“Similar to a hard drive, our genome may contain a lot of information to run our body, but at any given time, we are utilizing only parts of this information. Which parts are in use—which genes are expressed (turned on) or not (turned off)—is mainly influenced by our experiences and the meaning we assign to them (Dawson, 2008). Our genetic profile is therefore a snapshot at a particular point in time of all the molecular mechanisms involved in translating cues from our contexts into the expression of specific genes to create a particular physiological state or response—an outcome. Our genome thus acts as “a system to convert environmental information into molecular resources” (Cole, 2014) to respond to and evolve through our subjective experience.
Under the constant influence of our past and present life circumstances, it becomes difficult to develop a general model of gene expression to explain, let alone predict, individual health outcomes. But in a world largely defined by physical concepts, our natural tendency is to look for ways to control a system’s outcomes through the understanding and manipulation of its physical parts. For example, if we keep driving our car over potholes, chances are our car’s suspension will eventually get damaged. Our natural reaction is to upgrade our suspension. But if we do not change our driving habits and keep driving our car over potholes, we risk breaking our car’s suspension again. If not its suspension, then the tires will get damaged, or the rims will bend, or the wheel alignment will go out of whack. Similarly, making any ‘corrections’ to the mechanics of our gene expression may bring temporary relief or delay the onset of a disease, but if they do not address our history and life context—the ultimate orchestrators of genetic expression—it is very unlikely that the health issue will be permanently resolved. Since our genome is dynamic and many different combinations of expression states can lead to similar conditions, our genome eventually finds another way to respond and adapt to its context. Not unlike changing our driving habits to avoid costly repairs, fixing detrimental aspects of our lifestyle may be more efficient in achieving personal well-being than fixing the mechanical parts of our gene expression’s machinery.
When we program a software, for example, “we do not program at the level of electrons, Micro B, but at a level of a higher effective theory, Macro A […], that is then compiled down, without loss of information, into the microscopic physics [B]. Thus, A causes B. Of course, A is physically made from B […]. But from our perspective, we can view some collective B behavior in terms of A processes” (Gazaniga, 2011). Likewise, studying health outcomes in their contexts—as the results of interactions within ourselves, our social networks, and our environment—(Macro A) might be a better way to tackle the problem than decoding genes and genomes’ behaviors in health processes (Micro B). An approach focused on the interactions themselves rather than our genetic makeup has the potential to provide us with deeper insights into the etiology of diseases and the strategies to prevent them. “[W]e have to look at the whole picture, […] if we are to understand a more full set of forces in play” (Gazaniga, 2011).
To get the ‘whole picture’, however, both tangible and intangible aspects of our interactions must be considered. For quite some time already, scientists have been on the lookout for risk factors or other commonalities between individuals affected by or recovering from similar health conditions. But if they still cannot predict health outcomes with better accuracy, it is because concepts that fall outside of what is generally accepted by the scientific community have been generally excluded from these studies. This is especially true with regard to concepts of mind-body interactions, i.e., the influence of one’s or another person’s mental states and processes on a person’s physiological states.
In conclusion, I firmly believe the answers we seek are hidden in plain sight, within the subtle fabric of our experiences and our interactions with other people within our networks and communities. To retrieve these answers, however, science must open up to the subjective, the intangible, and start asking different questions.”
(Excerpt from Expanding Science (2020), Chap. 9, Beyond Gene Expression by Isabelle Goulet)
References
Cole, S. W. (2014). Human social genomics. PLoS Genet 10, e1004601.
Dawson, C. (2008). The genie in your genes: epigenetic medicine and the new biology of intention. Santa Rosa, California: Energy Psychology Press.
Gazzaniga, M. S. (2011). Who’s in charge? Free will and the science of the brain. New York: Harper Collins.