Genius germs: preliminary evidence, part IV

IV. Motivation from Behavior Genetics
(Part I here, II here, III here, V to follow.)

The cumulative evidence in Behavior Genetics (for pdf, see "Three Laws...") suggests ~50% of the variance w/in a population w.r.t. personality & g is left unaccounted for after considering the roles of the additive genetic effects plus the "shared environment" (SE) that is, anything that two siblings growing up in the same family share. What accounts for this leftover 50% is the "unique environment" (UE): it explains why identical twins (who share all their genes) reared together don't match each other 50% of the time. Now, that's surely a far greater concordance rate than for strangers or fraternal twins, but still, what could make up this UE that is as strong as the additive genetic effects plus SE combined?

In No Two Alike, Judith Rich Harris will present a three-piece model of personality to show how UE could make identical twins reared together look different. Razib of GNXP recently interviewed her here, and the Amazon review suggests that the heavy lifting is done by the new personality model: the systems for relationships, socialization, and status. We are thrilled to see a new personality model use "massive modularity" to make individual differences more tractable. Nevertheless, as w/ other "mind as a Swiss army knife" models (e.g., this), the more one stresses numerous components, local interactions, and complex interleaving of smaller parts, the more toys there are for microbes to subtly tinker w/ -- and the more likely it is that some bug or other has found a niche in the control panel of this most all-terrain of vehicles.

In the Behavior Genetics chapter of The Blank Slate, Steven Pinker devotes two pages (p. 396-7) to the role of chance in neural development: e.g., "...a neurotransmitter zigs instead of zags, the growth cone of an axon goes left instead of right..." But just what causes these chance events? The presence of microbes adds more possibilities for molecules to ping off of one another, though the process appears to use feedback loops to keep such events from snowballing into destruction. And what about the growth of axons? (An axon is the long fiber that caries the electrical impulse from the nerve cell body.) A puzzle in neuroscience is how neurons wire themselves up -- the growth cone of an axon is like a set of fingers that chemically feel their way through the environment in order to guide growth. That is, they can either be attracted to or repelled by chemical cues, but how they do this is largely unknown. If microbes were adapted to mimic such cues, they could guide axons in ways that benefited the host (as some gut flora digest the undigestible) or in ways that harmed the host (as some gut flora cause ulcers). More, the microbes might not be designed to do so, but perhaps their waste products after digestion mimic such cues, indirectly altering the neural wiring diagram. We do not propose these possibilities as an alternative to higher-level causes like Harris' but as a more strongly biological supplement in accounting for UE.

How could this alter personality or g, though? In example 1ii) in part III, we mentioned how it might affect g, so we now outline a subtle personality tweak: being a cat-lover. In my experience, cat-lovers seem to share some Big Five traits: the expected values for Introversion and Neuroticism would be somewhat above the population mean. Now, part of this could be that individuals who have a certain personality profile (for reasons having nothing to do w/ brain germs) seek out a pet most agreeable to their profile. But might the causal arrow also go the other way around? Could a brain germ compel you to seek out a certain pet, entailing subtle personality changes in the pursuit & maintenance of said pet?

Here's how it would work. The germ would make a copy of an existing (innate) cognitive algorithm for responding to and treating human infants -- e.g., {if GOAL = raise infant, then RUN 1, 2, 3...}; among these latter sub-routines would be things like {if input to visual system = search image (infant's face), then RUN happiness; RUN x, y, z... to acquire real-world correlate of search image (mate); treat infant in ways a, b, c...} The germ would then alter one symbol w/in that program, namely "infant" to "cat." Because there are two copies of the program, the affected person would seek out both -- relative priority to be determined in each case, though likely the cat takes lower priority. However, a more parasitic strain of the germ might alter the "infant" symbol to "cat" w/o making a copy -- the person would feel compelled to rear not infants but cats. (The reader has likely met both sorts of cat-lovers.) To best carry out these programs, personality must be subtly tweaked so that it agrees w/ average cat "personality," lest the host be turned off by their target "child's" solitary nature, for example.

But is there empirical support for such a hypothesis? In humans, not yet, but there is an clear parallel in rats: toxoplasma gondii. A rat becomes infected, say, from protozoa shed in cat feces. The protozoa enters the rat's brain & somehow dials down or switches off the rat's instinctual fear of the smell of cat urine, making it more likely to wonder near its natural predator and be killed. The protozoa then enters the cat, reproduces w/o apparently altering the cat's behavior (somewhat like falciparum malaria in the mosquito), and is shed in the feces, where it is then picked up by another rat, beginning the cycle anew. As for humans, we are a cat's natural caretakers, not prey, so a different strain of t. gondii could tweak our behavior to exaggerate our role accordingly. Say a human infant picks it up from indoor cats, the bug wires the human brain to cause cat-nurturing behavior, which throughout the human's life will bring the bug into contact w/ numerous other cats to infect, in whom it will reproduce & be shed, infecting some other infant, beginning the cycle anew.

Note that the longer the period between initial infection and reaching the microbe's ultimate goal, the more the selection pressure is for gentleness, lest it prematurely crash its hijacked vehicle. This parallels the case of the least harmful strain of HIV, which is passed from mother to child -- if the virus were too virulent, it would kill its vehicle before reaching its next host. Conversely, brain germs that are spread by unaffected vectors, contaminated water, or many-partner casual sex would undergo selection for increased virulence (presumably the nasty mental illnesses, e.g. tertiary syphillis). Paul Ewald develops this point in Plague Time.

We conclude w/ how microbes could partially account for regression to the mean -- i.e., the tendency for a child's value on some quantitative trait to be closer to the population mean than the values of the parents. The expected value of the child's trait is the parents' value (all expressed as z-scores) multiplied by the narrow-sense heritability (h^2), which in most cases is less than 1 and greater than or equal to 0. For example, if both parents are 1 SD above the mean in IQ, and h^2 = 0.4, then we expect the child to be only 0.4 * 1 = 0.4 SD above the mean. Similarly, if the parents were 1 SD below the mean, we expect the child to be only 0.4 SD below the mean. In whites, those numbers would be 115 for the above-avg parents, 85 for the below-avg parents, 106 for the above-avg child, and 94 for the below-avg child.

However, sometimes the actual value of the child is farther away from the mean than the expected value. In part this could be simply due to genetic noise occasionally foiling our expectations. But if microbes affect the brain during the long childhood of humans, this too could foil our expectations -- say, the child of below-avg IQ parents became even more below-avg than expected because he was infected w/ a germ that hogged the brain's energy resources. Or say a child of above-avg IQ parents is even more above-avg than expected because he was infected w/ a germ that helped cognition the way some gut flora help digestion. Perhaps it might help to think of a shorter time-frame. Exams are often used to illustrate regression to the mean: if a student gets an 85 on a mid-term where the mean was 70, we expect him to score closer to 70 on the final since some of his initial high-score might have been due to luck. But suppose he becomes infected w/ a germ that chemically mimics the effects of caffeine, which increases awareness & fights fatigue, allowing him to score in the 90s on the final. The same principle may operate over longer time-frames.

This discussion seems to have a heads-I-win / tails-you-lose quality to it: namely, that microbes could be invoked to partially account for any aspect of human (or animal) behavior. But then, in this respect microbes are no different from genes or "cultural differences." Moreover, in general genes do not harm the organism housing them in order to benefit themselves, one reason that motivated Ewald & Cochran's "new germ theory" of fitness-reducing traits (click 1st item of this search). But microbes are alive and rapidly evolving, meaning they can be invoked to account for either fitness-reducing or fitness-increasing traits in the host, depending on whether the bugs are mutualist or parasitic. Only empirical investigation can answer questions posed by hypotheses, but the hypotheses themselves should be as imaginative as possible, lest we leave an area of the truth unexplored. In part V, we will at last provide fairly solid (and to our knowledge, novel) empirical support that microbes do impact human cognition at the genius level.