A story on Science Daily says research suggests our so-called “free will” may be less free than we ever imagined. We may, instead, be meat puppets ruled by the desires and cravings of the smallest symbiotes we carry: our gut bacteria.
The story opens:
It sounds like science fiction, but it seems that bacteria within us — which outnumber our own cells about 100-fold — may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity… researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way… the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.
Actually this is not really surprising. It has long been known that human evolution has been affected by both viral and bacterial presence, as well as having our own DNA encoded with bits from them. And recently it was discovered bacteria can encode DNA from other animals – even dead ones – into their own.
The discovery of the recombinant DNA process should have alerted everyone to the wider possibility that there may be biological analogues already. After all, it only makes sense that in any symbiotic relationship, there must be some way for all parties to communicate with each other for mutual survival. The gut is a competitive environment with numerous species, so they also need a mechanism for cooperation and communication in ways that also help keep the host alive.
We have also learned that bacteria share genetic material among themselves – the process is called bacterial conjugation. They are capable of passing along information about resistance to drugs, studies showed. One story noted:
The study, published today in Nature, reveals the mechanism of bacterial type IV secretion, which bacteria use to move substances across their cell wall. As type IV secretion can distribute genetic material between bacteria, notably antibiotic resistance genes, the mechanism is directly responsible for the spread of antibiotic resistance in hospital settings. It also plays a crucial role in secreting toxins in infections — causing ulcers, whooping cough, or severe forms of pneumonia such as Legionnaires’ disease.
And, if bacteria (and viruses) can share genetic material with one another, why wouldn’t they be sharing some with us, their host?
We have already found ways to control bacteria behaviour through molecular exchange, why should we not expect bacteria are expressing similar molecules to control our behaviour? If their survival depends on our behaviour – our eating, sleeping, sexual patterns – it seems logical bacteria would need some mechanism to transmit to its host the patterns that are most preferential to the survival of the bacteria.
…evolution can only be properly understood through infectious disease dynamics and immunologic responses rather than natural selection and random mutation. All complex creatures are aggregates of these processes and need to be recognized as complete universes of cellular networks as distinct and individual vast collaboratives representing extended hologenomes.
In his book (p.22), Miller makes the claim that,
“All aggregated genetic material whether microbial, cellular or molecular, is sentient and can react, communicate, compete, cooperate and reproduce… This sentient capacity directly or indirectly underlies all biological change with every organism at every scale seeking its own favored environment and enhancing its own reproductive potential… This process of preference at the cellular level enables collective activities that yield complex environments or ecologies.”
I am not scientifically competent to comment knowledgeably on Dr. Miller’s work, but I am certainly fascinated by the debate he has opened and look forward to reading his book. William Harcombe’s dissertation has related content on how the evolutionary model works within microbial colonies and how species interact and cooperate.
For many years, I have read material on the topic of bacterial evolution and related areas, as well as genetics and Darwinian evolution.* It all fascinates me.
Meanwhile, I ponder whether my craving for, say, a sweet or salty food, or a cup of coffee, is the result of some deep biological urge or a chemical expression by my gut flora. Am I simply a machine for feeding the flora? That question reaches deep into our philosophical roots as to what we are, who we are and the nature of consciousness.
* Evolution is not simply a biological process, but also occurs at the molecular level, according to this story on Science Daily: “At the molecular level, evolution reshaped some of the enzymes that help complete chemical processes — such as converting food into energy — in humans and all other life forms.”
They studied “humanized” forms of an enzyme that originated with the common bacterium E. coli in order to relate the action of protein dynamics and catalysis to the process of enzyme evolution. They found that enzyme dynamics evolved over millions of years to optimize a specific catalyzed reaction that occurs in humans.