In a previous post, I argued against the assumption that the mind and the brain ought to function as a unified system without internal contradictions or disharmony, citing the recent revolutionary discovery of “anti-correlated” brain networks associated with mentalistic versus mechanistic cognition as a case in point. Indeed, in another post I added further reasons why it is naïve and out-dated to assume that at the most basic, biological level we are products of a single genetic design. I pointed out that internally we are all confronted with the mental conflicts thrown up by imprinted genes which express the conflicting biological interests of our parents.
A recent paper by Peter Kramer and Paola Bressan gives a beautifully clear and concise account of imprinting—not to mention of the imprinted brain theory—but also goes on to discuss much more. As they put it:
Unbeknownst to many people, our emotions, cognition, behavior, and mental health are influenced by a large number of entities that reside in our bodies while pursuing their own interests, which need not coincide with ours. Such selfish entities include microbes, viruses, foreign human cells, and imprinted genes regulated by viruslike elements.
This well-written review deserves the wide readership the authors intend, and provides “a broad overview of the consequences of our coexistence with these entities.” The authors’ “aim is to show that we are not unitary individuals in control of ourselves but rather ‘holobionts’ or superorganisms—meant here as collections of human and nonhuman elements that are to varying degrees integrated and, in an incessant struggle, jointly define who we are.”
The diagram at the top gives an overall view of what is covered. In the case of microbial brain parasites, the authors discuss Toxoplasma gondii, which originally evolved in felines and rodents, but which now infects 10%−70% human beings worldwide, depending on age. The parasite can only complete the sexual phase of its life-cycle inside a cat, so when it finds itself in a rodent it alters the animal’s behavior so that it loses its fear of cats, all the more likely to be eaten by one! Intriguingly, this implies an attack on the brain systems responsible for the fear-response, which are in the lower, limbic brain. In mice the limbic system is known to be the work of paternal but not maternal genes, and something of the same may be true in human beings. Indeed, according to the imprinted brain theory, this might explain why toxoplasmosis in humans is a major risk factor for psychoses such as schizophrenia. As I argued in The Imprinted Brain, the theory’s explanation is that attacking the paternal, more autistic parts of the brain disturbs the mental balance in the maternal, more psychotic direction. But Kramer and Bressan add another, entirely compatible suggestion:
A possible mechanism for how Toxoplasma interacts with us—for example, causing schizophrenia—relies on the fact that, in the presence of the parasite, we mount an immune response that breaks down the amino acid tryptophan. Neurochemical changes that typically result from the breakdown of tryptophan have been observed in the brains of schizophrenia patients and are implicated (…) in schizophrenia-associated deficits in perception, spatial working memory, contextual learning, and pre-pulse inhibition (the attenuation of a startle reflex to a strong stimulus by prior adaptation to a weaker one).
They also discuss the effects of gut bacteria on the brain and behaviour, pointing out that “The human gastrointestinal tract houses up to 100 trillion micro-organisms, belonging to more than 7,000 strains; collectively, these contain 10 times the number of human cells and 100 times as many genes as our genome (…).” They add that “the process of bacterial colonization initiates signaling mechanisms that irreversibly affect behavior, by both turning genes on or off and altering the communication between neurons in specific brain regions. In animals, the evidence is overwhelming…” In humans, bacteria are capable of modulating gastro-intestinal inflammation, and chronic, low-grade inflammation has been implicated in schizophrenia and in mood disturbances, notably anxiety and depression, as I mentioned in an earlier post on the so-called Old Friends Hypothesis. Indeed, Kramer and Bressan note that this may explain why so-called pro-biotics (micro-organisms with health benefits, typically bifid bacteria and lactobacilli) can be therapeutic.
Where exploitation of humans by viruses is concerned, cytomegalovirus infects the majority of the world’s population. In the USA in the period 1988–1994, it was estimated to be present in nearly 60% of people over 6 years of age and in more than 90% of those over 80. The infection is usually benign. But some people with a particular variant of a gene involved in learning and memory have a five-fold increased risk of developing schizophrenia thanks to maternal cytomegalovirus infection during their development before birth. And as in the case of T. gondii, cytomegalovirus appears to attack the limbic system.
Another way that viruses have exploited us is by retro-viruses copying their DNA into our genome. As these authors note, “The DNA of human endogenous retroviruses occupies at least 8% of our genome; genetic material of so-called jumping genes, which resemble retroviruses and may also have a viral origin, comprises another 37%.” They add that
harmful viral elements that are normally inactive can be reactivated by various pathogens (…). The influenza virus (…), for example, is capable of reactivating normally inactive endogenous retroviral elements that (a) can cause neuroinflammation, along with white matter and myelin degeneration, and (b) have been implicated in bipolar disorder and schizophrenia (…), although both independent replication and a clarification of the mechanism involved in the reactivation are still lacking.
But the invaders don’t have to belong to other species, they can be human:
Evidence is mounting that our brain (and behavior) can also be permanently modified by the invasion of selfish entities that are not micro-organisms or viruses but the cells of another person. The likeliest time of infiltration would have been when we were fetuses, with either our mother or our twin as the intruders. As we will see, some of these foreign cells go on to multiply and form large patches of the host’s body and brain; hence, their integration is exquisite—they literally become the cells of their hosts.
The H-Y antigen (also discussed in The Imprinted Brain) is expressed in the male fetal brain, and no other theory but one invoking the build-up of maternal antibodies to this antigen can explain why the more older brothers—but not sisters—a man has, the higher his likelihood of being homosexual. As Kramer and Bressan note, “Remarkably, a man is twice as likely to be homosexual if he has, on average, 2.5 older brothers than if he has none and three times as likely if he has four older brothers.”
Additionally, the authors discuss chimerism: the presence in one person of cells from another person. Actual examples discussed are embryonic or fetal male cells inside a mother’s and/or female co-twin’s brain and the likely effects on brain development and behaviour. And as I remarked at the beginning, Kramer and Bressan review the imprinted brain theory and conclude with some practical suggestions for future research and therapy.
Psychotherapists in particular might benefit from these suggestions, touching as they do on issues that are normally ignored but which this remarkable review suggests are crucial, not only for mental health, but for our very concept of ourselves as organisms. As these authors conclude, "It is time to change the very concept we have of ourselves and to realize that one human individual is neither just human nor just one individual."
(With congratulations and thanks to Peter Kramer and Paola Bressan, and apologies for taking so long with this post.)