We have to think differently. It’s time to think not like 8 billion human individuals, but as a species that understands who we are and how we got to where we are. The human world has changed in the past 10,000 years for one simple reason: we have advanced our technological prowess to the point that we let technology and science make decisions for us. We especially love science and technology when we get what we desire.
However, it’s important to note that there exists a basic misunderstanding of the difference between science and technology. The confusion is really the difference between basic science and applied science. Basic science is a process for discovery and understanding, and it is impersonal in the sense that scientific decisions are based on facts rather than desire.
For example, when evolutionary biologists announced in the 1950s that insect resistance to pesticides and bacterial resistance to penicillin were clear demonstrations of the Principle of Natural Selection, we did not listen, because that was not the voice we wanted to hear.
Simultaneously, the applied science world (technology) was proclaiming that the early problems with pest control were expected symptoms of the trial-and-error process of basic science, and that new information would result in improved technological solutions.
The voice of applied science was the voice we wanted to hear. This voice promised the kind of world we thought we wanted to live in. This world is one where humans are in charge of everything, Nature must submit to our desires, and Science is the tool for achieving those desires.
And so, our burgeoning population (one that grew from 1.6 billion in 1900 to 2.5 billion in 1945 to nearly 8 billion today) has continued to think as it has always thought. We worry about people as individuals, we worry about food as something that keeps our bodies alive, and we readily accept whatever technology can offer to assist us. And we are missing a big point.
Humans are not individuals. Not in a biological sense. This failure to understand who we are as organisms is at the root of the problems we face as a species in the 21st Century.
Humans are somewhat self-contained mobile ecosystems containing many trillions of partners within our microbiomes. The terrestrial macro-ecosystems surrounding us create the context through which we move. Like all animals, we are “somewhat self-contained” in that each of us is an independently moving ecosystem, but also one that actively makes exchanges with the external ecosystem, albeit through highly filtered exchanges. Under stable conditions we don’t really need inputs from the external world (other than food). If our food environment never changed, we could probably exist quite well without added inputs from the outside.
Unfortunately, our world is not stable. We experience constant flux in terms of the kinds of food we eat, the pathogens we are exposed to, and the chemicals in our environment that affect our bodies and our internal ecosystems. And while our internal ecosystems are resistant and resilient, our modern technological world now wields large hammers that are capable of completely restructuring the microbiome almost instantaneously.
Antibiotics are just such a hammer. One by one, each antibiotic eventually fails through bacterial resistance, but we make bigger and better hammers to satisfy our (still) naïve impulse to define the rules of life. In terms of medicine, the release of penicillin in 1945 was the biggest hammer blow to disease in history. It hit the bacteria living in the human body hard and almost nothing stood in its path.
The unpleasant side effects on humans could also be quite fierce: nausea, vomiting, diarrhea, abdominal pain, rashes and itching, thrush, swollen tongue, headache, and occasionally anaphylaxis, seizures, and anemia. For a medicine that kills a wide range of presumably unnecessary bacteria, that’s quite a list of negative responses for a human suffering from the effects of only one of those bacteria. Perhaps we should have wondered more about that.
Doctors like to use antibiotic hammers because quite often the exact pathogen causing a health problem is not known, so “kill all to get one” is considered a reasonable approach. After all, they’re just bacteria. And it usually works. Pharmaceutical companies also like big hammers because they want to sell something that can be used in a variety of situations. The unfortunate reality of the pharmaceutical world is that the development of specific antibiotics is just as expensive as that of broad-spectrum antibiotics. However, the narrow spectrum drug will sell fewer units and therefore each unit must be more expensive for the consumer.
And so, doctors often prescribe broad-spectrum antibiotics for general malaise. That is, if a patient is feeling poorly and there isn’t an obvious connection to a pathogen, a doctor’s approach is that a broad-spectrum antibiotic will cover a lot of territory, it won’t do any particular harm, the patient will feel better about being treated, and the patient almost always recovers (anyway) in a few days.
In fact, most pediatricians know that 90% of the children being brought in as “sick” will recover within a few days to a week whether or not the doctor prescribes anything. This is because most childhood illnesses are viral and kids usually have great immune systems. Because the child and especially the parent would like to have a prescription, it would make more sense for doctors to default to a placebo rather than to antibiotics, which are prescribed inappropriately about 75% of the time.
The fact that patients almost always recover is a testament to the strength and resilience of the immune system and therefore to the microbiome. However, the current medical system is dominated by worries of malpractice suits; if the doctor failed to prescribe an antibiotic and the patient contracted an unrelated secondary infection, the legal consequences for the doctor would be catastrophic. Better to prescribe the antibiotic; no harm done.
But what happens when the antibiotic fails or makes matters worse? When an antibiotic fails to eliminate a bacterial problem, the typical approach is to prescribe a different broad-spectrum antibiotic and to keep doing so until the patient shows signs of improvement. In cases of a stubborn illness, even intravenous antibiotics may be given. While this approach may ultimately and apparently eliminate the stubborn pathogen, the serial application of strong antibiotics can be disastrous for the microbiome and can lead to life-threatening conditions.
For example, consider Clostridium difficile or C. diff. Chronic and untreatable C. diff. infections and the increasingly favored cure for that infection may be the most talked about example of the relationship between the microbiome and intestinal disorders, and perhaps the best example of a reason for changing some current medical practices.
The difficult thing to understand is how and why C. diff becomes such a problem. It is one disease that is clearly linked to serial antibiotic use and to particular antibiotics.[i] We know that a series of different antibiotics can (apparently) facilitate the infection and can also make an existing infection worse. Both outcomes are clearly linked to the major disruption of the gut microbiome by the antibiotics. We know that stopping antibiotic treatment does not make the problem go away which means the microbiome has been so disturbed that it cannot right itself. The standard treatment is more antibiotics, but even those antibiotics that are known to be effective against C. diff. fail a significant percent of the time.
We also know that C. diff did not become a problem merely because it was introduced to the system and just took over. No, C. diff is a relatively common resident in the large intestine, just like the common cold virus in our noses and Streptococcus bacteria in our throats. Something facilitated the change in ecosystem balance; something weakened the system and allowed C. diff to become dominant and entrenched. C. diff is an opportunistic pathogen that lies in wait until the conditions are favorable for a coup, an overthrow of the system, but the system must be greatly weakened first. This happens when the microbiome is simplified and isolated from the outside world. Reversing the dominance of C. diff. is not easy. Unfortunately, a massive input of beneficial and diverse bacteria from the food we eat (i.e., probiotics) is an unlikely occurrence because of the strong filters as bacteria pass through the upper digestive system.
Fortunately, there is another way for a massive input to arrive in the lower digestive tract. We now know that the most effective way of treating C. diff is a fecal transplant, that is, seeding a healthy microbiome into the damaged system. While the mere suggestion of a fecal transplant will raise a few eyebrows, a better than 90% success rate – much higher than the antibiotic success rate – should allay those concerns. When a strong herbicide is applied to a pasture and kills all of the plants there, the only way to re-establish the plants is from seed. Likewise, when the microbial community in a colon has been so devastated by a series of antibiotics that even the appendix can’t restart the system, a large infusion of bacteria from a healthy colon is the answer.
C. diff. is just one example of the importance of having a diverse ecosystem in our colon and also an example of the resilience of the system and the human body. Even after months of disease and damage from C. diff., the system can be restored and it can happen within hours to a few days. Unfortunately, C. diff. is also just one of many examples of the damage we are causing to the microbiome when we consider antibiotics to be the best and sometimes only tool in the toolbox.
And again, when we see C. diff. in a patient, we have little to no understanding of the influence of age, developmental stage, personal history, genetics, and diet in the severity of the disease. What we can see is this: applying a series of drugs (i.e., technology) that are hugely destructive to bacteria seems to have facilitated an apparently incurable disease, but one that can be cured almost instantaneously by reinstating the diverse bacterial community from a healthy person’s colon. What do we learn from a lesson that essentially is this: the cure for a bacterial problem is more bacteria.
If it is true that we are each highly diverse, dynamic, contextual, independent ecosystems and the health of the host absolutely depends on care of that ecosystem, then how should we live as humans? How do we maintain our health in a world that is changing faster than we even know? Perhaps more importantly, what do we eat for lunch?
If you watch TV, you already know this is the multi-billion-dollar question and the food and drug companies are earnestly trying to convince you they know the answers. (Hint: they don’t.) They are operating on only the tiniest of clues. The scientists actively researching the microbiome and human health don’t have a handle on it. The surface has just been scratched, the first layers of the onion have been peeled back, and we’re still in the “counting on our fingers” stage of documenting the diversity and some of the more obvious interactions.
The good news is that the problem for you and me is not as complicated. We don’t actually have to understand the microbiome for us to be active caretakers. We know that the microbiome is not an accidental assemblage of bacteria, that it has been there for ages, that it may be crucial to our digestive processes, and that some of the bacteria are providing nutritional and protective services. We know that diversity is good and simplification is bad. We know that the microbiome feeds on plant material and that food diversity supports bacterial diversity. We know that flexibility in the face of change is an asset and that diverse systems are more flexible.
We know many of the basic rules of external ecosystems and we can pretty safely assume that such rules apply to the internal ecosystem. Let’s take the rules we know from external ecosystems and apply them to our microbiome.
[i] Buffie, C.G. and Pamer, E.G., 2013. Microbiota-mediated colonization resistance against intestinal pathogens. Nature Reviews Immunology 13:790-801.