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Mind
A Unified Theory of Life and Intelligence
By Frank T. Vertosick Jr. OPEN ROAD INTEGRATED MEDIA
Copyright © 2013 Frank T. Vertosick, Jr., M.D.
All rights reserved.
ISBN: 978-1-4804-9578-4
CHAPTER 1
THE MICROBIAL MIND
... 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 Worlds
Tom 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 a pack of cigarettes 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 footholds 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?
To make matters worse for bacteria, we not only injected our drugs into sick humans but fed them to farm animals, sprayed them on crops, and dumped them by the boxcar load into our rivers, oceans, and ground water. The earth's bacteria, nearly a third of the planet's living substance, could easily have been annihilated. As brain chauvinists, we didn't give much thought to the welfare of single-celled creatures like bacteria, nor did we seriously consider what it meant to us if they all perished at our hand.
Imagine for a moment that Fleming had discovered a substance capable of killing every bird on the planet. We would treat this bird-killing drug like plutonium and transport it in a lead box under armed guard, not feed it to dairy cattle. Thankfully (since the vast majority of bacterial species are beneficial, not harmful, to life), bacteria rose to the challenge with a vengeance, and, I dare say, with no small amount of ingenuity. By contaminating the entire biosphere with our drugs, we incited the global network of bacteria to rebellion. Like some vast industrial community, they soon set to work deciphering our drugs and foiling our plans.
I'm reminded of a science fiction story I read as a boy, in which a scientist discovers a race of highly intelligent, though tiny, beings. He kidnaps them and establishes a colony in his laboratory, cultivating them like so many ants in a toy farm. One day, he's struck with a cruel inspiration: he places a gigantic weight over the colony and starts lowering it a fraction of an inch each day. He then provides his colony with bauxite—raw aluminum ore —and unlimited electric power. The beings, once content in their well-fed confinement, quickly realize they are soon to be crushed and commence making aluminum beams to shore up the weight. Ordinary aluminum proves too flimsy and the beams snap like twigs, but within weeks the beings invent a new aluminum alloy ten times stronger than anything known to humans. The scientist patents their discovery and grows rich. He proceeds to torment his pets in other ways, hoping to tap their ingenuity further. Though he can scarcely see the organisms who accomplish these feats, he knows they're intelligent because, in keeping with Turing, they produce tangibly intelligent outputs.
Fleming and Florey began lowering their great antibiotic weight onto the world's bacteria in 1940 and, in response, the bacteria immediately began throwing up their beams. Barely a year after penicillin's first commercial application, sporadic reports of bacterial resistance to the drug began to appear. Gradually, the beams hardened; by the mid-1950s, nearly every global species of bacteria merely laughed at the thought of penicillin, and the wonder drug was a wonder no more. Florey and Fleming garnered a Nobel Prize for a discovery that took them decades to accomplish, and some bacterial "simpletons" chewed up and spat out their miracle in less than half that time. And what prize did they attain for mocking our arrogance? Survival, the only prize that mattered to them.
If we conducted a Turing test using the language of pharmacology instead of words, who would look more intelligent to an impartial observer: Fleming, or his staph cultures?
* * *
Before continuing, I need to provide a little technical background.
Living things are built from huge, carbon-based (organic) molecules known as macromolecules. In general, organic macromolecules are polymers formed by joining similar molecules into long chains. We now know that all genetic information is carried by polymers known as nucleic acids; included in this category is the now famous DNA (deoxyribonucleic acid), which consists of two polymer chains of deoxyribose (a sugar) twisted together in the "double helix" configuration first deduced by James Watson and Francis Crick nearly five decades ago. Bridging the two strands, like rungs on a ladder, sit a series of paired molecules known as the nucleotide bases. DNA uses just four bases: adenine, thymidine, guanine, and cytosine, abbreviated A, T, G, and C.
The pairing of bases is not random: A pairs only with T, and C only with G. Thus, if a strand contains the following base sequence, ATTGCATG, then the complementary strand must contain the mirror sequence, TAACGTAC. When DNA replicates, its twin strands untwist to form single strands; each strand then reconstitutes a new partner by attaching free bases in the appropriate sequence—an exposed A binds a new T, an exposed C binds a new G, and so on. In this fashion, genetic information is permanently "digitized" in the unique base sequence of a single DNA strand while the other strand merely goes along for the ride.
Another class of polymer macromolecules is the proteins, which are formed by linking together smaller sub-units, known as amino acids; all living proteins are built from just twenty different types of amino acids and may range in size from a few amino acids to long chains containing many hundreds. Unlike filamentous DNA strands, which tend to stay in a stringlike form, proteins typically fold themselves into complex globular shapes as the different amino groups adhere to one another. The intricate three-dimensional shape of a protein determines its unique biochemical functions. For example, the unique shape of hemoglobin—the main protein in red blood cells—contains a cleft just the right size for an iron atom. The iron, in turn, is used to carry oxygen. As will be seen in ensuing chapters, the ability of proteins to assume a variety of shapes is critical to the living process and to the generation of biological intelligence.
A protein's shape is determined entirely by its unique amino acid sequence. To understand why this is so, consider this analogy: assume we have a long metal chain and wish to twist part of it into a loop. We attach Velcro fasteners to two links and stick them together. The size of the loop will then be determined by which links have fasteners. If we place the fasteners twenty links apart, we'll create a loop twenty links in size. If, however, we place the fasteners only five links apart, the geometry of the chain may not permit us to make a loop at all. The stiffness of the links may prevent the fasteners from coming into close enough opposition to bind. If we distribute multiple fasteners along the chain and then tumble it in a clothes dryer, we will end up with a tangled three-dimensional shape determined entirely by the one-dimensional sequence of fasteners along the chain's length.
Certain amino acids act like Velcro fasteners, causing a protein chain to loop back upon itself. Thermal agitation at the molecular level acts like the clothes dryer, insuring that sticky amino groups will rapidly seek out and bind together. The position of the amino acid "fasteners" determines the protein's shape, but what determines the amino acid sequence of the protein chain is the base sequence of its corresponding DNA gene. (Although the terms DNA and gene are often used interchangeably, they are by no means synonymous. A gene is a sequence of bases that directly codes for the amino acid sequence of a single protein. Much of our DNA has nothing to do with coding for proteins and cannot be considered "genetic" per se.)
DNA encrypts an amino acid sequence using the triplet code: three sequential bases code for each amino acid in the protein's chain. For example, the triplet AGA codes for the amino acid serine. (Triplets are also called codons.) The triplet code is redundant, or degenerate, in that more than one codon can correspond to any given amino acid. In addition to AGA, three other codons code for serine. When a gene becomes activated, or "expressed," its base sequence is converted (translated) into the amino acid sequence of a real protein. Only a small fraction of a cell's genes are active at any one time; the rest lie dormant and unused. At the time of activation, the DNA gene unwinds and exposes its base sequence; the sequence is then copied (or, to use the correct term, transcribed) onto a piece of ribonucleic acid, also called RNA (a close cousin of DNA). In general, RNA is smaller than DNA and prefers to remain in a single-stranded form. These characteristics make it ideal for carting small chunks of genetic information around in a readable format. RNA is the workhorse of the genetic factory. If DNA is an encyclopedia, RNA is an office memo or work order.
After transcribing the gene sequence, this messenger RNA, or mRNA, leaves the DNA and journeys to the cell's cytoplasm, where it binds to tiny protein factories called ribosomes. A ribosome reads the mRNA, translates each codon in the base sequence into the corresponding amino acid, and then attaches that amino acid to the lengthening protein chain. (In addition to coding for amino acids, the triplet code contains "start" and "stop" codons that signal the ribosome when to begin and end a given protein chain.)
(Continues...)
Excerpted from Mind by Frank T. Vertosick Jr.. Copyright © 2013 Frank T. Vertosick, Jr., M.D.. Excerpted by permission of OPEN ROAD INTEGRATED MEDIA.
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