In this informed but plainly speculative work, the surgeon-author of the well-received Why We Hurt (2000) asserts that biology on the molecular and cellular scales is intelligent. That this opinion is unorthodox is evident in Vertosick's regular asides to skeptics or, as he refers to them, "brain chauvinists." Vertosick's argument rests on two supports: a detailed description of chemical "learning" by bacteria, the human immune system, and enzymes; and a view that these structures behave as networks. A telling weakness to this argument is Vertosick's admission that "[his] belief that network architecture underlies all living systems . . . can't be proven to everyone's satisfaction with the available evidence." Yet his strength is the clarity and energy with which he explains the remarkable adaptability of, for example, bacteria in evolving strains resistant to penicillin--though he would call it "genetic learning" rather than plain old evolution. Even if they don't subscribe to Vertosick's thesis, readers will find much to learn and delight in here. Gilbert Taylor
Copyright © American Library Association. All rights reserved
Review
PRAISE FOR WHY WE HURT
"Writing with eloquence, clarity and wit, Dr. Vertosick has given us a masterful book on a subject of concern to us all."--Rabbi Harold Kushner, author of When Bad Things Happen To Good People
"To my surprise and delight, Dr. Frank T. Vertosick, Jr., a practicing
neurosurgeon, performs a feat of literary alchemy."--Dr. Jerome Groopman, The New York Times Book Review
"Fascinating . . . Falls squarely in the territory of Oliver Sacks."--Newsday
About the Author
Frank T. Vertosick, Jr., M.D., is a neurosurgeon and the author of Why We Hurt and When the Air Hits Your Brain. A former president of the Pennsylvania Neurosurgical Society and a Fellow of the American College of Surgeons, he lives in Pittsburgh, Pennsylvania.
Frank T. Vertosick, Jr., M.D., is a neurosurgeon and the author of Why We Hurt and When the Air Hits Your Brain. A former president of the Pennsylvania Neurosurgical Society and a Fellow of the American College of Surgeons, he lives in Pittsburgh, Pennsylvania.
Excerpt. © Reprinted by permission. All rights reserved.
1THEMICROBIALMIND"...the Martians-dead-slain by the putrefactive and disease bacteria...slain, after all man's devices had failed, by the humblest creatures that God, in his wisdom, has put upon this earth."-H. G. Wells, The War of the WorldsTom was eighty-three years old. He ate sensibly, drank little alcohol, took his vitamins, and walked a local high school track for exercise. His sole vice was smoking: Tom had smoked one cigarette pack every day for over six decades. He had never given much thought to quitting; for most of his life, he felt fine. But tobacco finally exacted a toll on his health in his later years. When he was young, Tom rarely got sick and never missed a day of work because of a cold or flu. Upper respiratory infections were now frequent visitors, each one harder on him than the last. When he arrived in our emergency room one chilly autumn evening, Tom could scarcely breathe. A recent bout of influenza had quickly progressed into bacterial pneumonia. Influenza causes a raw inflammation of the trachea and bronchi, the air passages leading to our lungs. The inflamed surfaces ooze a viscous fluid, which is normally swept upward toward the mouth and nose by the incessant beating of microscopic hairs called cilia. After reaching the upper trachea, the fluid is coughed away. Viruses force us to hack and sneeze our way through our illness so they can spread to new hosts. By expectorating virus-laden fluids at other people, we complete their life cycle. Cigarette smoke kills cilia, leaving denuded airways smooth as porcelain. Unhindered, a smoker's viral secretions slide downhill and collect in the tiny air sacs comprising the lungs. Pooled secretions become contaminated with airborne bacteria, and microbes quickly thrive in the warm, moist darkness. Although the immune system fights back valiantly (more on that in the next chapter), the defenses of elderly smokers can easily become overwhelmed by bacterial growth. So it was with Tom. His body could no longer combat the burgeoning population of bacteria infesting his diseased lungs and he sought the help of doctors, armed with modern antibiotics, to save him. We, his doctors, would wage war on the bacterial cells now fulminating in Tom's body; it would be a war of modern medicine versus ancient, one-celled beasts. Our enemy, cunning and resilient, would not surrender without a fight. Nevertheless, we had the combined genius of the multibillion-dollar pharmaceutical industry in our camp. For Tom, this would be a battle for a single life-his own. For the bacteria, it would be yet another skirmish in their eternal struggle against extinction. Could we, with our human brains, outfox the microbial mind, a vast, global intelligence flowing from the stunning plasticity of bacterial DNA? A better question: does a "microbial mind" exist at all? I say that it exists, for I have felt its presence. We need to leave Tom for a moment and explore our battle against bacteria in some detail. Our chief weapons (besides our own immunity, of course) are antibiotics, substances that kill bacteria or halt their growth by crippling key components in their metabolic machinery; different classes of antibiotics attack different biochemical pathways. In this age of designer drugs, we often forget that the first known antibiotics were natural substances excreted by molds and other simple organisms. Ironically, some antibiotics come from the bacteria themselves. Biologists speculate that bacteria and molds use natural antibiotics to eliminate their competition and establish a foothold in overpopulated environments. Most people are familiar with the legend of Sir Alexander Fleming. In 1928, Fleming, a microbiologist from St. Mary's Hospital in London, discovered that his staphylococcal cultures were being inhibited by mold contamination; he speculated that the mold, a common Penicillium species found in soil, was producing some chemical substance lethal to his staph. By sheer serendipity, Fleming had happened upon one of the miracles of modern medicine. He called his new substance penicillin; the discovery, although monumental, stirred little immediate interest. Years later, a group of Oxford researchers led by Howard Florey teamed with an American pharmaceutical company to isolate and synthesize penicillin in the pure quantities needed for widespread clinical application. Their initial trials were startling: infections once thought to be incurable quickly abated after the administration of concentrated penicillin. The world rightly hailed penicillin as a godsend. The Oxford team didn't invent penicillin-Nature took care of that detail. However, they devised a way of delivering this natural substance into the human bloodstream at an unnaturally high purity and concentration. The bacteria of the world were caught completely flat-footed by this development. To us, purified penicillin was a lifesaver, but to them, our enhanced antibiotics looked more like hydrogen bombs. True, bacteria had long encountered naturally occurring antibiotics, and a few species had even evolved defenses against them. Not surprisingly, antibiotic-producing bacteria proved particularly adept at detoxifying the poisons-spiders rarely get trapped in their own webs. Nevertheless, few bacterial species possessed a good defense against penicillin, and the defenses of those that did proved far too weak to handle the extraordinary doses we could now administer. And we didn't stop with penicillin. Twentieth-century medicine would soon unleash a slew of poisons into the environment, poisons more potent and diverse than anything previously encountered in the microbial world's billion-year history. Bacteria faced a veritable holocaust. Microbial species that succumb to an antibiotic are said to be sensitive; those that survive its presence are called resistant. Modern studies conducted on species collected between 1914 and 1950 (the Murray collection) showed that bacteria from the "pre-antibiotic" era were universally sensitive to our purified antibiotic preparations, proving that pre-1950 microbes were ill equipped to handle the souped-up drugs that began appearing after World War II. In the earliest days of commercial antibiotic use, our hopes ran high that we could win the battle against bacterial infections once and for all. We were brilliant humans, full of hubris, pitted against mindless simpletons. We had found the answer, and our foe was now defenseless. Even if bacteria could further evolve to counter our attacks, how quickly could they do so? Their pre-1950 antibiotic resistance, inadequate as it was, had taken millions of years to evolve. Now, in a matter of decades, they would be confronted with a bewildering array of concentrated doom. By the 1970s, chemists could modify antibiotic molecules almost at will, producing new drugs at a swift pace, and in the 1990s, we even enlisted the help of supercomputers to design new drugs. Now, not only do bacteria have to neutralize purified versions of natural substances, they have to deal with novel molecules of human design, molecules never before seen on earth. If they couldn't meet this challenge, they would soon be exterminated. The arms race was on. Could we produce new drugs faster than bacteria could evolve to defend themselves? Which would prove smarter, the pharmaceutical industry or the microbial mind?Copyright © 2002 by Frank T. Vertosick, Jr., M.D.All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher.Requests for permission to make copies of any part of the work should be mailed to the following address: Permissions Department, Harcourt, Inc., 6277 Sea Harbor Drive, Orlando, Florida 32887-6777.
