Contagion (Law of Contagion)

Domains, Evolution and Origins of Contagion

Contagion effects appear in domains as diverse as food transactions, contact with microbially contaminated entities, contact with other (especially unfamiliar) persons, contact with morally tainted entities, and contact with loved or greatly admired persons (positive contagion). This breadth raises questions about the evolutionary origin of contagion and the cultural history of expansion of the domain of contagion. We briefly consider four accounts of the origin of contagion, keeping in mind that it appears to be uniquely human. Two accounts are based on an origin of contagion as an adaptive means of avoiding microbial contamination, which shares with contagion the fundamental properties of importance of physical contact, the ability to produce a major effect with a minimal dose, and negativity bias (there is no potent positive opposite to germs).

According to the first account, contagion originated in association with disgust, the rejection of a set of potential foods as offensive. On this view, contagion arose as a means of avoiding microbial contamination from foods. Pinker (1997) notes that animal foods are much more likely than plant foods to be vehicles for the transmission of potentially harmful microorganisms. The principal risk from plant foods is toxins; toxins do not have contaminating properties, in the sense that they cannot multiply, and microbes in plants are much less likely to find a compatible host in animals. Almost all potential food elicitors of disgust are of animal origin (Rozin & Fallon, 1987), and almost all examples of negative food contagion effects involve foods of animal origin. Interpersonal contagion is often manifested in the domain of food because food is a highly social entity that is typically procured, handled, prepared, or eaten and shared by others. These multiple other-contacts with one’s food allow for widespread interpersonal contagion influences, no doubt enhanced by the particular intimacy of the act of ingestion. There is evidence for a widespread traditional belief in “You are what you eat” – that is, the idea that one takes on the physical, behavioral, intentional, and moral properties of what one consumes (Nemeroff & Rozin, 1989; Stein & Nemeroff, 1995). This belief is a very concrete form of contagion. In the interpersonal domain, taken literally, it would apply only to other humans for the rare cases of cannibalism. However, when coupled with the principle of contagion, “You are what you eat” promises an enormous range for passage of personal influence by food (Rozin, 1990). Now, the food someone has raised or prepared becomes a vehicle for their essence.

A second account locates the origin of contagion in the interpersonal as opposed to the food domain. Illness transfer in humans usually involves a human vector, and therefore is interpersonal. Common vehicles are food, air, physical contact with infected persons, and shared objects and residues. On this account, there is no reason to specially privilege the food vehicle as the original source of contagion. Widespread avoidance of physical contact with or close proximity to ill or dead people suggests the possibility that the core issue in the origin of contagion is microbial contamination, whatever the source.

The third account does not attribute the origin of contagion to negative, microbial effects, but rather to positive effects. Although the relative weakness of positive contagion suggests that it might be an accidental overextension of the negative contagion principle, it is also possible that positive contagion has its own origin or adaptive value. An obvious function for positive contagion is in the support of kin relations and love bonds. It could well function to strengthen important blood bonds, with their obvious link to fitness. Sharing food is a particularly common behavior that centers on kin-related groups, and sexual intimacy involves highly contagious contact. Positive contagion includes valuing objects that belonged to and were in contact with ancestors, living loved ones, or greatly admired persons; Grandmother’s ring, food prepared by a loved one, or Princess Diana’s clothing are salient examples.

The relative weakness of positive contagion could be simply a result of the negativity dominance discussed previously. Alternatively, it could be a result of the fact that positive contagion virtually always competes with illness risk and disgust. The microbial risks of intercourse are well illustrated by sexually transmitted diseases. A deep kiss involves exchange of saliva, which is both a disgusting body fluid and a potential disease vector, when examined out of the context of love or lust (Nemeroff, 1988; Nemeroff & Rozin, 1994, 2000).

A final account of the origins of contagion is based in the work of Johnson and Lakoff (e.g., Johnson, 1987; Lakoff, 1987; Lakoff & Johnson, 1980), who write about the “embodied” nature of cognition. Our bodies, they say, provide us with preconceptual structures that shape our abstract thoughts. Body movements and perceptual interactions with the world, which are fundamentally based in the experience of having a human body, give rise to “image-schemata” that are “metaphorically projected” to structure our domains of thought. By this account, the contagion principle would arise from our phenomenological experience of our bodies as containers (having an inside, a boundary, and an outside), combined with other schemas such as trajectory, force, links, and so on. This account easily explains the breadth of magical contagion, although it does not address the negativity bias.

Given some initial locus for the origin of contagion, an account is still needed for the great breadth of contagion in contemporary humans. The problem of the spread of contagion is paralleled by the spread of disgust from its likely original food origin to a wide range of elicitors, including interpersonal contacts and especially contacts with ill or immoral persons. The range of disgust in contemporary humans overlaps substantially with the range of contagion. Indeed, our definition of disgust invokes contagion as a critical feature: Contact with a disgusting substance renders an otherwise acceptable entity (e.g., a food) unacceptable (Rozin & Fallon, 1987). Our account of the cultural evolution of disgust invokes the process of preadaptation; that is, the application of an adaptation that evolved for one purpose to a new purpose. We trace the cultural evolution of disgust as an expansion of elicitors from its origin as a response to distasteful foods through reactions to offensive foods, other animal properties of our existence (e.g., sex, death), interpersonal contacts, and certain types of moral offenses (Rozin, Haidt, & McCauley, 1993; Rozin, Haidt, McCauley, & Imada, 1997). The extension of contagion could have occurred by this same type of process, whatever its origins. Of course, once contagion became linked to disgust, either in origin or later on, its domain could have spread as the domain of disgust spread.

We commonly ask people why they reject juice that had brief contact with a cockroach. The answer almost always refers to toxins and microbes; the disease-generating properties of the roach. This, of course, relates to some of the views we have expressed about the microbial origins of contagion. However, in the laboratory, we often follow up this response by repeating the process with a new glass of juice, now contaminated by a sterilized roach – that is, a germ-free roach just removed from an autoclave. In the experiment, we present this roach as safer than the average fork and the juice as safe to drink. Subjects almost always continue to reject the juice, while admitting, in an embarrassed way, that their initial microbial harm account must have been invalid or at least incomplete. It is the offensive roach properties that have been passed into the juice, somewhat independent of any physical threat of harm. We find the same sort of results with hypothetical sweaters (on questionnaires) that have been worn by someone with an infectious disease. They are rejected even after sterilization (Nemeroff & Rozin, 1994; Rozin, Markwith, & McCauley, 1994). Furthermore, the pattern of rejection is quite similar to the rejection of sweaters previously worn by morally tainted but healthy individuals. Also, those who are most inclined to reject “hepatitis sweaters” are generally the same as those most inclined to reject “healthy murderer sweaters.”