical—or wise—for the doctor to nourish the patient’s mystical belief in medication?  An increasing number of doctors believe they should not encourage their patients to expect prescriptions, for they know how easy it is to deepen the patient’s physiological and phychological dependence on drugs—or even on placebos, for that matter.  If enough doctors break this habit, there is hope that the patient himself will come to regard the prescription slip in a new light.

In the end, the greatest value of the placebo is what it can tell us about life.  For what we understand ultimately is that the placebo is only a tangible object made essential in an age that feels uncomfortable with intangibles.  If we can liberate our selves from tangibles, we can directly connect hope and the will to live to the ability of the body to meet threats and challenges.  Then the mind can carry out its difficult and wondrous missions unprompted by little pills.

When the Curtains of Death Parted

When the Curtains of Death Parted

By MARTIN C. SAMPSON, M.D.

It was a hot Philadelphia summer day, and the air in the old Pennsylvania Hospital hung heavy and still.  I had been up all night in a vain fight to save a little girl from meningitis.  In reaction of her death I was feeling completely disheartened.  As a young intern I had seen so much of dying in the past months that life seemed fragile and meaningless.  I was face to face with cynicism.  Faith seemed to exist only to be mocked by death.

The first patient I was to examine that morning was a man I shall call John Bradley.  He was in his late 40s, with deep-set brown eyes and a gentle face.  During the few weeks since his admission his condition had declined steadily.  As I looked through the window of his oxygen tent I saw that his lips were blue, his breath fast and strained.  I knew that his heart had been weakened by rheumatic fever in his youth, and that in recent years hardening of the arteries had taxed it even more.

I couldn’t help thinking of his wife, a small, white-haired woman with a face in which the shadows of work and sorrow mingled with faith and trust.  She and her husband had constantly looked to me for help.  Why, I thought bitterly, did they ask so much of me?

I went over Bradley’s medications again in my mind, hoping to think of something new to relieve his suffering.  He was getting digitalis to control his failing heart, an anti-coagulant to prevent the formation of clots in its damaged wall, and injections to help rid his body of excessive water.  The amount of oxygen being pumped into his tent had been increased.  This day, as on many previous days, I inserted a needle to draw off any fluid that had accumulated in his chest.  Still, when I left him I had the feeling that all my efforts were fruitless.

Shortly after six o’clock that evening the nurse in charge of Bradley’s ward called me to come at once.  I reached his bed within seconds, but already his skin was ashen, his lips purple and his eyes glazed.  The pounding of his heart could be seen through the chest wall, and the sound of his breath was like air bubbling through water.

“One ampoule of lanatoside C and start rotating tourniquets, quickly,” I said to the nurse.

Intravenous lanatoside C would give the rapid action of digitalis.  The tourniquets would keep the blood in his legs from circulating and temporarily relieve the failing heart—but only temporarily.

An hour later Bradley began to breathe more easily.  He seemed aware of his surroundings and whispered, “Please call my family.”

“I will,” I said.

He closed his eyes.  I was just leaving when I heard a deep gasp.  I wheeled and saw that he had stopped breathing.  I put my stethoscope to his chest.  The heart was beating, but faintly.  His eyes clouded over, and after a second or two his heart stopped.

For a moment I stood there, stunned.  Death had won again.  In that moment I remembered the little girl who had died the night before and a wave of fury came over me.  I would not let death win again, not now.

I pushed the oxygen tent out of the way and started artificial respiration, meanwhile asking the nurse for adrenalin.

When she returned, I plunged the syringe full of adrenalin into the heart.  Then I whipped the needle out and listened through my stethoscope again.  There was no sound.  Once more I started artificial respiration, frantically trying to time the rhythm of my arms to 20 strokes a minute.  My shoulders were aching and sweat was running down my face.

“It’s no use,” a flat voice said.  It was the medical resident, my senior. “When a heart as bad as this one stops, nothing will start it again.  I’ll notify the family.”

I knew he had the wisdom of experience, but I had the determination born of bitterness.  I was desperately resolved to pull Bradley back though the curtains of death.  I kept up the slow rhythmic compression of his chest until it seemed so automatic it was as if a force other than myself had taken over.

Suddenly there was a gasp, then another!  For a moment my own heart seemed to stop.  Then the gasps became more frequent.  “Put the stethoscope in my ears.” I said to the nurse, “and hold it to his chest.”  I kept pumping as I listened.  There was a faint heartbeat!

“Oxygen!”  I called triumphantly.

Gradually the gasps lengthened into shallow breaths.  In a few minutes Bradley’s breathing grew stronger and so did his heartbeat.

Just then the screen around the bed was moved slightly, and Mrs. Bradley stood beside me.  She was pale and frightened.  “They told me to come right away.”

Before I could answer, Bradley’s eyelids quivered.  “Helen,” he murmured.

She touched his forehead and whispered.  “Rest, John, dear—rest.”

But he struggled for speech.  “Helen, I told them to call you.  I knew I was going.  I wanted to say good-bye.”

His wife bit her lip, unable to speak.

“I wasn’t afraid,” he went on painfully. “I just wanted to tell you—“ he paused, his breathing heavier,”—to tell you that I have faith we’ll meet again—afterward.”

His wife held his hand to her lips, her tears falling on his fingers.  “I have faith, too.”  She whispered.

Bradley smiled faintly and closed his eyes, a look of peace on his face.

I stood there, filled with a mixture of exhaustion, wonder and excitement.  The mystery of death was right on this room.  Could I, in some way, begin to understand it?  I leaned forward and very softly asked, “John, do you remember how you felt?  Do you remember seeing or hearing anything just now, while you were—unconscious?

He looked at me for a long moment before he spoke.  “Yes, I remember,” he said.  “My pain was gone, and I couldn’t feel my body.  I heard the most peaceful music.”  He paused, coughed several times, and then went on: “The most peaceful music.  God was there, and I was floating away.  The music was all around me.  I knew I was dead, but I wasn’t afraid.  Then the music stopped, and you were leaning over me.”

“John, have you ever had a dream like that before?”

There was a long, unbearable moment; then he said, with chilling conviction, “it wasn’t a dream.”

His eyes closed, and his breathing grew heavier.

I asked the ward nurse to check his pulse and respiration every 15 minutes, and to notify me in case of any change.  Then I made my way to interns’ quarters, fell across my bed and was instantly asleep.  The next thing I heard was the ringing of the telephone beside my bed.

“Mr. Bradley has stopped breathing.  There is no pulse.”

One glimpse of his face told me that death had won this time.

Why, then, had the curtains of death parted briefly to give this patient another few minutes on earth?  Was that extra moment of life the result of chance chemical factors in his body?  Or did it have a deeper, spiritual meaning?  Had his spirit been strong enough to find its way back from death just long enough to give message of faith and farewell to his wife?  Could it also have been meant to give a small glimpse of eternity to a troubled and cynical young intern?

Whatever the meaning, and whether of not it had a purpose, the incident made a deep impression on me.  This was my first step toward acceptance of certain mysteries as an essential part of life.  This acceptance, the gift of a dying patient whom I could not save, put me on the road back to faith.

Can Science Produce Life?

Can Science Produce Life?

By RUTHERFORD PLATT

For years scientists have carried on a wave of unprecedented laboratory experiences to test their theories of how life on Earth began.  The results have been amazing.  Retracing the probable steps by which the raw, lifeless elements of space became organic matter, they now have produced primitive cell-like structures that have many of the properties of living cells.  Here is the dramatic story:

When Planet Earth was born it slowly cooled to form a hardened crust of black volcanic rock.  In time, masses of silicon mixed with mineral elements were squeezed to the surface by the pressures of internal fires, and crystallized as big islands of granite, which formed the foundations of continents.  The whole crust heaved and bulked, cloudbursts drenched the rocks, and sterile water collected in wide depressions to form the earth’s first seas.  Countless volcanoes and fissures continuously gushed methane, steam, ammonia and perhaps carbon dioxide, to give the earth its first atmosphere.  That ‘air’ contained the four chief elements of life—carbon, oxygen, hydrogen and nitrogen.  But they were in the form of gases deadly to present-day life.  Moreover, the atmosphere was flooded with ultraviolet radiation and stabbed by incessant lightning.

How, in this elemental turmoil, did life on earth begin?  Many have tried to supply the answer.  Among the first was Anaxagoras of Greece, who in the fifth century B.C. declared that life comes down to earth in raindrops, in the form of spermata [little seeds].  Came the 20^th century, and the origin of life was still a mystery.

Then in 1924 the Russian scientist A.I.Oparin stated that life might have arisen out of inanimate matter in a prolonged process of ‘preorganic evolution.’  He showed how, in theory, atoms of carbon, oxygen, hydrogen and nitrogen could have formed molecules basic to life, even under the raw, inhospitable conditions of the primordial earth—and how self-reproducing clusters of these molecules might have adhered together and then evolved toward more complex forms.

Three years later the English biochemist J.B.S.Haldane wrote that although such substances would be destroyed by microorganism, “before the origin of life they must have accumulated till the primitive oceans reached the consistency of hot, dilute soup.”  And when the ultraviolet light radiated the surface of this soup, inorganic compounds would have been converted into organic molecules—molecules containing carbon.  At once time scientists believed that only living things could produce such organic molecules.

By the 1050s the scene was shifting from the theorist’s armchair to the laboratory, where scientists were striving to demonstrate that the molecular constituents of life could have emerged under primordial condition.

Using the cyclotron at Berkeley to create high-energy particles to represent cosmic rays, Dr. Melvin Calvin of the University of California bombarded a mixture of carbon dioxide and water vapor; ingredients he thought likely to have been present in the earth’s ancient atmosphere.  Some organic compounds were formed.

Dr. Harold C. Urey, atomic scientist then at the University of Chicago, reasoned that methane, ammonia and hydrogen were probable constituents of the original atmosphere.  What would happen, he wondered, if these raw lifeless substances were placed in a flask and then stabbed repeatedly by electric flashes to represent lightning?  In 1953 his student Stanley L. Miller performed this now classic experiment.  To their delight, they found that amino acids had been formed.

Amino acids are the building blocks of protein and hence of all life.  They are also believed to have been involved in the first stage of the evolution toward life.  The theory is this:

The colossal retort of the primordial earth must have yielded myriads of molecules as ephemeral as bubbles.  But, because of their peculiar molecular structure, the molecules of amino acids are especially stable.  The four elements of life—carbon, oxygen, hydrogen and nitrogen—are assembled in every amino-acid molecule into two opposing groups so well-matched in their electrical charges that they are stabilized like wrestlers locked in equal combat.  Thus the tenacious amino acids could have survived in the chaos to become an early link between no-life and life.

In experiments that followed, a surprising fact turned up.  The basic molecules of life could also have been produced by many other forces in those fierce, elemental times, including X rays, cosmic rays, ultraviolet light and volcanic heat.

After the creation of amino acids, two even larger problems remained.  Giant protein molecules, discovered everywhere in living things, are made of long chains of amino acids.  How did the amino acids get hooked up into these long chains?  And then how did these twisted protein giants turn into living cell?

Giant proteins are fantastically elegant structures—“the noblest piece of architecture produced by nature” in the opinion of biologists.  One molecule of the vital protein of blood, hemoglobin, for example, has 8954 atoms fitted together in a dazzling pattern.  The problem is that all the complicated proteins in life around us—living cells create those, which make flesh, blood, bone, hair, eggs, milk, seeds, and feathers—.  Those living cells in turn are made of protein.  How could protein be created in the first place, when there were no living cells?

This question is puzzling many scientists around the world.  No one has yet developed a foolproof theory that explains which steps came first of what triggered them.  One line of reasoning, first put forward by Dr. George Wald of Harvard, is that there may be conditions occurring in nature in which amino acids might themselves furnish the answer.  And so they did—quickly and beautifully—when the stage was set for them by Dr.Sidney W. Fox, then of the Institute of Molecular Evolution in Miami, Florida.  The “miracle” occurred when amino acids were permitted to dry out.  The thinking was that solutions of amino acids, billions of years ago, had puddled in warm, dry spots.  What would happen to such solutions today if the water was allowed to evaporate?  The scientists who watched this experiment saw a marvelous event.

As the spot on the warm test tube dried, its amino acids formed long, submicroscopic thread-like structures.  These chains some with hundreds of little molecules jointed end to end, were named proteinoids.  The sum of their electric energies endowed them with power to bend and fold!

There are 20 kinds of amino acids common to the proteins of life, and the precise order in which these are lined up in the chains spells what their protein creates—flesh of bone, hair of feather.  The scientists have been able to manufacture all these amino acids under presumed primordial conditions.  Dr. Kaoru Harada was able to synthesize 14 in a single experiment.

So the answer to one question is found.  Amino acids by themselves can produce primitive protein-like material under certain conditions—no need for a cell to help them.

Still, the final question remains.  How could these proteins from a living cell, with its millions of atoms and molecules carefully arranged in a precise pattern?

The primitive proteins came long before living cells appeared.  The precisely ordered proteins of present-day plants and animals would have acquired their amino-acid arrangement in the course of many millions of years of evolution.  Dr. Calvin estimated that molecular life must have evolved for two billion years before the first living cells appeared.

Duplicating this great leap, making a whole living cell in the laboratory, may take a while.  But it now appears that we’ve begun.  The most striking experiment, which has produced crude cell-like spheres that maintain their identity and are capable of dividing themselves, is truly fantastic and has taken us a giant step along the pathway toward understanding the origin of life.

Again, Dr. Fox did the experiment.  To reconfirm his laboratory findings, he climbed up the broad slope of a cinder cone in Hawaii, looking for spots where conditions might have permitted primitive proteins to form in the pre-life world.  He was surprised to discover that large areas of the cone were oven-hot just beneath the surface.  Might not this warm primitive earth have been the womb of the molecules of life—where they could bake and boil, before being washed through the loose lava by a cloudburst and so into the sea?  What would this have done to the elemental amino acids?

Dr. Fox took hunks of lava back to the laboratory and placed on them amino acids coined from methane, ammonia and water.  With everything sterilized to avoid contamination, he baked this concoction for a few hours in a glass oven at 338-degree F., the temperature he found four inches under the surface of the cinder cone.  When the materials cooled, a brown, sticky residue was left clinging to the lava.  He then deluged the lava with sterile water, and a brown soupy liquid resulted.

This unpromising stuff turned out to be very exciting.  As seen through an ordinary optical microscope a wonderful galaxy of spheres swarmed across the field of vision.  The amino acids had first united to make proteinoids—and then these had combined to form little spheres!  Dr.Fox named these fascinating strangers ‘microspheres’.n  they looked like, in many ways behaved like, and were the same size as certain simple bacteria, and they clung together in chains as do the one-celled blue green algae.  Bacteria and blue-green algae are two of the most elementary forms of life that exist on earth.

Although these spheres are not true cells—they have no DNA genes and they are simpler than any contemporary life—they do possess many cellular properties.  They have stability: they keep their shapes indefinitely.  They stain in the same way as the present-day protein in cells, an important chemical test.  But the real significance of these micro spheres is that scientists did not synthesize them piece; they simply set up the right conditions—and micro spheres produced themselves.

In the meantime, scientists working independently in other laboratories are making DNA and other essential constituents of the living cell could have formed.  It becomes hard to avoid the premise that life is inherent in matter, and that life will exist on other planets whenever the conditions are right.

Wonder of the Firstborn

Wonder of the Firstborn

By LAURIE LEE

She is, of course, just an ordinary miracle, but she is also the particular late wonder of my life.  This girl, my child, this parcel of will and warmth, was born last autumn.  I saw her first lying next to her mother, purple and dented like a bruised plum.  Then the nurse lifted her up and she came suddenly alive, her bent legs kicking crabwise.  Her first living gesture was a thin wrangling of the hands accompanied by a far-out Herbridean lament.

This moment of meeting seemed to be a birth time for both of her first, my second life and us.  Nothing, I knew, would be the same again, and I think I was reasonably shaken.  Then they handed her to me, stiff and howling.  I kissed her, and she went still and quiet, and I was instantly enslaved by her flattery of my powers.

Only a few weeks have passed since that day, but already I’ve felt all the obvious astonishment.  Newborn, of course she looked already a centenarian, exhausted, shrunken, bald, tottering on the brink of an old crone’s grave.  But with each day of survival she has grown younger and fatter, her face filling, drawing on life, every breath of real air healing the birth-death stain she had worn so witheringly.

The rhythmic tides of her sleeping and feeding spaciously measure the days and nights.  Her frail self-absorption is a commanding presence, her helplessness is strong as a rock, so that I find myself event to her silences as though some great engine were purring upstairs.

When awake, and not feeding, she sports and gobbles dryly, like a ruminative jackdaw, or strains and groans and waves her hands about as though casting invisible nets.  I see her hauling in life, groping fiercely with every limb and muscle, working blind at a task no one can properly share, in darkness where she is still alone. Each night I take her to bed like a book and lie close and study her.  Her dark-blue eyes stare straight into mine, but off-center, not seeing me.  Already, I suppose, I should be afraid for her future, but I am more concerned with mine.  I fear perhaps her first acute recognition, her first questions, and the first man she makes of me.  But for the moment she stares idly through me, at the pillow, at the light on the wall.

Meanwhile, as I study her, I find her early strangeness insidiously claiming a family face.  Here she is, brand-new, my daughter whom I must guard.  A year ago this space was empty; not even a hope for her was in it.  Now she’s here with our name upon her, and no one will call in the night to reclaim her.  She will grow, learn to run in the garden, run back and call this home.  Or will she?

All those quick lively tendrils seem so vulnerable to their own recklessness—surely she’ll fall on the fire or roll down some crevice or kick herself out of the window?  I look at those weaving hands and complicated ears, the fit of the skin around that delicate body, and I realize I’m succumbing to the new-parenthood shakes.  My daughter is so new to me still that I can’t yet leave her alone; I have to keep digging her out of her sleep to make sure that she’s really alive.

Her face is a sheaf of masks, which she shuffles through aimlessly.  I watch eerie rehearsals of those emotions she will one day need, random, out-of-sequence, but already exact, automatic, yet strangely knowing: a quick pucker of fury, a puff of ho-hum boredom, a beaming after-dinner smile, perplexity, slyness, a sudden wrinkling of grief, pop-eyed interest, fat-lipped love.  Ever since I was handed this living heap of expectations, I can feel nothing but simple awe.

What have I got exactly?  And what am I going to do with her?  And what for that matter will she do with me?

I have got a daughter, whose life is already separate from mine, whose will already follows its own directions, and who has quickly corrected my woolly preconceptions of her by being herself.  I am merely the keeper of her temporary helplessness.  With luck, she can alter me; indeed, is doing so now.  She will give me more than she gets, and may even later become my keeper.

But if I could teach her anything at all, by unloading upon her some of the ill-tied parcels of my years, I’d like it to be acceptance and a holy relish for life.  To accept with gladness the fact of being a woman—when she’ll find all nature to be on her side.  If pretty, to thank God and enjoy her luck.  To be willing to give pleasure without feelings loss of face, to prefer charm to the vanity of aggression, and not to deliver her powers and mysteries into the opposite camp by wishing to compete with men.

In this way, I believe—though some of her sisters disapprove—she might know some happiness and also spread some around.

And, as a brief tenant of this precious and irreplaceable world I’d ask her to preserve life both in herself and others.  To prefer always Societies for the Propagation and Promotion of rather than those for the Abolition or Prevention of.

I’d ask her never to persecute others for the sins hidden in herself, nor to seek justice in terms of vengeance; to avoid like a plague all acts of mob righteousness and to accept her frustrations and faults as her own personal burden, and not to blame them too often, if she can possibly help it, or young or old, whites of blacks, East, West, Jews, Gentiles, television or bingo.

For the rest, may she be my own salvation, for any man’s child is his second chance.  In this role I see her leading me back to my beginnings, reopening rooms I’d locked and forgotten, and stirring the dust in my mind by re-asking the big questions—as any child can do.  With my tardy but bright-eyed pathfinder I shall return to that wood which long ago I fled from but which together we may now enter and know.

How I Beat the Tyranny of Cataracts

How I Beat the Tyranny of Cataracts

By EARL SELBY with MIRIAM SELBY

Two summers ago, I noticed deterioration in the vision of my right eye.  A tennis ball, when seen through this eye for backhand shots, was a blurry blob until it was almost on top of me.  At night, the lights of oncoming cars splattered into distracting shears of glitter.  I could read a newspaper only I held it close to my nose.

Although I felt no pain, I went to see an ophthalmologist.  Placing a corrective lens in front of my right eye, he asked me to read the wall chart.  What chart?  Not one letter was visible.  After a through examination, he said, “You have a cataract.”  I didn’t exactly know what a cataract was, but the diagnosis quickly sharpened my interest.

A cataract, I learned, is a cloudiness of the eye’s lens that occurs when the lens’s clear protein becomes opaque.  Normally, light rays pass through the cornea to lens, which focuses the rays on the retina, triggering the impulses we translate into sight.  A cataract impedes vision by preventing rays from reaching the retina.

Cataracts are among the worlds leading causes of blindness.  They can appear in one of both eyes, at any age and may be congenital, trauma0induced or, most commonly, associated with aging.  The National Society to Prevent Blindness estimates that 44 million Americans age 40 and over has cataracts.  Fortunately, only a small percentage has vision sufficiently impaired that they must have the lens surgically removed—the single cure.  In the United States, there are about 400,000 cataract operations a year.

Medical wisdom used to caution against surgery until cataracts were ‘ripe,’ or matured into grayish, hard kernels.  But this was not necessarily the best time for patients, struggling with failing sight for years while awaiting the operation.  Today, however, cataract victims almost always have the option of scheduling the operation at their convenience, when impaired vision forces significant changes in life-style.

I saw the shadow of my cataract everywhere—on my reading, driving, recreation and job.  Once the cataract was diagnosed, I had to stop flying an airplane, which is essential in my work; I could no longer pass the pilot’s medical examination.  I needed surgery; the only available treatment for cataracts.

Vaguely, I recalled horror stories of cataract operations in which patients were hospitalized for weeks, eyes bandaged, heads locked in sandbags.  A neighbor of mien who had twice undergone cataract surgery eased my fears.  He said modern techniques could reduce hospitalization to a day or two.

Somewhat relieved, I considered the options I’d have after surgery.  Once a clouded lens is removed, something must be substituted to focus light rays on the retina.  Cataract eyeglasses or contact lenses are the traditional alternatives.  But each has definite limitations for certain people.

On being introduced to thick cataract eyeglasses, most patients feel they have moved into the fun house’s crazy-mirror room.  Parallel lines bend.  Door frames bow inward.  Floors are wavy.  Peripheral vision is severely restricted.  The eyeglasses magnify about 30 percent, meaning they can’t be worn when one eye is normal.

Contact lenses, which cause a 6 to 10 percent enlargement, are compactable with a normal eye, but can be difficult to manage, especially for anyone with shaky hands, arthritis or poor coordination.  Patients with dry eyes or allergies also have difficulties with them.  Most contacts must be taken out daily for cleaning, and to rest the eye.

To escape either of these choices, a growing number of cataract victims—approximately 100,000 in the United States last year—are turning to intraocular lenses [IOLs].  Pioneered in Europe, IOLs duplicate nature’s way of creating sight: a plastic lens surgically implanted in the eye gives vision [essentially no magnification] 24 hours a day and never has to be touched, adjusted or cleaned by the patient.  Still, because implants require additional surgical steps, they do involve greater risk of complications than simple cataract extractions coupled with spectacles of contacts.

IOLs are not for every eye.  It takes a skilled ophthalmologist to ascertain when IOLs are advisable, and a well-trained surgeon to implant them.  In general, IOLs are not recommended for relatively young patients.

In September 1979 the National Eye Institute sponsored a Consensus Conference to determine guidelines for the use of the intraocular lens.  Participating ophthalmologists, research scientists, consumers and others recommended that, in general IOLs be used in elderly patients.  They also suggested that use be restricted to one eye unless special needs of the patient indicated otherwise.

Before deciding on an IOL implant, I sought information everywhere, especially since the ophthalmologist I consulted had shown no enthusiasm for the technique.  I again talked with my neighbor, who had implants in both eyes and could read without glasses.  He mentioned friends who also had good vision with IOLs.  I talked with his ophthalmologist, Dr. Steven G. Cooperman of Beverly Hills, California.

Also, I asked a neurosurgeon friend to refer me to other ophthalmologists.  One said that implant techniques were steadily being improved and lens designs refined; he considered implants safe.  Another said that he did not perform implants.  That was not surprising.  Until the 1970s, implants weren’t used much by U.S. doctors, and not all ophthalmologists are trained to do implants. [Others feel they cannot conscientiously recommend them because of the greater risks.]

I read everything I could from the Food and drug Administration, including what was to me a rather scary statement explaining why the agency is investigating the safety of IOLs.  May be implants are too dangerous, I thought, and began to waver.  Then I came across an article in the FDAs “Drug Bulletin.”  It said there was “widespread acceptance” of IOLs by doctors, adding that 3000 ophthalmologists in 2500 U.S. hospitals were doing implants.  That certainly did not indicate gloom and doom.  I could not believe that one in four ophthalmologists would be inserting IOLs if there were an intolerably high risk.

So, in august 1978, I elected to have an implant and went to Dr. Cooperman.  Within three weeks of my original cataract diagnosis, I was in a hospital, prepared for the operation.

There are several methods for removing cataracts; the surgeon chooses the procedure best suited to the patient.  In one method, the ‘intracapuslar” extraction, the entire lens and its surrounding capsule are taken out.  Although this means a relatively large incision [half an inch or so], the procedure is quick and is used by most ophthalmologists.

In my case, Dr. Cooperman went to and “extracapsular” extraction.  Looking through a microscope, he cut an eighth-of-an-inch incision at the outer edge of the cornea and lifted the corneal flap out of the way.  He then separated the lens nucleus from its capsule and cased the nucleus through the pupillary hole into the eye’s front chamber.  Then he inserted a hollow titanium needle, and with high-frequency sound vibrations softened and liquefied the cataract.  ] NewYork’s Dr. Charles Kelman developed this process, called phacoemulsification,] the fragments were removed by suction through the hollow needle, along whti the front portion of the lens capsule, leaving its back in place.

From among the many styles of implant lenses, my surgeon had selected a two-looped Binkhorst type [named after Cornelius Binkhorst, a Dutch doctor famous for his implant surgery.  To insert a quarter-inch plastic disc into my eye, Cooperman first widened the corneal incision to accommodate the lens.  Them be maneuvered it into place and anchored it by slipping under iris the two plastic loops extending from its sides.  The wound was stitched shut, the eye medicated and patched.  The surgery had taken 21 minutes.

The patch came off the next morning, and after 20 hours in the hospital I was discharged.  Three rules were lay down: prescribed drops three times a day for a month; don’t strain in heavy lifting; sleep for several nights with the eye covered by a protective shield.

How was my sight?  Blurry.  Although I could work and read with my good eye, I was worried.  I would stare at digital clock, wanting to strangle the numbers into recognizable shapes.  I tested the implanted eye continually.  One night a star I had not previously been able to make out suddenly popped into view.  It was my own personal miracle.

The blurriness gradually tapered off until the eye just had double vision.  Tennis court No. 2 was 22. On the second post-surgery visit to my doctor he found minuscule swelling around the sutures, which was pulling the cornea slightly out of shape and causing the dual images.  This is not unusual.  Once he had snipped three stitches to relieve the pressure, my vision cleared.  With a corrective lens, my eye tested 20/20.  Absolutely normal!

At the 1979 international symptom of the American Interlobular Implant Society, I heard Miami’s Dr. Norman S. Jaffe, a veteran of more than 4000 implants, report that 90 percent of his IOL patients got essentially normal vision, good enough at least for a driver’s license.  ‘Most of the remaining 10 percent had other conditions that prevented a similar degree of improvement].  He contended that good surgeons, using high-quality IOLs, have the same success rate.

The society’s president, Dr. Robert C. Drews of St. Louis, declared, “IOLs have come of age.”  Referring to the continuing FDA investigation, which after one year of monitoring all implants found no reason to suspend the procedure as unsafe, Drews called IOLs an “overwhelming success.”

Since I am in the FDA study, let me add some details.  One year after the surgery, my implanted eye tested 20/15 with ordinary glasses—better vision than I’d had in years.  For distance vision, I am 20/20 without glasses.  My new driver’s license says I do not need corrective lenses.  And the Federal Aviation Administration has approved me once again to be a plot.  One surgeon has an apt expression for all this.  He calls it IOL.  “Happiness factor.”

The Disease That Always Killed

The Disease That Always Killed

By GEORGE H. WHIPPLE, M.D., as told to J.D.RATCHLIFF

It was a pure horror of a disease.  It started innocently enough.  Victims noted that everyday chores tired them more than usual.  Soon they were finding difficulty rising from a chair.  Their skin took on a waxy, yellowish cast; tongues became flaming red and sore.  Some sufferers became addle-headed; a few went on to paralysis.

Pernicious anemia was a leisurely killer.  It might take two to five years to claim its victims.  But, eventually, all died.  When they finally expired, blood counts were often down from a normal five millions red cells per cubic millimeter of blood to a watery 500,000—not enough to carry the needed amount of oxygen around the body.  Slowly, tissues and organs were asphyxiated.

Physicians fought futile battles against this doom.  A mysterious poison was killing some thought the red cells off.  Others made a better guess; that the bone marrow, which manufactures red cells, had, for unknown reasons, forgotten how to produce the trillion new cells needed each day.  Still others believed that the spleen played some role in the disease and that its surgical removal would help.  Such patients did well for a while, and then began slipping again.  Whatever the treatment, the end result was always the same: death.

The conquest of this disease was, I believe, one of the first instances in medical history in which a universally fatal illness was converted into a minor inconvenience.  Today, tens of thousands of people live normally with pernicious anemia, scarcely aware that they have it.  Here is the story of how this came about.

Both my grandfather and father had been country doctors in New Hampshire, and I was tempted to follow in their footsteps.  But, while studying at Johns Hopkins, I became interested in pathology; the study of disease itself.  Blood in general, and the anemias in particular, fascinated me almost from the start.  I studied the anemia, which accompanies hookworm disease, and observed tropical anemia in Panama in 1907 while the Panama Canal was under construction.  Opportunity to get at the problem in a concentrated way came in 1914, when I was invited to San Francisco to head the new Hooper Foundation, the research arm of the University of California’s Medical School.

The anemia, of course, is a wide spectrum of diseases, and even in those days most of them were curable.  But pernicious anemia was different.  The normal lifespan of a red blood cell is 120 days.  As each dies, it must be replaced—ten million are needed each second.  In pernicious anemia the new cells were not produced in adequate number.  It seemed obvious to me that the only source of building material for red cells was food, and I blocked out a study along these lines.

The first step was to produce artificial anemia in dogs.  Form neck artery I intermittently withdrew blood until the level of hemoglobin—the vital red coloring matter in blood cells—was 40 to 50 percent below normal.  [The procedure, incidentally, did not seem to bother the animals at all.]  Then various diets were tried to see which, if any, hastened production of new red cells.

At this point a compact, blond young woman appeared in my lab and demanded a job.  German-born Frieda Robscheit—later she would Americanize her name to Robbins—was absolutely determined.  ‘I am going to work with you, whether you like it or not,” she said.  I hired her, and she turned out to be one of the finest collaborators any researcher can ever had.

Our first problem was to devise a basal diet for our dogs, one that would provide essential nourishment but would be the poorest possible for building blood.  Then we would supplement this diet with various foods to see which would hasten production of red cells.

Months, years, passed.  Thousands of red-cells counts were made as the work crawled methodically along.  Scores of foods were tried as blood builders—milk, eggs, lettuce, Naturally, we also tried a variety of meats.  A slaughterhouse near the lab furnished whatever we required in this line; spleen, pancreas, bone marrow, brains, sweetbreads.  And in time an extraordinary performer emerged.  It was liver in as little as two weeks liver restored low-red-cell dog blood to normal.  We found it difficult to believe that any food could act with such speed and efficiency.

But our work was by no means completed.  If liver was to be the hero in conquering anemia, the fact had to be nailed solidly down—which meant trials on many more dogs, with time of recovery exactly measured.

In 1921, I moved to Rochester, New York, to become dean of a medical school then being started.  As soon as the new laboratory was ready, Frieda Robbins came east by train, accompanied by our kennel.  Finally, in 1925, we felt confident enough to report: “Liver feeding remains the most potent factor for the sustained production of hemoglobin and red cells.”  Now, somebody else had to extend our findings to treatment of pernicious anemia in human.

Dr. George R. Minot of Hayward was one of the very finest in Boston medicine.  Tall, rail-thin, fastidious, reserved, he was totally dedicated to his patients.  When he heard of our work on dogs he determined to try liver on his pernicious anemia cases.

Not at all well himself—he suffered from diabetes—he enlisted the help of a younger colleague, dr. William P.murphy, then at Peter Brigham Hospital.  The two almost literally stuffed their patients with all the liver they could get down protesting gullets.  Sometimes Murphy mixed ground raw liver with orange juice and poured this in.  Patients in a coma got ground liver via stomach tube.

The response was almost beyond belief.  Within a few days, patients looked better, felt well, and their red-cell counts were climbing.  May be these people weren’t doomed after all!

On May 4, 1926, Minot, in his flat New England voice, read a paper before his peers at the annual meeting of the Association of American Physicians.  He reported that he and Bill Murphy had stuffed 45 patients with liver.  Some had had blood counts lower than on million, now all but one had near normal counts.  That one was an elderly lady who so despised liver that she said she preferred death to eating it.  Most of the other patients were up and about—no longer breathless, no longer weary.  Most were back at normal occupations.  Minot’s report was acclaimed by a standing ovation.

Ata hospital in Boston next morning, doctors were preparing to give an elderly man a transfusion—the only thing that had kept him barely alive for several years.  “Why not just let me die?” the weary sufferer asked.  A young doctor burst in.  “Did you see the morning paper?” he asked.  A news report had summarized Minot’s paper.  Liver diet was started immediately, and within a week the patient had new life in his limbs.

Such events were soon being enacted all over the world.  A year later, Minot and Murphy reported on 105 patients.  There had been three deaths: one in an auto accident, one from cerebral thrombosis, one from unknown causes—but none from pernicious anemia.

In 1934, Minot, Murphy and I received identical cablegrams from Stockholm.  We had been accorded medicine’s highest honor, the Nobel Prize.

A way had been found to rescue the doomed—but the story was still by no means complete.  Even at outset it was clear that it wasn’t liver that was working such wonders, but some elusive X substance in liver.  The problem was to get rid of useless components and concentrate on the substance.  Dr. Edwin J. Cohn, the gifted Howard chemist, took this job upon himself.  Soon he had an extract, one tablespoon of which was the equivalent of half a pound of liver.  Next came an injectable liver extract 400,000 times as potent as the mother stuff; a short every two to four weeks was sufficient to keep blood normal.

The search for the X substance came to an end at last in 1948, with the cornering of Vitamin B12.  An invisibly small amount of it—a millionth of a gram a day—was sufficient to control a disease once totally deadly.

Pernicious anemia, which had probably plagued man from the beginning, at last could be rendered harmless.

New Hope for Retarded Children

New Hope for Retarded Children

By SARA D. STUTZ

Jordy is mongoloid.  When he was born, the pediatrician suggested that his parents put him in an institution.  Fortunately for Jordy, his parents ignored the doctor’s advice and took him home.  Within a few months they enrolled him in the Infant Development Program of the Exceptional Children’s Foundation in Los Angeles.  At three, he’s functioning so well that he has been accepted in a pre-school for normal children.

·       Linda, normal at birth, suffered massive brain injury in an auto accident when she was sent to Lanterman State Hospital in Pomona, California, where her parents expected her to be a crib case for the rest of her life.  But now, through special sensory motor training, Linda is learning to walk and talk again.  She’ll never return to normal, but she’ll soon function in a manner her family can manage at home.

·       At nine months, Christy was hospitalized with malnutrition and other evidences of parental neglect.  She was unresponsive and slow for her age.  Now, enrolled in the developmentally delayed infant education project at the Nisonger center in Columbus, Ohio, she is, at 13 months, feeding herself, crawling, and trying to talk.  It looks as if Christy is going to catch up.

Jordy, Linda and Christy aren’t miracle babies.  They are typical of the youngsters being served by infant intervention programs, a new and highly promising concept in education.  “With early intervention, many developmentally delayed children may be entered in regular classes of helped so that their disabilities require less extensive special services,” said James J. Gallagher, former associate commissioner of education for the handicapped, at HEW.

There are an estimated 2.2 million retarded persons in the United States. Dr. GeorgeTharjan, professor of physiology at ULCA, testifying before President’s Committee on Mental Retardation, estimated that as many as 50 percent might have been classes as “normal,” had they had the benefit of early training.  Not only could they be leading more satisfying lives, but also society could be spared the expense of their lifetime institutional care.  The cost of such care for a person from age six can be $300,000 to $1.5 million.

Babies learn from experience.  If they can take in what’s happening around them, and if their surroundings contain an average amount of stimulation, they develop to their full potential.  But, if their ability to absorb their environment is limited, they don’t get the experiences they need for mental development.

“Any infant suffers is his original capacity to inquire, to seek, to explore, is stifled.  Sterility of the early childhood environment, especially the absence of daily conversational exchange with the mother and others in contact with the infant, seems to impose a permanent limitation on intelligence,” noted John W. Kidd, former president of the Council of Exceptional Children.

When a profoundly retarded infant is put in a crib and given only the necessary custodial care, as was common practice until recently, he merely lies there, explains Clara Lee Edgar, the physiologist who developed a training program a lanterman State Hospital.  He has no way of making anything happens.  He cannot learn anything.

But if that same child is taken out of the crib and strapped t a scooter board on wheels with his toes hanging down on the floor, he can, with the slightest amount of wiggling, make the board move.  He seems to say to himself, “Hey, I can go somewhere.”  In subsequent periods on the board he learns to scoot across the room.  Eventually, he begins to hold his head up while doing it and even use his arms and hands to guide him.  He’s having experiences that will increase his intelligence.

Now, with the new intervention programs, which have sprung up in the past 15 years, babies with developmental delays, are being helped to have the experiences they need to make mental and physical progress.  Most programs are open to any developmentally delayed baby—a preemie, the baby having difficulty relating to people, the child of overanxious parents, the slow walker—not just children with known physical of mental impairment.

Babies enter programs through a verity of channels.  Some, usually low-birth-weight preemies or babies who have experienced unusual difficulties at birth, become part of a program while in the newborn nursery.  Many are referred to programs by their pediatricians or public-health nurses because of obvious medical conditions such as Down’s syndrome [mongolism], hydrocephaly [enlargement of the brain because of an abnormal drainage of cerebral fluid], microcephaly [abnormally small skull] of spina bifida [open spine].

Babies who have developmental problems evident at brith may cry all the time or they may be very ‘good.’  They might not cry or fuss for attention for a verity of reasons.  Without being neglectful, a mother would leave such a child in the crib all day except for feeding and changing him.  Yet this is the baby who most needs an environment that provides a maximum of social and sensory experience.

Directors of infant programs usually request mothers to bring their babies once a week to a center where special equipment is available, and where trained personnel can show them how to teach their babies.  Group activities are offered when babies are old enough to work on the self-help and language skills necessary for entry into pre-school.

At the Early Childhood Intervention Center in Dayton, Ohio, I followed a group of seven Mongoloid youngsters, one and-a-half to three years old, through a morning’s activities that would be almost unbelievable to the person conditioned the think of Down’s Syndrome as a totally incapacitation handicap.  After a period of free play with specially chosen toys to improve coordination, the children sang songs that helped them to identify their own names.  Then they divided up, one group going to draw with crayons and play simple ball games while the other had a lesson in identifying colors and matching shapes.  At snack time, all the children fed themselves.  In half-hour discussion periods, the mothers were told what the children would be learning next and how to reinforce it at home.

Rural areas, as well as cities, can have such special services.  In 1969, the Office of Special Education and Rehabilitation, part of the Department of Education, provided fund to develop a model rural program in Portave, Wisconsin.  “We expected the first to build a special school and bring in children for classes,” said David Shearer, director of the project.  “But we soon rejected that.  The area we’re responsible forcovers 3600 square miles of farms and villages.  Since youngsters with prblems may live 100 miles apart, we use ‘home trainers’ instead.”

The home trainers—women who either have had instruction in special education or are paraprofessionals—come once a week for an hour-and-a-half lesson.  They show parents how to conduct similar lessons the other days of the week, and leave any equipment that is needed.  Results?  The average child in the Portage project gained 13 months in an eight-month period.

Lanterman State Hospital at Pomona, California, is showing that there is no level at which children are ‘hopeless.’  Severely retarded youngsters—ones who are often crib cases for life—are trained so well that they can often return to their families.

Therapists are talking severely retarded children through the developmental stages that the normal child experiences.  For a verity of reasons, the retarded youngster cannot effectively use his body to deal with the world around him.  Research has shown that by improving his balance and other sensory motor skills the child can be helped toward more normal behavior.  I watched the most advanced group go to the dining room for lunch, where one bright-eyed little girl carefully set the table and served the rolls to her classmates.  It was hard to imagine that she had been a crib case.

Will the community be ready to accept these children?  The teachers and parents I talked with said yes, if the public is given adequate information about developmental problems.  I heartily agree.

My youngest child, Eric, is afflicted with Down’s syndrome.  He has been a much-loved member of the family ever since he was born.  Friends and acquaintances with which we have openly discussed his condition are interested in his development and are rooting for him in a truly heartwarming way.

Several years ago, when Eric was hot quite three, I took him on one of our routine trips to the supermarket.  I held his hands as he walked into the store for the first time.  As we passed through the turnstile, we were startled by the sound of loud applause.  The checkers were clapping for him and his small chest swelled with pride.

At that moment thought of what might have been crossed my mind.  Even with early stimulation and training, Eric is slower than the ‘average’ mongoloid child.   He could easily be a hopeless, unreasoning hospital patient instead of a lively happy little boy embarking now on a program of special public education.  Where he was born and the kind of advice we were given have made that much difference in his life.

The Miracle of Muscle

The Miracle of Muscle

By J.D.RATCLIFF

Events that take place when a dog wags its tail, a baby toddles across the floor or you scratch your nose with your forefinger dwarf in complexity the workings of a hydrogen bomb.  All are examples of muscular contraction—so commonplace we pay it no heed, yet so mysterious that it has baffled the most gifted scientists.

More than half of the human body is muscle—“the most remarkable stuff in nature’s curiosity shop,” as one scientist had said.  From birth to death, muscles play a critical role in everything we do.  They propel us into the world in the first place—when the womb suddenly empties itself.  They provide nearly all our internal heat.  They push food along the digestive tract, suck air into lungs, and squeeze tears from lachrymal glands.  And finis is written for fails and us when the heart muscle, after beating two and half billion times in a 70-year life span, flatters.

We speak of “muscles of iron.”  Yet the working or contractile element in muscle is a soft jelly.  How this jelly contracts to lift 1000 times its own weight is one of the supreme miracles of the universe.  An elaborate series of chemical and electrical events, which would require hours of days to duplicate in the laboratory, occur almost instantaneously when a muscle contract—the twitch of an eyelids, for example.

There are three types of muscle in the human body.  One is the striated muscle, which looks like a sheaf of hair-sized filaments.  These are the muscles of motion—that propel us when we walk, that lift a forkful of food, that nod our heads.  Next come the “smooth” muscles.  These control such involuntary actions as the churning of intestines during digestion, the dilation of the pupil.  A third type is found in the heart.  In structure, it is midway between the other two.  All types of muscle are startlingly efficient machines for converting chemical energy [food] into mechanical energy [work]. 

Hundreds of books and scientific papers have been written on muscles—but none explains fully the process by which muscles contract, how you wiggle a tow.  “It is essential that we understand these puzzles,” said Dr. Albert Szent-Gyorgyi, Nobel Prize winner and scientific director of the National Faundation for Cancer Research.  “In one was or another, failure of muscles to contract porperly accounts for the vast majority of deaths—from heart failure, high blood pressure and other diseases.”

It is the riddles such as these that Dr. Szent-Gyorgyi and his co-workers went years seeking to solve.  Fiber by fiber and molecule by molecule they have taken muscles apart, and then fitted them together again trying to discover the mechanics of muscular action.

Research suggests that muscle is never thoroughly relaxed.  Because it is partially tensed—something like a taut spring—it is ready for almost instantaneous action when an electrical message from the brain orders it to contract.

TWP proteins, Dr. Szent-Gyorgye has found, are mainly responsible for the contraction—actin and myosin.  Alone, neither is contractile.  But when an electrical impulse from the brain orders the batting of an eye, or the wrinkling of a nose, actin and myosin combine to form actomyosin, which is contractile.

In a sense of actomyosin is the muscular ‘engine.’  Its fuel is a remarkable chemical substance, adenosine triphosphate—ATP for short.  ATP is a submicroscopic bombshell of energy.  Actomyosin fibers contract violently on contact with it.  At death, ATP disintegrates rapidly and muscles become hard, inelastic.  This is rigor mortis.

To demonstrate the critical importance of ATP, Dr. Szent Gyorgyi stored rabbit muscles, which had been washed free of the chemical, in freezers for periods up to a year.  Taken out, thawed and touched with ATP, the hard, brittle muscles spring to life; once again they show the elasticity they had when they propelled a rabbit in its hopping gait.

Creating ‘living’ tissue in the laboratory has been something of a scientific will-o-the-wisp.  But muscle researchers have come close to it.  Dr. Szent-Gyorgyi mixed jelly-like actin with jelly-like myosin.  Then, with the aid of a tiny glass nozzle, he spun this material into gossamer filaments.  Watching through a microscope, he added a droplet of ATP to the fluid surrounding the filament.  There was violent contraction!  He had created artificially perhaps the most fundamental of all life processes—muscular contraction.  “It was, “he says, “the most exciting moment of my life.”

Where are such experiments leading?  They may open a new frontier of attack on some of mankind’s greatest ills.  There is no logical reason why the human heart should beat two billions times during a lifetime, the suddenly fail.  Almost nothing is known about the cruel crippling of muscular dystrophy; or why muscles in blood-vessel walls should tighten to produce the misery of hypertension; of why the uterine muscles of many women become crumply contracted each month to cause painful distress.  Once the mechanics of muscular action are thoroughly understood, we may be at the beginning of a new biology, a new medicine.

Meanwhile, there is a great deal all of us can do to keep our muscles functioning well.  First, they must be promptly fed.  Generally speaking, the average diet includes all the protein needed for muscle repair, and all the carbohydrate required for muscle fuel.  But muscles can starve through lack of exercise—witness hospital patients who eat perfectly balanced meals and get out of the bed too weak to walk.  Reason: muscles are nourished by thousands of miles of hairline capillaries, which transport food and carry off wastes.  In the sedentary adult, large numbers of these capillaries are collapsed, out of business, nearly all the time.  Exercise alone can open them up and provide better muscle nutrition.

A number of studies have shown the beneficial results of exercise on the heart muscle.  A study in London bus drivers, for example, showed that drivers, who sat all day, had far more heart trouble than conductors, who were constantly on the move.  Similar checks have shown office workers more prone to heart disease than postal workers.

Often, muscles become unduly fatigued when required to work at too fast a rate.  One housewife rushes at her chores and is worn out by noon, while her more leisurely sister accomplishes just as much and finishes the day still fresh.  A series of treadmill experiments tells why.  In one, subjects were paced at 140 steps a minute.  Gradually speed was increased to 280.  At the doubled rate, oxygen requirements of muscles increased eightfold supplying such demands are fatiguing in it.  All work and exercise should be paced to get the most of our muscles.

Like all other body organs and tissues, muscles must have rest.  Millions of people sleep the traditional eight hours, and then get up exhausted.  The most likely explanation: one set of muscles has been cramped, tensed all night—wearing out the rest of the body.  The best way to avoid this is to become acquainted with your own muscles.

Lie quietly in bed, legs straight, and arms at the side.  Contract one set of muscles at a time, and consciously relax them.  Start with the feet and work upward.  In a matter of minutes, real relaxation can be achieved—leading to more restful sleep.

Overburdened or weakened muscles sometimes require additional support.  This is particularly true of the back muscles, whose chief function is to hold the body erect.  Often, low-back pain can be traced to weakness of these muscles. Every physician has his favorite set of exercises to provide new strength.  But until exercises are well under way, extra support is sometimes necessary.  A strong extra-wide belt is useful for this purpose.

It is best, of course, not to wait until muscles are weakened before giving them the care and consideration they deserve.  For, to a great degree, we are what our muscles make us—sick or well, vigorous or droopy, alive or dead.