Our understanding of complex natural ecosystems is not particularly good, but we have had an appreciation of the importance of species diversity for a very long time. In recent years, we’ve begun to talk about the importance of both “vertical” and “horizontal” diversity to ecosystem stability. By vertical, I mean the importance of having the different levels of the trophic system intact.[i]
To have top carnivores, there must be sufficient food, which means other animals, which means herbivores, which means plants. A lot of plants. A pride of three-hundred-pound African lions requires a large number of gazelles and they in turn require a large year-round supply of plant material. And that’s just for one of the big African carnivores. If plant life is scarce, we can’t expect high diversity of large carnivores because there wouldn’t be enough food to support self-sustaining populations of other species in the food web.
Vertical diversity is also important because it helps to prevent dominance by one or a few species at the other trophic levels. Carnivores are predators that act as a top-down control on herbivore abundance, which reduces habitat damage caused by overly abundant herbivores. An example would be the environmentally ruinous number of white-tailed deer after wolves were exterminated on the East Coast of the US. (Of course, the number of deer is reduced periodically by overeating of the food supply and by disease outbreaks.)
By horizontal diversity, I mean “redundancy” in the sense that each trophic level has many species each doing very similar things. A stable ecosystem has many species of plants and many species of herbivores eating those plants. If one species is lost, the ecological function that species provides is not lost because there are many other species filling that ecological role. We understand that horizontal diversity (that is, ecological redundancy) is critical for creating and maintaining stability in ecosystems. In short, there are basic rules that govern the organization and the actions of the natural world.
However, even as we have come to understand a great deal more about natural ecosystems and the fundamental importance of diversity, humans hold themselves apart from the natural world. And our growing reliance on technology has enhanced that separation.
Our use of technology is typically a one-size-fits-all approach yet we know that all interactions within an ecosystem depend on context. While we acknowledge that every person is genetically unique and that each of us has an ethnic history reflected in our genotype, we continue to treat humans and the human environment as if we were all the same.
This one-size-fits-all approach is particularly prevalent in the medical industry where prescriptions are absolutely uniform, but drugs affect each of us very differently. For one person, a 200mg dose of ibuprofen is effective, but another person might require 400mg for the same response. The rapidity at which a drug works, how long it is effective, the effective dosage, whether is make us sleepy or restless or constipated or causes loss of appetite, all differ from one person to the next. The effectiveness of a great many drugs depends on an individual’s medical history, such as childhood trauma, or current medical status such as diabetes or recovery from recent medical procedures. Many drugs cannot be taken in conjunction with other drugs. Drug efficacy may depend on patient age or gender or obesity or metabolism.
Our individuality in terms of medicine is the basis of emerging technologies for managing our genetic differences. It is now a very simple procedure to submit a DNA sample and receive a detailed description of many of the particular genetic variants (alleles) each of us possesses and this can be very useful for understanding what genetic disorders we might potentially experience in our lives. Getting a genetic screen can inform you about, for example, a tendency in your family for heart disease or cancer.
But can the presence of a particular allele tell you whether you will get heart disease or cancer? No, it cannot. It can only offer the barest of knowledge that you possess the allele and there is an estimated probability of contracting the disease and that estimate is based on some number of other people who have (or had) the same allele and did or did not contract the disease. This uncertainty about how genes are expressed and how they affect us is the crux of the problem.
Let’s say 100 people are carrying an allele for a particular disease. How many will get that disease? And when? And will it be lethal or disabling? There is no answer to any of those questions. The probability can only be estimated and not very accurately. Each person has a unique life history filled with a huge number of experiences that affect their health and an infinite number of combinations of experiences could potentially influence how they react to new experiences. Our internal biochemistry is an incredibly complex, dynamic, and constantly adjusting world and each person’s reaction to the outside world depends on their genetics and their personal history.
The medical and genetic research world has a limited understanding of the interactions of the genes and the proteins they produce and even less understanding of how the genetic variation within humans affects those interactions. The best a medical specialist can say is “there is a 30% chance of developing this disease,” which is potentially a more frightening statement than saying nothing at all. It’s the same as saying, “There is a 30% chance you have a bomb in your body, but we won’t know until it goes off. Until then, HAVE A GREAT DAY! ”
And when it comes to antibiotics, in which an attempt is being made to eradicate a particular living organism from inside our bodies, the consequences of this one-size-fits-all approach are magnified. The problem begins with the application: we ingest or inject the antibiotic into the entire human system and expect it to disperse throughout the entire body regardless of the site of the infection. Even when the infection is very localized and can be treated locally, doctors will typically prescribe a broad-spectrum oral antibiotic “just in case”.
Antibiotics are indiscriminate; they kill all bacteria of particular types regardless of the role they might be playing and regardless of whether or not they are pathogenic or are the cause of the particular medical problem. Thus, bacteria in the tissues, in the organs, and in the gut are all attacked simultaneously. The negative effects of the target pathogen are indeed reduced and the body’s own defenses are able to regain control, but any positive effects the non-target bacteria might have been providing are also reduced.
Because we are all different, this is where the consequences become very interesting. For some people, this loss of potentially beneficial bacteria can have long-term indirect effects and we have literally no idea how that works because we tend to interpret all effects in terms of causes that we can observe right now. For example, if a patient takes an antibiotic series for a bowel problem and a year later develops acid reflux, it is highly unlikely a medical practitioner would make a connection between the two diseases.[ii]
Same but different bacteria too?
Recent studies reveal that species composition of the human microbiome is similar among people within a culture and becomes increasingly similar the closer two people are to each other, whether they are related or not. Similarly, members of the same family will tend to have very similar bacteria in their microbiome, but only when they are living together. But these general similarities belie the amazing differences between individuals within our society.
The microbiome is strongly affected by events that occur at birth and immediately afterward. For example, the use of antibiotics on infants and toddlers has a much greater long-term effect than antibiotics taken later in life after the microbiome has been established. The damage to the microbiome early in life may not be reversible because physiological and developmental processes that occur in the infant and toddler cannot be revisited once they are completed. This research is both stunning and startling because the implications are that antibiotic use in babies can cause irreversible developmental damage.
The microbiome is strongly positively affected by the food we eat, especially plants, and strongly negatively affected by the drugs we take, particularly antibiotics. These effects are influenced by age, gender, birth conditions, disease history, trauma, local environment, and genetics. The interactions of the variables that can affect the microbiome are manifold, often indirect, impossible to tease apart, and may never be fully understood. This last part is ultimately the point of this blog: the interactions within our ecosystem are dependent on such a large number of variables that we may never be able to understand them. The complexity of human physiology is now magnified by possible interactions at different times and under different conditions with bacteria that may or may not be interacting with other bacteria.
Our approach to scientific research on this unbelievable complexity called the microbiome (and this is essentially unavoidable) is that of a black box. This phrase, of course, relates to any activity in which something goes into an unknown place and we watch to see what comes out and then try to determine what must have happened during the time we were unable to observe the process. For example, we commonly apply a medical treatment to the whole person and examine the outward effect of the treatment on specific things.
Perhaps the most perfect example of black box research, and again this is essentially unavoidable, is to give a patient a drug orally and then to examine the patient fecally. I say this is unavoidable because there is no way to study a human gut in real time and in great detail or how the gut interacts with the rest of the body. At best we can say that the drug changed certain aspects of the feces in either “positive” or “negative” ways. In fact, there is no way to study and separate direct and indirect effects in systems that have a large number of variables. At best, a correlation can be established between one action and one consequence, but it is impossible to establish causation. This is the nature of complex systems and has been captured rather well by the quote at the top of the chapter from Emerson M. Pugh:
“If the human brain were so simple that we could understand it,
we would be so simple that we couldn’t.”
From a technological point of view, in order to construct a complete working model of a human brain, it would have to actually be a human brain. Pugh is intimating that to do so we would have to understand every aspect of humanness down to the tiniest detail, but that’s a level of complexity we can’t possibly comprehend. We cannot fully comprehend our own complexity. We cannot know all there is to know about knowing. How much harder would it be then to completely comprehend an ecosystem made up of thousands of different species, one of which is us? And in fact, this kind of “knowing” implies linear and predictable and uniform processes, which is not the way living systems or ecosystems work.
It is, however, the way our brains work. Human logic systems do not handle probabilistic events particularly well (although the entire mathematical genre of Game Theory is one approach). And so, we focus on the black box and manipulate the inputs and scrutinize the outputs and look for hints about the nature of what it means to be human. And in the end, concerning human health and the microbiome, our efforts are comparable to Plato’s cave where an individual must attempt to divine the nature of the world by examining the shadows cast on the walls.
It is important to understand why technology, as it applies to medicine, pest control, and food production, is failing us. It isn’t from an inherent flaw in technology. Technology is inert. It’s a flaw in the human application of the technology. Were we androids (i.e., robots with human form), all of our solutions would be technological and our “lives” would be simple because there would be a technological fix for every situation. But as I will discuss next, as biological entities, our solutions cannot be technological without inviting a constant barrage of negative consequences. It’s the cost of being biological and it means that all of our solutions to biological problems must take that reality into account.
[i] In this case, trophic level means a feeding level. Typically, these are producers (plants), herbivores, carnivores, and top carnivores. Terrestrial systems may have 3-5 trophic levels and highly productive oceanic systems can have as many as 6-7. Humans are invariably at the top of the food chain. [ii] See the book Missing Microbes (2015) by Dr. Martin Blaser for a more detailed presentation on the potential links between antibiotics and certain diseases outside of the colon.