Long Live the Microbes

The twentieth century may well go down as the century of war against microbes, mainly the bacteria (and some viruses) that were found to be responsible for infectious diseases like malaria, cholera, tuberculosis, smallpox, and the common cold and flu. Most of these diseases are communicable, so much of human hygiene became the struggle to keep ourselves clean and free of “germs,” up to and including the overuse of antibiotic soaps that were the rage a few years ago. Chlorine bleach became as common in western kitchens as salt. More recently, however, we are being told that all this cleanliness that we thought next to godliness may not be so great for us after all. Rodney Dietert’s new book, The Human Superorganism (Dutton: 2016), takes this idea to the next level. Dietert, a professor of immunogenetics at Cornell, goes so far as to state that “human mammals are not really viable. As mammals devoid of microbial partners, we lack what we need to exist” (p. 28). In this view, all that cleaning with disinfectant and the overuse of antibiotics in both children and farm animals (chickens were given antibiotics in their feed because the normal chicken immune response against pathogens caused muscle loss—and muscle loss meant small chicken breasts, while producers, and consumers, wanted large breasts, i.e. lots of white meat) has led to an epidemic of non-communicable diseases (NCDs); the latter being the result of our war on what is literally an indispensable part of ourselves—the microbiome. That is, we are composed in large part of bacteria, something that the biologist Lynn Margulis pointed out years ago. Some estimates of bacterial cells in the human body range as high as 90 percent of the total cells. This astonishing number refers to the more than 10,000 different microbial species in and on our bodies from our gut to our mouths to our skin: “one square inch of our skin can contain up to six billion microorganisms!” (5). This, in short, is what Dietert means by calling humans a “superorganism”: we humans are made up of thousands of species (mostly bacterial), including the genetic information we carry, which is not, as we have been instructed most recently, just the 22,000 genes in our mammalian genome. No, Dietert points out, “ninety-nine percent of the genetic information within the space we call you is not from your genome” but from all those microbes in your microbiome. Ten million of them.

            Does this matter? It matters crucially, according to Professor Dietert. And the reason is that with deficiencies in our microbiome, countless processes that we need for digestion, for our immune systems, for our very preferences for food and our partners derive from the work of our microbiome. Without the full complement of microbes, that is, we humans are incomplete. And the consequence of being incomplete is the current epidemic of NCDs the world population is suffering from: obesity, autism, heart disease, asthma, and all the allergies and auto-immune diseases that plague many of us these days. Dietert quotes the World Health Organization to the effect that these NCDs now kill three times as many people as infectious diseases (68% to 23%). That’s because defects in the microbiome (occurring through drugs, diet, oversanitation, stress, and exposure to chemicals) lead directly to defects in the immune systems which determine what gets through to our cells, tissues and organs, and what does not.

            Is there scientific evidence that this is the case? Consider one study done by Derrick McFabe at the University of Western Ontario. McFabe demonstrated that simply by altering the concentration of one gut bacterial metabolite, the short-chain fatty acid known as propionic acid, he could make normal mice antisocial to the point where they ignored their littermates and obsessed on a ball. In the same vein, John Cryan and researchers at University College in Cork, Ireland, raised germ-free mice (bubble mice) and found that, lacking normal gut microbes, the mice had “altered gene expression” in the amygdala. They lack social cognition, are generally antisocial, and “have eerily similar social interaction profiles to those of autistic children” (247). As Dietert summarizes it, these metabolites (or products of bacterial metabolism), including such things as the vitamins B₃, B₅, B₆, B₁₂, and K, and critical brain chemicals like serotonin, dopamine, acetylcholine and norepinephrine, “can influence virtually every physiological system and tissue in the body” (70). They influence what we like to eat, whom we are attracted to, if anyone, and whether we can function normally or live our lives plagued by excessive inflammation leading to diseases like atherosclerosis. Again, as Dietert puts it, virtually every NCD (non-communicable disease), which is itself often due to loss of the full integrity of the microbiome, “has unhealthy inflammation with excessive oxidation at its core” (129).

            How does this happen, and why is it happening so much now? As noted above, modern conditions are major contributing factors to the compromising of our microbiome, our microbial partners. Dietert lists six factors contributing to the epidemic: 1) antibiotic overreach; 2) the food revolution and diet; 3) urbanization; 4) birth-delivery mode; 5) misdirected efforts at human safety; 6) mammalian-only medicine. Antibiotic over-use has received a great deal of attention in recent years, and many food producers have now cut back or eliminated the use of antibiotics in animal feed. But not all. And one of the areas where antibiotic use still reigns, as far as I can tell, is in its use to compensate for the obscene crowding that takes place in feedlots for cattle and in poultry cages. Disease cannot help but be rampant amid such intolerable crowding, and antibiotics are required to help keep diseases in check. In addition, doctors have routinely prescribed antibiotics for minor ailments like ear infections, and thus led to the compromise of not just the offending bacteria but to all the bacteria in and on our bodies. Use of probiotics like yogurt can help, but Dietert and others now recommend a major effort to limit the use antibiotics to only dire cases. One other area where antibiotics have been used routinely is in childbirth. Dietert makes much of the fact that Cesarean sections have increased exponentially in recent years, doubling and tripling in many countries. Today, Cesarean sections in the U.S. are up to 33% of all births, compared to 24% in England, 40% in parts of India, and 46% in China. One major result of this, according to Dietert, is that the newborn fails to get the contact with vaginal microbes that it needs to complete its own microbiome—so it is born incomplete. In addition, Cesarean sections run the risk of infection, so antibiotics are routinely employed pre-surgically, compromising the mother’s microbiome, and thereby her infant’s, even before birth.

            One other factor deserves mention here (though all of them are important). That is the role of chemicals with which our environment, our food, and our bodies have been flooded.  A simple thing like food emulsifiers (the chemicals that smooth things like ice cream, chewing gum, artificial tears), such as Polysorbate 80 and carboxymethylcellulose, have been “found to alter gut microbe populations by thinning the mucus layer and increasing inflammation” (167). In this experiment on mice, eventually the mucus thinning led to inflammation-driven NCDs in the mice. Bisphenol A, the infamous endocrine disruptor found in plastic baby bottles, food packaging and other plastics has also been found to compromise the gut barrier, again leading to increasing inflammation and NCDs. And that scourge of our planet, glyphosate, the chief agent in Monsanto’s Roundup pesticide, has been found to “selectively alter the ecosystem of environmental microbes (in the soil), such as favoring the formation of some types of biofilms” (256). This leads to reduction in the presence of some fungi needed by grass roots, which in turn leads to less foraging areas for ungulates. In a study of chicken gut microbes, pathogenic bacteria were found to be more resistant to glyphosate than were the helpful bacteria—thus helping the pathogens! And in Germany, glyphosate was found to affect the microbe mix in cows, reducing the normal protection their gut bacteria (Enterococcus) provided in restricting the growth of botulism spores. The result: an increase in botulism-related diseases in cattle in recent years.

            Enough said. Even if Dietert has overstated his case, it seems clear that a revolution in human health and food intake is under way. Dietert’s main recommendations call for a reduction in the flagrant use of antibiotics, a return to natural forms of childbirth where possible, and an increase in the use of probiotic foods. This gets to another point he makes: that traditional cultures, before the advent of cold food transport and frozen foods, used fermentation processes to keep foods from spoiling. Sauerkraut, kimchi, miso, tempeh, chichi, wines and beers, and of course yogurt were used by various cultures to keep foods edible, the side effect being that all of these foods have bacterial cultures that promote and restore the gut microbes we need to digest most of our foods. Some doctors have been for years recommending the use of yogurts after antibiotic treatment, precisely to restore the favorable gut fauna. Now Rodney Dietert’s book is providing the scientific rationale for even more attention to the microbes that foster our health and our very lives. It wouldn’t take much—except of course for the resistance sure to be mounted by industries like Big Pharma, which are quite content with the epidemics that keep millions sick and them wealthy. In that regard, we can expect lots of ‘scientific’ studies to prove that diseases like obesity, autism, asthma, and the rest are genetic. For myself, though, eating yogurt regularly and even preparing sauerkraut in my own kitchen seems like a much better option—until, that is, the world wakes up and outlaws GMOs, glyphosate, and Monsanto, and many others like them. At the least, it’s worth thinking about.

Lawrence DiStasi

Our Malevolent Doppelganger

-->

When I first heard of Siddartha Mukerjee’s prize-winning book, The Emperor of All Maladies, I decided I wanted no part of it. Why read a book about cancer when we already hear far too much about this insidious horror of a disease? But then I read Mukerjee’s second book, The Gene, and realized that he is the latest in that enduring trend of physicians (William Carlos Williams, Lewis Thomas, Abraham Verghese) who are also brilliantly accomplished writers. So I decided to take a look at The Emperor of All Maladies (Scribner: 2010). I’m truly glad I did. Mukerjee is the real thing—a physician who seems to have maintained his humanity, his soul, his sensitivity to words, even as he maintains a killing schedule as an oncologist. Both aspects of his persona give him the necessary insights to write the book he has: a ‘biography of cancer’ that crackles with the suspense of a good mystery. The mystery, of course, involves finding the biology and genesis of cancer as a disease—the scientific pursuit—and ferreting out the medications that might promise a cure—the therapeutic pursuit. Both, though with a heavy emphasis on finding the cure, comprise what came to be known as The War on Cancer. It was a public-relations ploy designed to raise money to pay for research: money for trials for new procedures such as drugs for chemotherapy, surgery for tumor removal, X-rays to kill the offending cells; and also for the pure research into the fundamental biology of cancer cells to finally discover what, in fact, was causing cancer. What was the cellular malady that turned normally functioning cells into maniac proliferators of the tumors that were choking the body—always more and more bodies, it seemed—to death? And though the War on Cancer succeeded in raising an astonishing amount of money for cancer research and therapy, both from the U.S. Government and from private foundations, it never quite lived up to its promise. This is because the metaphor of war automatically implies taking aim and destroying an outside enemy—a virus or a bacterium that invades the body. But what Mukerjee leads us to in the end is the discovery, made gradually over the years, that the enemy is not something external to the human body. The enemy is within. Within the body. Deep within the cell. As Pogo once famously said, “we have met the enemy and it is us.”

            This is really the main thrust of Mukerjee’s book for me: cancer is not something that invades the body from without; cancer is a relentless and sometimes beautiful (Mukerjee actually uses this word) perversion of the most basic process of the human body: cell division or mitosis. The body must reproduce its cells constantly in order to live, to survive (blood cells are produced in our bone marrow at the astonishing rate of 300 billion per day!). And cancer hijacks this process in a way that makes it a virtual duplicate of ourselves. Here is how Mukerjee puts it early on:

To confront cancer is to encounter a parallel species, one perhaps more adapted to survival than even we are….This image—of cancer as our desperate, malevolent, contemporary doppelganger—is so haunting because it is at least partly true. A cancer cell is an astonishing perversion of the normal cell…Like the normal cell, the cancer cell relies on growth in the most basic, elemental sense: the division of one cell to form two (38).

What is even more mind-boggling is that cancer is not simply a fierce replica of our own ability to produce cells; the resultant cells also have the ability to evolve, to change in response to our attempts to kill or halt them. Mukerjee again:

Every generation of cancer cells creates a small number of cells that is genetically different from its parents. When a chemotherapeutic drug or the immune system attacks cancer, mutant clones that can resist the attack grow out. The fittest cancer cell survives (39).

So though we might want to think of cancer as simply a “dumb” result of basic chemical processes, we are forced to realize that cancer, like all “dumb” life, possesses a deep and deeply-ingrained intelligence. It recognizes attempts to extirpate it, bides its time, and works out strategies that allow it to survive and thrive (though here, as elsewhere in contemplating disease, I have never been able to quite figure out how “survival” fits a disease whose end game seems to be to destroy its host, and thereby, itself). Leukemia cells under attack from poisonous chemicals (combination chemotherapy), for example, seem to know enough to be able to migrate (metastasize) to the brain, where these chemicals are helpless to cross the blood-brain barrier. Mukerjee calls the brain, in this instance, “a natural ‘sanctuary’ for cancer within the body,” for a leukemia that seems almost conscious: “sensing an opportunity in that sanctuary, [it] had furtively climbed in, colonizing the one place that is fundamentally unreachable by chemotherapy” (147).

            Mukerjee gives us a detailed history of how cancer came to be recognized as a specific disease (as far back as ancient Egypt), and the many therapies developed to combat it: surgery (his description of mastectomies to extirpate breast cancer leaves us fascinated, and horrified at the more and more radical excisions that surgeons like William S. Halsted recommended in their mania to cut out every bit of a remaining cancer—all this mutilation, in the end, to no avail); chemotherapy, which found drugs almost by chance, by trial and error, and evolved to include higher and higher doses of more and more drugs, often leaving the patient half-dead from nausea (combination drug, X-ray and spinal-tap therapy was called, at St. Jude’s, “total hell”); to radiation therapy from higher and higher doses of X-rays, which themselves led to mutations; all in the effort to make the War on Cancer pay off with what was hopefully referred to as a “moon shot.” Mukerjee describes each of these phases in detail, often animated with case histories of some of his patients—the most memorable being Carla Reed. In her quest to stop her leukemia, we are told, Carla in 2004 entered “total hell,” visiting the clinic 66 times, with 58 blood tests, seven spinal taps, and several bone-marrow biopsies, in addition to multiple chemotherapies and radiations. Mukerjee cites a writer, a former nurse, describing a typical course of this “total therapy” at St. Jude’s hospital:

“From the time of his diagnosis, Eric’s illness had lasted 628 days. He had spent one quarter of these days either in a hospital bed or visiting the doctors. He had received more than 800 blood tests, numerous spinal and bone marrow taps, 30 X-rays, 120 biochemical tests, and more than 200 transfusions. No fewer than twenty doctors—hematologists, pulmonologists, neurologists, surgeons, specialists and so on—were involved in his treatment, not including the psychologist and a dozen nurses” (169).

But at least some of the patients suffering these agonies earned extensions of their lives. Mukerjee is harder on the results of the radical surgeries that were, and still, though rarely, are, the preferred treatment for breast cancer: 

Between 1891 and 1981, in the nearly 100 years of the radical mastectomy, an estimated 500,000 women underwent the procedure to “extirpate” cancer….Many were permanently disfigured; many perceived the surgery as a benediction…When radical surgery fell, an entire culture of surgery thus collapsed with it. The radical mastectomy is rarely, if ever, performed by surgeons today (201).

            The good news (if one can call it that) in Mukerjee’s story has to do with the long process of discovery about cancer biology, and the linking, finally, of these discoveries with therapies and drugs designed to match that knowledge. First, the discoveries (and it should be noted that all I can do here is provide a truncated sketch of what was and is a very complicated process). Beginning with a hunch by an Italian scientist named Boveri, biologists began to hone in on the mechanisms whereby the tightly regulated process of mitosis (cell division) in normal cells became chaotic in cancer cells. Bruce Ames, with his famous test on Salmonella bacteria in the late 1960s, found that a gene mutation would allow Salmonella to grow on sugar (galactose). He then saw that chemicals that scored high as mutagens (causing mutations) also tended to be carcinogens (causing cancer). Carcinogens, in short, had a common property: they could alter genes (mutation). One of the first carcinogens to be identified in the lab was a virus: the Rous Sarcoma Virus that could insert a viral gene into cells and make them cancerous. Though many scientists then became convinced that all cancer was caused by viruses, Howard Temin soon saw that it wasn’t the virus but what it had done that was key. By examining the Sarcoma virus, several scientists next found a specific gene, a single gene, that had done the damage. The gene was called src (pron. “sarc”), and it became one of a class called “oncogenes”—genes capable of causing cancer. It was then found how the src gene functioned: it encoded a protein whose main function was to modify other proteins by attaching a chemical, a phosphate group, to these proteins. Such protein enzymes were already known as kinases, and they acted as “molecular master switches,” often switching a cell “on” which then turned another “on” until with many cells turned “on” the target cell switched from a non-dividing to a dividing state, all under tight control. Src, by contrast, was a kinase on hyperdrive, turning normal cells into endlessly-dividing machines, the hallmark of cancer.

            One final mystery remained: how did src evolve into an oncogene? Two scientists at UCFS (University of California at San Francisco), J. Michael Bishop and Harold Varmus in the 1970s began to study src and came up with the solution. They discovered that src was not some foreign gene that had infiltrated normal cells; src was everywhere in normal cells from ducks to mice to fish to humans. But these normal src genes were not identical to the ones in the Rous virus. They were kinases, but not hyperactive ones; they were tightly regulated to act only during normal cell division. In short, they did not have the mutation that the viral genes had that made them permanently activated. Out of this, Varmus and Bishop developed a theory: normal src was a precursor to the cancer-causing viral src. It was a normal part of the cell, endogenous to the cell, that needed a mutation to turn it into a cancer-causer, an oncogene. Here is how Mukerjee sums up this vital discovery and insight:

The crucial implication of the Varmus and Bishop experiments was that a precursor of a cancer-causing gene—the “proto-oncogene,” as Bishop and Varmus called it—was a normal cellular gene. Mutations induced by chemicals or X-rays caused cancer not by “inserting” foreign genes into cells, but by activating such endogenous proto-oncogenes (362).

Mukerjee goes on to put this in historical perspective: “The Greeks had been prescient with their name for cancer, onkos (meaning load or burden). Cancer was intrinsically ‘loaded’ in our genome, awaiting activation” (362)—often by an environmental insult like cigarette smoke or radiation. He also cites a wonderful image from Harold Varmus’ speech when he and Bishop received the Nobel Prize in 1989, revealing the cancer cell to be “like Grendel (the monster in Beowulf), a distorted version of our normal selves” (363). 

            With many modifications and extensions (further research found that there were two “flavors” of cancer genes: positive ones like src that drive cell growth into hyperactivity [Bishop compared these to a “jammed accelerator”]; and negative genes, like Rb, that normally suppress cell division, but, with mutations, lose their suppressing function so that cell division goes on unhindered [as in “brakes” that don’t work]), this has become the dominant theory in cancer research. It has also, finally, led to targeted therapies that have allowed drugs to be specifically targeted to a specific kind of cancer-causing gene. Among these new targeted drugs was one called Herceptin, which targeted a breast-cancer oncogene labeled Her-2. In 1991, a patient named Bradfield was given Herceptin in combination with an older chemical, cisplatin, designed to kill breast cancer cells. Two months into her therapy, Bradfield’s neck tumor disappeared, and after 18 months of therapy, she was in full remission and survives today. Another is known as Gleevec, a drug developed by Ciba-Geigy (now Novartis) for Chronic Myeloid Leukemia or CML. Though it at first refused to spend money for drug trials for Gleevec (not enough patients would use it for Novartis to make money), Novartis finally relented and agreed to a few trials. As of 2009, CML patients treated with Gleevec were surviving an average of thirty years after diagnosis, proving that targeted cancer therapy really does work.

            But lest we forget, Mukerjee reminds us that cancer is the wiliest of all diseases. Soon, doctors were noticing that some cancers were demonstrating Gleevec resistance (similar to bacteria that become resistant to antibiotics). It is worth trying to describe this Gleevec resistance to demonstrate the phenomenal intelligence Mukerjee is at pains to make us see. I have already described cancers that migrate into the brain to escape drugs; but there is another, a cancer cell mutation that, almost fiendishly, activates the cellular pumps that normally rid the cell of natural poisons—to get rid of the chemotherapy drugs! Gleevec-resistant cells did something more astonishing: they acquired mutations that precisely altered the structure of the leukemia-causing oncogene Bcr-abl, “creating a protein still able to drive the growth of leukemia but no longer capable of binding to the drug” (442). That is, where normally Gleevec slips precisely into a “narrow, wedgelike cleft in the center of Bcr-abl” to literally pierce its heart and kill it, the mutations altered this molecular “heart” so that the drug could no longer penetrate it (it no longer fit), thus making the mutated cancer immune. As Mukerjee puts it, “To escape targeted therapy, cancer had changed the target” (442).

            I don’t know about you, but this kind of (apparently) non-cognitive intelligence, even in a form that most of us would not hesitate to call “evil,” leaves me gasping for words. It does the same to Mukerjee, though he is quite adept at providing brilliant phrases and sentences in this captivating book. But let me give you some of the thoughts that it has evoked in me, and then end with Mukerjee again. It occurred to me today that if cancer is a perversion of our normal selves, our normal processes, as Mukerjee says, then we might say that it is a perversion because it is uniquely and brilliantly concerned only with its own survival. I have always had a problem with those who insist that the only thing that matters in life is survival. Because if survival is the end game, then cancer does it even better than we do. Cancer, as we see countless times in Mukerjee’s story, is the ultimate survivor. He even says, at one point, “Some day, if a cancer succeeds (in finding immortality), it will produce a far more perfect being than its host—imbued with both immortality and the drive to proliferate” (459). Cancer, that is, is better than we humans are at survival. The question becomes, is that all we are? Are we simply here to survive? Designed to outlast everything and everyone else? If that is the case, then we are on the “right” path, moving ourselves and the planet towards destruction as we do so. In this way, we are indeed just like cancer. Our monomaniacal drive for survival moves inevitably towards the destruction of our host, the only home we know. Which is why it is here that I part company with the survivalists. Though it is difficult to say how, and to what degree, humans, human being, is/are more than simply the number of years we survive or the sum of those who survive. Human being involves others, involves all other being. It matters to humans if others survive. It must matter, as we know from the cases where such mattering is thrust aside—and we see the horrors that have marked our century, and the horrors that may yet be coming if we do nothing but look out for our own survival, either as individuals, as a country, as a continent, as a hemisphere. We can easily predict the outcome of that kind of survivalism; we are already getting a taste of it today. No. Human being, again, is more than mere survival, and that is how we differ from cancer.

            So though Mukerjee ends with a reiteration of his overall theme (“Cancer is a flaw in our growth, but this flaw is deeply entrenched in ourselves. We can rid ourselves of cancer, then, only as much as we can rid ourselves of the processes in our physiology that depend on growth—aging, regeneration, healing, reproduction”), when he says this he is speaking strictly as a scientist, as someone looking at cancer, at humans, as strictly physical processes. Though I have nothing but admiration for his ability to do this, and for his ability to make us see how elegant and intertwined this dread disease is with our own fate, I part company with him here. For here, after all, is where we as humans have the capacity to look deeply into this flaw in our being, contemplate it, even come to terms with it, perhaps accept it (at least in the abstract)—and in so doing, comprehend it. We, that is, comprehend it; it does not comprehend us, other than as obstacles to its survival. And that makes all the difference.

Lawrence DiStasi

Wonders

I am thinking today of the wonders that exist all around us and that usually either don’t get our attention, or are not available until someone points them out. The fact that we even exist is, of course, the first one. How does it happen that in a universe unimaginably large and cold, and with objects—whatever they are—so far apart that most cannot even be perceived without special equipment (not to mention the wholly imperceptible ‘dark matter’ that makes up most of the universe), how on an undistinguished rock 93 million miles from its parent star, does matter suddenly take on attributes that allow it to reproduce itself, and eventually, move where it wishes, direct its intelligence to solving problems, and produce theories about what it is, why it is here, and where it comes from? For that matter, how does it happen that there is matter in the first place? No one knows. And yet we are here, we are alive, we have minds that can ask such questions, and we take most of it for granted. We shouldn’t.

At the other extreme, we humans tend to have an exaggerated opinion of ourselves compared to other life forms. We shouldn’t do that either. We shouldn’t imagine, that is, that we’re somehow so exalted that we have no contact or common investment with other life forms, or anything in common with them either. Because even the humblest of the manifestations of what we call life, especially animal life, exhibit commonalities with us that are wonders both in themselves and in the intelligence they display. Consider slime molds. Molds and slime are normally things we consider with revulsion. In fact, the colloquial name of one species is “dog vomit slime mold,” because that’s exactly what it looks like. But these little buggers are truly amazing, both in their ability to “think,” and in their causal transformations. According to Robert Burton in A Skeptic’s Guide to the Mind (2013), the individual cells in a slime mold communicate through release of a chemical called adenosine monophosphate (AMP). These cells live conventional lives when there’s enough food around. But when food gets scarce, the individuals (I’m not sure we can think of them as ‘individuals’ in our sense, but that’s what Burton calls them) gather together with their relatives and form giant amoeba-like aggregations that conform to our usual image of slime molds. More important, they become incredibly efficient at finding food. This ability has been tested in the laboratory and the tests show that slime molds can find their way through complex mazes to reach food. They do it by sending out networks of tube-like legs, each of which explores alternate routes until it finds the best path to the favored food. Then all consolidates into a single blob, which takes the shortest route to the food. The experimenters used oat flakes (one of this slime mold’s favorites) placed on a map of England to attract the slime molds, with the starting oat flake placed where London would be. What the experimenters found, to their astonishment, was that the solution to finding other oat flakes (placed where different cities would be) exactly duplicated the British intercity network of highways. In other words, this “mindless” creature, using pseudopodia (the tube-like legs acting as scouts) to feel its way towards food, duplicated the same routes that had required trained highway engineers long years to figure out. Japanese researchers found the same thing, this time with the slime molds exactly duplicating intercity rail routes from Tokyo. Now, I know what you’re thinking: given the stupidities evinced by highway engineers in recent years, especially in setting up the San Francisco Bay Area’s highway routes after the 1989 earthquake, it’s no wonder slime molds can do as well or better. But the wonder still stands: nature has somehow equipped one of its humblest and apparently simplest creatures with the kind of intelligence that we might have thought was limited only to us, or at least to mammals more or less like us in having a brain. Nothing of the kind. Intelligence seems to be a feature of nature at its simplest levels.

Here’s another example Burton provides. Locusts are familiar to most of us from the bible stories about “plagues of locusts” that overwhelmed ancient communities when they swarmed and ate everything in sight. But the precursors to locust swarming remind us of that same intelligence seen in slime molds. Like slime molds, individual locusts are normally solitary creatures—when the supply of food is sufficient for them. But when droughts occur, locusts begin to crowd together, usually in areas that still have some vegetation. It is this close contact from crowding that triggers remarkable changes in locusts. They begin marching together, seeking always to increase their numbers, and soon they are eating everything in sight, including each other. How does this happen? Australian researchers found what appears to be the tipping point. At densities of around thirty individuals, amazing physiological changes take place: the locusts change color, from brown to yellow-and-black. More “Hulk-like,” their leg muscles enlarge and seem to automatically begin marching movements. Their brains increase in size by some thirty percent, and reorganize, with areas normally devoted to visual processing for solitary food-finding minimized, and areas providing higher-level visual processing for group foraging growing larger. All these changes, in turn, were found by the researchers to be the product of rubbing each other’s hind-leg leg hairs (itself the product of the greater density of individuals). This rubbing of leg hairs triggers an outpouring of the neurochemical serotonin, which is known to regulate moods such as anger, aggression, and appetite. And voila, nature’s solution to drought for locusts is an aggregation impulse that leads them to become the fearsome consumers of everything in sight needed for their survival.

One other wonder, though this one’s from the dark side. As noted in the recent Frontline Documentary, Hunting the Nightmare Bacteria, some 2 million people get antibiotic resistant infections each year, many from the very hospitals where they go to get treated. Some are particularly hair-raising, such as the one that infected a pre-teen girl with something that started with strange sores and would not respond to any treatment. The infection finally got to her lungs, and, with no antibiotics to treat it, she had to have a lung replacement to save her life. The infection is still not gone, and her chances are only so-so, her life by now having been turned upside down. A young man got a similar resistant infection on his leg, and finally had to have the leg amputated. Again, the infection is still there. What is happening is that bacteria, one of the oldest and most ubiquitous life forms on this planet, are evolving resistance faster than we can create new antibiotics to fight them. Part of the problem, of course, is overuse of the antibiotics we have had, not just in fighting human infections, but also in our farm animals: their keepers does them with large quantities of antibiotics to keep them alive in the horrific conditions they’re raised in. Some researchers say that we are entering a new age—rapidly reverting to the time when we had no antibiotics at all. And the worst part is that drug companies have pretty much given up on costly research to find new antibiotics because these drugs get used only once for a few days; what they like to develop are drugs for heart disease—that have to be used for a lifetime. More profit, you know. But aside from the ignorance in entrusting our health to profit-making corporations, what we have to take note of is the amazing intelligence at work in our sometime adversaries, the bacteria. They have not only evolved new genes to protect them against our antibiotics, but have even learned how to pass the resistant genes on to other bacteria! The result is that more and more infectious bacterial species are becoming resistant to our increasingly vain efforts to control them.

I don’t know about you, but thinking about the subtle mechanisms at work in our fellow creatures—all without primate brains, or writing, or labs or computers—simply leaves me wonder-struck. It makes me want to bow before the inconceivable wonder we’re all engaged in, but also to wonder how anyone could, as billions of us now do, dismiss with such arrogance all other wonders besides our own. And it reminds me that though we may, through our arrogance and ignorance, finally do ourselves in via global warming or chemical poisoning or nuclear armaggedon, we won’t do in nature or our planet. It will go on, merrily giving birth to new and better adaptations that in some future eon may come up with a little wiser, humbler, and even happier organism than Homo sapiens sapiens.

Lawrence DiStasi