The Case Against Ball Lightning

by Steuart Campbell

Ball lightning (BL) is popularly described as a slowly-moving luminous ball not more than twelve inches (30 cm) in diameter occasionally seen at ground level during a thunderstorm. Scientists usually understand it as an electrical discharge phenomenon somehow associated with normal lightning.

The existence of BL is controversial with opinions and explanations changing over time. While many theories have been advanced to explain it, none of them account for all the reported characteristics, Further, it has not been created in laboratory conditions with all these characteristics, and reliable accounts of it are rare and often suspect. Because of perceptual and memory problems, anecdotal evidence is of doubtful value. There is no photograph, film or video recording that can be accepted unreservedly as showing BL. Many forget the null hypothesis, which has explained many postulated phenomena, such as phlogiston and the ether, that turn out to be nonexistent. The null hypothesis may also explains BL, which could be a chimera, a pseudo-phenomenon.

Skepticism regarding the existence of BL goes back at least to Michael Faraday and Francois Arago in the nineteenth century. In 1839 Faraday, while allowing that balls of fire might appear in the atmosphere, doubted that they had anything to do with lightning or atmospheric electricity (Barry, p.133). More recently, Karl Berger reported that, in over 20 years of study as a meteorologist and lightning investigator, he had never observed BL. He concluded that it did not exist (Barry, p.133). Other scientists have reached the same conclusion. James Lovelock put tales of BL in the same category as those of spontaneous human combustion and crop circles (Lovelock, p. 86). Even Barry allows that unbiased examination of reports leads to the conclusion that a great percentage are highly questionable and could be interpreted in several ways (op. cit. p.134). Among those ways is the persistence of vision theory proposed by Lord Kelvin in 1888. He claimed that the uniform size reported in many cases was ascribed to an illusion associated with the blind spot in the eye (Singer, p.19). Lovelock reported such a case after a lightning flash (p. 86). Other sources of deception proposed have been will-o’-the-wisp and owls with luminous wings, but the existence of both of these is itself doubtful. In recent years, some scientists have accepted the existence of BL, but with little evidence.

Reports of BL suffer from defects inherent in the human perceptual and memory systems. Because both perception and memory are reconstructive processes, what we perceive is not necessarily what the sense organs receive. This is demonstrated by various well-known optical illusions, such as the moon illusion. Distant stationary lights are subject to several movement illusions, all of which attribute movement to the light. The most famous is the autokinetic illusion, in which a stationary light (usually a star) will appear to move about at random.

The size or distance of an unknown object cannot be determined by observers without additional information. Observers usually make a guess about either the size or distance of an object and then determine the other parameter from their guess. In fact both can be wrong. The size of distant objects seen near the horizon can be exaggerated (the moon illusion), as can an object’s altitude (angle above the horizon). Nor can observers usually distinguish between change in size of an object and change in its distance, usually interpreting a change in size as a change in distance. A phenomenon called size constancy can interfere with size perception. Even estimates of time-span are unreliable; fascination tends to shorten it. Estimates of brightness are meaningless (it is a relative term) and observers tend to make false associations, drawing unwarranted conclusions from what they perceive. They may associate effects with the wrong cause. In the case of anomalous luminous phenomena, observers try to identify them by reference to the models they carry in their minds. Clearly they can only identify a phenomenon as BL if they have heard of it. Conversely they are likely to identify an anomalous object as BL simply because they have heard of it.

explain (Singer, p. 62). However such contradictions might be explained if the observers are reporting many different phenomena, none of which are actually BL. Among the objects mistaken for BL are bright astronomical objects at low altitude, sometimes seen in mirage (Campbell 1988a).

Because anecdotal reports are unreliable, so are illustrations based on these reports. However, it is more difficult to explain reports of physical damage and photographic evidence. It is sometimes alleged that BL can penetrate closed windows and the literature contains several alleged examples. When a mysterious hole appeared in a window of his department during a storm, a professor of meteorology in Edinburgh concluded that BL was the cause. However later investigation showed a simpler explanation—mechanical damage (Campbell 1981a). Almost circular cracks can appear in sheet glass when subjected to the appropriate sudden stress.

Reports of extensive damage such as fires or explosions may more easily be explained as the result of ordinary lightning strikes. Such reports are not clarified by the popular belief that lightning strikes are the result of something called a ‘thunderbolt’.

Barry demonstrated that a long-lived luminous ball phenomenon can be produced by spark-initiated combustion of low-density hydrocarbon gas at atmospheric pressure (p.108). This may explain the 1975 report from a housewife in Smethwick (English Midlands) that BL appeared over her gas cooker (Campbell 1988b). Normal lightning may ignite hydrocarbon gases in the atmosphere, producing similar phenomena, but this is not what is understood as BL.

Photographs alleged to show BL are as suspect as anecdotal reports and sketches. The camera cannot lie, but what it shows can be misinterpreted and the photographer can lie. Until the early 1970s, a photograph taken in 1961 at Castleford (Yorkshire, England) had been interpreted as showing the path of BL. Even New Scientist magazine described it as the ‘Path of a Thunderbolt’. But a decade later it was claimed that it showed the pulsed trace from a street lamp (Davies and Standler) and a decade after that it was demonstrated that this was correct (Campbell 1981b): the photographer incautiously moved the camera while the shutter was still open. A Russian photograph taken in 1957 had the same explanation, but not before a member of the Soviet Academy of Sciences endorsed the picture on the basis of similar pictures he had seen in a 1939 US journal (Campbell 1987). He did not know that the pictures were all produced by lamps, presumably as hoaxes.

Many alleged pictures of BL are deliberate fakes. They appear to include the picture produced in 1966 by a former Canadian Air Force pilot, which misled the American editor of Aviation Week and Space Technology, who used it on the cover of his skeptical books on UFOs (Campbell 1988c).

Although it is fairly easy to take a photograph, or to fake one, which many mistakenly interpret as showing BL, it should be less easy to produce a film or video sequence that could fool anyone. However, in 1973 a film appeared that was claimed to show BL traveling slowly across the horizon near Aylesbury (England). It shows a bright ball of light moving on a steady horizontal course for twenty-three seconds until it suddenly vanishes. Because it was reported initially as a UFO, the film has been shown many times at UFO conferences and has featured in a BBC TV program about UFOs. But it was also thought that it showed BL. Later it was demonstrated that the ‘ball’ was burning fuel being dumped from a damaged US fighter-bomber; the aircraft itself, nearly four miles (6 km) away, was not visible beside the fireball and too far away to be heard (Campbell 1991).

In 1989 a TV station in south-east England screened a video of a smudgy spherical object with a hole which was captured accidentally as the videographer attempted to video normal lightning; he had not seen anything unusual during the recording. The videographer thought it might show BL and this explanation was initially endorsed by Professor Roger Jennison of the University of Kent (he has himself reported seeing BL). However, it was later demonstrated that the object in the sequence was a combination of an artifact of the camera itself and a distant street light (Bergstrom and Campbell).

IT SEEMS BIOLOGY (NOT RELIGION) EQUALS MORALITY

by Marc D. Hauser

For many, living a moral life is synonymous with living a religious life. Just as educated students of mathematics, chemistry and politics know that 1=1, water=H2O, and Barack Obama=US president, so, too, do religiously educated people know that religion=morality.

As simple and pleasing as this relationship may seem, it has at least three possible interpretations.

First, if religion represents the source of moral understanding, then those lacking a religious education are morally lost, adrift in a sea of sinful temptation. Those with a religious education not only chart a steady course, guided by the cliched moral compass but they know why some actions are morally virtuous and others are morally abhorrent.

Second, perhaps everyone has a standard engine for working out what is morally right or wrong but those with a religious background have extra accessories that refine our actions, fuelling altruism and fending off harms to others.

Third, while religion certainly does provide moral inspiration, not all of its recommendations are morally laudatory. Though we can all applaud those religions that teach compassion, forgiveness and genuine altruism, we can also express disgust and moral outrage at those religions that promote ethnic cleansing, often by praising those willing to commit suicide for the good of the religious "team".

None of my comments so far are meant to be divisive with respect to the meaning and sense of community that many derive from religion. Where I intend to be divisive is with respect to the argument that religion, and moral education more generally, represent the only — or perhaps even the ultimate — source of moral reasoning. If anything, moral education is often motivated by self-interest, to do what's best for those within a moral community, preaching singularity, not plurality. Blame nurture, not nature, for our moral atrocities against humanity. And blame educated partiality more generally, as this allows us to lump into one category all those who fail to acknowledge our shared humanity and fail to use secular reasoning to practise compassion.

If religion is not the source of our moral insights — and moral education has the demonstrated potential to teach partiality and, therefore, morally destructive behaviour — then what other sources of inspiration are on offer?

One answer to this question is emerging from an unsuspected corner of academia: the mind sciences. Recent discoveries suggest that all humans, young and old, male and female, conservative and liberal, living in Sydney, San Francisco and Seoul, growing up as atheists, Buddhists, Catholics and Jews, with high school, university or professional degrees, are endowed with a gift from nature, a biological code for living a moral life.

This code, a universal moral grammar, provides us with an unconscious suite of principles for judging what is morally right and wrong. It is an impartial, rational and unemotional capacity. It doesn't dictate who we should help or who we are licensed to harm. Rather, it provides an abstract set of rules for how to intuitively understand when helping another is obligatory and when harming another is forbidden. And it does so dispassionately and impartially. What's the evidence?

To experience what subjects in some of our studies experience, see the moral sense test . It asks for information about gender, age, nationality, education, politics and religion. Once logged in, there is a series of scenarios asking participants to judge whether a particular action is morally forbidden, permissible or obligatory.

Most of the scenarios involve genuine moral dilemmas. All are unfamiliar, for a reason. Unfamiliar and artificial cases have an advantage over familiar scenarios, such as abortion, euthanasia and charitable donations: no one has a well-rehearsed and explicit moral argument for such cases, and for all the cases we create, neither the law nor religious scripture provides any guidance.

For example, if five people in a hospital each require an organ to survive, is it permissible for a doctor to take the organs of a healthy person who happens to walk by the hospital? Or if a lethal gas has leaked into the vent of a factory and is headed towards a room with seven people, is it permissible to push someone into the vent, preventing the gas from reaching the seven but killing the one? These are true moral dilemmas — challenging problems that push on our intuitions as lay jurists, forcing us to wrestle with the opposing forces of consequences (saving the lives of many) and rules (killing is wrong).

Based on the responses of thousands of participants to more than 100 dilemmas, we find no difference between men and women, young and old, theistic believers and non-believers, liberals and conservatives. When it comes to judging unfamiliar moral scenarios, your cultural background is virtually irrelevant.

What guides your judgments is the universal and unconscious voice of our species, a biological code, a universal moral grammar. We tend to see actions as worse than omissions of actions: pushing a person into the factory vent is worse than allowing the person to fall in. Using someone as a means to some greater good is worse if you make this one person worse off than if you don't. This is the difference between an evitable and inevitable harm. If the person in the hospital or in the factory is perfectly healthy, taking his life to save the lives of many is worse than if he is dying and there is no cure. Distinctions such as these are abstract, impartial and emotionally cold. They are like recognising the identity relationship of 1=1, a rule that is abstract and content-free.

If this code is universal and impartial, then why are there are so many moral atrocities in the world? The answer comes from thinking about our emotions, the feelings we recruit to fuel in-group favouritism, out-group hatred and, ultimately, dehumanisation.

Consider the psychopath, Hollywood's favourite moral monster. Clinical studies reveal that they feel no remorse, shame, guilt or empathy, and lack the tools for self-control. Because they lacked these capacities, several experts have argued that they lack the wherewithal to understand what is right or wrong and, consequently, to do the wrong thing. New studies show, however, that this conclusion is at least partially wrong. Psychopaths know full well what is right and wrong but don't care. Their moral knowledge is intact but their moral emotions are damaged. They are perfectly normal jurists but perfectly abnormal moral actors. For the psychopath, other humans are no different from rocks or artefacts. They are disposable.

Here lies the answer to understanding the dangers of nurture, of education and partiality. When we fuel in-group biases by elevating and praising members of the group, we often unconsciously, and sometimes consciously, denigrate the "other" by feeding the most nefarious of all emotions, the dragon of disgust.

We label the other (the members of the out-group) with a description that makes them sub-human or even inanimate, often parasitic and vile, and thus disgusting. When disgust is recruited, those in the in-group have only one way out: purge the other.

When the Dalai Lama stated that the Chinese were attempting "cultural genocide" against the Tibetans by attempting to stop protests, he was not only making a statement about the Chinese per se but about a particular form of moral education, one that fails to acknowledge autonomy, preaches partiality and feeds disgust and dehumanisation. The Chinese must stop their attempt to purge the Tibetans of their cultural heritage and right of cultural expression. And the nations of the world, and their diverse peoples, must remain vigilant against any attempts at cultural decimation.

The good news about the psychology of prejudice, of creating distinctive classes of individuals who are in the tribe and outside of it, is that it is flexible, capable of change and — viewed from an evolutionary perspective — as abstract and content-free as the rules that enter into our moral grammar.

All animals, humans included, have evolved the capacity to create a distinction between members of the in-group and those in the out-group. But the features that are selected are not set in the genome. Rather, it is open to experience.

For example, we know from studies of child development that within the first year of life, babies prefer to look at faces from their own race to faces of a different race, prefer to listen to speakers of their native language over foreigners, and even within their native language prefer to listen to their own dialect. But if babies watch someone of another race speaking their native language, they are much more willing to engage with this person than someone of the same race speaking a different language.

These social categories are created by experience, and some features are more important than others because they are harder to fake and more indicative of a shared cultural background. But, importantly, they are plastic. Racial discrimination is greatly reduced among children of mixed-racial parents. And adults who have dated individuals of another race are also much less prejudiced. On this note, moral education can play a more nurturing role by introducing all children, early in life, to the varieties of religions, political systems, languages, social organisations and races. Exposure to diversity is perhaps our best option for reducing, if not eradicating, strong out-group biases.

Lest there be any confusion about the claims I am making, I am not saying that our evolved capacity to intuitively judge what is right or wrong is sufficient to live a moral life. It is most definitely not and for two good reasons.

For one, some of our moral instincts evolved during a period of human history that looked nothing like the situation today. In our distant past, we lived in small groups consisting of highly familiar and often familial individuals, with no formal laws. Today we live in a large and diffuse society, where our decisions have little-to-no impact on most people in our community but with laws to enforce those who deviate from expected norms. Further, we are confronted with moral decisions that are unfamiliar, including stem cells, abortion, organ transplants and life support. When we confront these novel situations, our evolved system is ill-equipped.

The second reason is that living a moral life requires us to be restless with our present moral norms, always challenging us to discover what might and ought to be. And here is where nurture can re-enter the conversation. We need education because we need a world in which people listen to the universal voice of their species, while stopping to wonder whether there are alternatives. And if there are alternatives, we need rational and reasonable people who will be vigilant of partiality and champions of plurality.

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A Conversation with Robert Sapolsky

In the endless sort of struggle that neurobiologists have — in terms of free will, determinism — my feeling has always been that there's not a whole lot of free will out there, and if there is, it's in the least interesting places and getting more sparse all the time. But there's a whole new realm of neuroscience which I've been thinking about, which I'm starting to do research on, that throws in another element of things going on below the surface affecting our behavior. And it's got to do with this utterly bizarre world of parasites manipulating our behavior. It turns out that this is not all that surprising. There are all sorts of parasites out there that get into some organism, and what they need to do is parasitize the organism and increase the likelihood that they, the parasite, will be fruitful and multiply, and in some cases they can manipulate the behavior of the host.

Some of these are pretty astounding. There's this barnacle that rides on the back of some crab and is able to inject estrogenic hormones into the crab if the crab is male, and at that point, the male's behavior becomes feminized. The male crab digs a hole in the sand for his eggs, except he has no eggs, but the barnacle sure does, and has just gotten this guy to build a nest for him. There are other ones where wasps parasitize caterpillars and get them to defend the wasp's nests for them. These are extraordinary examples.

The parasite my lab is beginning to focus on is one in the world of mammals, where parasites are changing mammalian behavior. It's got to do with this parasite, this protozoan called Toxoplasma. If you're ever pregnant, if you're ever around anyone who's pregnant, you know you immediately get skittish about cat feces, cat bedding, cat everything, because it could carry Toxo. And you do not want to get Toxoplasma into a fetal nervous system. It's a disaster.

The normal life cycle for Toxo is one of these amazing bits of natural history. Toxo can only reproduce sexually in the gut of a cat. It comes out in the cat feces, feces get eaten by rodents. And Toxo's evolutionary challenge at that point is to figure out how to get rodents inside cats' stomachs. Now it could have done this in really unsubtle ways, such as cripple the rodent or some such thing. Toxo instead has developed this amazing capacity to alter innate behavior in rodents.

If you take a lab rat who is 5,000 generations into being a lab rat, since the ancestor actually ran around in the real world, and you put some cat urine in one corner of their cage, they're going to move to the other side. Completely innate, hard-wired reaction to the smell of cats, the cat pheromones. But take a Toxo-infected rodent, and they're no longer afraid of the smell of cats. In fact they become attracted to it. The most damn amazing thing you can ever see, Toxo knows how to make cat urine smell attractive to rats. And rats go and check it out and that rat is now much more likely to wind up in the cat's stomach. Toxo's circle of life completed.

This was reported by a group in the UK about half a dozen years ago. Not a whole lot was known about what Toxo was doing in the brain, so ever since, part of my lab has been trying to figure out the neurobiological aspects. The first thing is that it's for real. The rodents, rats, mice, really do become attracted to cat urine when they've been infected with Toxo. And you might say, okay, well, this is a rodent doing just all sorts of screwy stuff because it's got this parasite turning its brain into Swiss cheese or something. It's just non-specific behavioral chaos. But no, these are incredibly normal animals. Their olfaction is normal, their social behavior is normal, their learning and memory is normal. All of that. It's not just a generically screwy animal.

You say, okay well, it's not that, but Toxo seems to know how to destroy fear and anxiety circuits. But it's not that, either. Because these are rats who are still innately afraid of bright lights. They're nocturnal animals. They're afraid of big, open spaces. You can condition them to be afraid of novel things. The system works perfectly well there. Somehow Toxo can laser out this one fear pathway, this aversion to predator odors.

We started looking at this. The first thing we did was introduce Toxo into a rat and it took about six weeks for it to migrate from its gut up into its nervous system. And at that point, we looked to see, where has it gone in the brain? It formed cysts, sort of latent, encapsulated cysts, and it wound up all over the brain. That was deeply disappointing.

But then we looked at how much winds up in different areas in the brain, and it turned out Toxo preferentially knows how to home in on the part of the brain that is all about fear and anxiety, a brain region called the amygdala. The amygdala is where you do your fear conditioning; the amygdala is what's hyperactive in people with post-traumatic stress disorder; the amygdala is all about pathways of predator aversion, and Toxo knows how to get in there.

Next, we then saw that Toxo would take the dendrites, the branch and cables that neurons have to connect to each other, and shriveled them up in the amygdala. It was disconnecting circuits. You wind up with fewer cells there. This is a parasite that is unwiring this stuff in the critical part of the brain for fear and anxiety. That's really interesting. That doesn't tell us a thing about why only its predator aversion has been knocked outwhereas fear of bright lights, et cetera, is still in there. It knows how to find that particular circuitry.

So what's going on from there? What's it doing? Because it's not just destroying this fear aversive response, it's creating something new. It's creating an attraction to the cat urine. And here is where this gets utterly bizarre. You look at circuitry in the brain, and there's a reasonably well-characterized circuit that activates neurons which become metabolically active circuits where they're talking to each other, a reasonably well-understood process that's involved in predator aversion. It involves neurons in the amygdala, the hypothalamus, and some other brain regions getting excited. This is a very well characterized circuit.

Meanwhile, there is a well-characterized circuit that has to do with sexual attraction. And as it happens, part of this circuit courses through the amygdala, which is pretty interesting in and of itself, and then goes to different areas of the brain than the fear pathways.

When you look at normal rats, and expose them to cat urine, cat pheromones, exactly as you would expect, they have a stress response: their stress hormone levels go up, and they activate this classical fear circuitry in the brain. Now you take Toxo-infected rats, right around the time when they start liking the smell of cat urine, you expose them to cat pheromones, and you don't see the stress hormone release. What you see is that the fear circuit doesn't activate normally, and instead the sexual arousal activates some. In other words, Toxo knows how to hijack the sexual reward pathway. And you get males infected with Toxo and expose them to a lot of the cat pheromones, and their testes get bigger. Somehow, this damn parasite knows how to make cat urine smell sexually arousing to rodents, and they go and check it out. Totally amazing.

So on a certain level, that explains everything. Ah ha! It takes over sexual arousal circuitry. This is utterly bizarre. At this point, we don't know what the basis is of the attraction in the females. It's something we're working on.

Some extremely nice work has been done by a group at Leeds in the UK, who are looking at the Toxo genome, and we're picking up on this collaboratively. Okay, Toxo, it's a protozoan parasite. Toxo and mammals had a common ancestor, and the last they did was God knows, billions of years ago. And you look in the Toxo genome, and it's got two versions of the gene called tyrosine hydroxylase. And if you were a neuro-chemistry type, you would be leaping up in shock and excitement at this point.

Tyrosine hydroxylase is the critical enzyme for making dopamine: the neurotransmitter in the brain that's all about reward and anticipation of reward. Cocaine works on the dopamine system, all sorts of other euphoriants do. Dopamine is about pleasure, attraction and anticipation. And the Toxo genome has the mammalian gene for making the stuff. It's got a little tail on the gene that targets, specifies, that when this is turned into the actual enzyme, it gets secreted out of the Toxo and into neurons. This parasite doesn't need to learn how to make neurons act as if they are pleasurably anticipatory; it takes over the brain chemistry of it all on its own.

Again that issue of specificity comes up. Look at closely related parasites to Toxo: do they have this gene? Absolutely not. Now look at the Toxo genome and look at genes related to other brain messengers. Serotonin, acetylcholine, norepinephrine, and so on, and you go through every single gene you can think of. Zero. Toxo doesn't have them, Toxo's got this one gene which allows it to just plug into the whole world of mammalian reward systems. And at this point, that's what we know. It is utterly cool.

Of course, at this point, you say well, what about other species? What does Toxo do to humans? And there's some interesting stuff there that's reminiscent of what's going on in rodents. Clinical dogma is you first get a Toxo infection. If you're pregnant, it gets into the fetal nervous system, a huge disaster. Otherwise, if you get a Toxo infection, it has phases of inflammation, but eventually it goes into this latent asymptomatic stage, which is when these cysts form in the brain. Which is, in a rat, when it stops being anything boring like asymptomatic, and when the behavior starts occurring. Interestingly, that's when the parasite starts making this tyrosine hydroxylase.

So what about humans? A small literature is coming out now reporting neuropsychological testing on men who are Toxo-infected, showing that they get a little bit impulsive. Women less so, and this may have some parallels perhaps with this whole testosterone aspect of the story that we're seeing. And then the truly astonishing thing: two different groups independently have reported that people who are Toxo-infected have three to four times the likelihood of being killed in car accidents involving reckless speeding.

In other words, you take a Toxo-infected rat and it does some dumb-ass thing that it should be innately skittish about, like going right up to cat smells. Maybe you take a Toxo-infected human and they start having a proclivity towards doing dumb-ass things that we should be innately averse to, like having your body hurdle through space at high G-forces. Maybe this is the same neurobiology. This is not to say that Toxo has evolved the need to get humans into cat stomachs. It's just sheer convergence. It's the same nuts and bolts neurobiology in us and in a rodent, and does the same thing.

On a certain level, this is a protozoan parasite that knows more about the neurobiology of anxiety and fear than 25,000 neuroscientists standing on each other's shoulders, and this is not a rare pattern. Look at the rabies virus; rabies knows more about aggression than we neuroscientists do. It knows how to make you rabid. It knows how to make you want to bite someone, and that saliva of yours contains rabies virus particles, passed on to another person.

The Toxo story is, for me, completely new terrain — totally cool, interesting stuff, just in terms of this individual problem. And maybe it's got something to do with treatments for phobias down the line or whatever it is to make it seem like anything more than just the coolest gee whiz thing possible. But no doubt it's also a tip of the iceberg of God knows what other parasitic stuff is going on out there. Even in the larger sense, God knows what other unseen realms of biology make our behavior far less autonomous than lots of folks would like to think.

With regard to parasite infections like Toxo in humans, there is a big prevalence in certain parts of the world. There's a higher prevalence in the tropics, where typically more than 50 percent of people are infected. Lower rates in more temperate zones for reasons that I do not understand and do not choose to speculate on. France has really high rates of Toxo infection. In much of the developing world, it's bare feet, absorbing it through soil, where cats may have been. It's food that may not have been washed sufficiently and absorption through hands. It's the usual story that people in the developing world are more subject to all sorts of infectious stuff.

A few years ago, I sat down with a couple of the Toxo docs over in our hospital who do the Toxo testing in the Ob/Gyn clinics. And they hadn't heard about this behavioral story, and I'm going on about how cool and unexpected it is. And suddenly, one of them jumps up, flooded with 40-year-old memories, and says, "I just remembered back when I was a resident, I was doing a surgical transplant rotation. And there was an older surgeon, who said, if you ever get organs from a motorcycle accident death, check the organs for Toxo. I don't know why, but you find a lot of Toxo." And you could see this guy was having a rush of nostalgic memories from back when he was 25 and all because he was being told this weird factoid ... ooh, people who die in motorcycle accidents seem to have high rates of Toxo. Utterly bizarre.

What is the bottom line on this? Well, it depends; if you want to overcome some of your inhibitions, Toxo might be a very good thing to have in your system. Not surprisingly, ever since we started studying Toxo in my lab, every lab meeting we sit around speculating about which people in the lab are Toxo-infected, and that might have something to do with one's level of recklessness. Who knows? It's very interesting stuff, though.

You want to know something utterly terrifying? Here's something terrifying and not surprising. Folks who know about Toxo and its affect on behavior are in the U.S. military. They're interested in Toxo. They're officially intrigued. And I would think they would be intrigued, studying a parasite that makes mammals perhaps do things that everything in their fiber normally tells them not to because it's dangerous and ridiculous and stupid and don't do it. But suddenly with this parasite on board, the mammal is a little bit more likely you go and do it. Who knows? But they are aware of Toxo.

There are two groups that collaborate in Toxo research. One is Joanne Webster, who was at Oxford at the time that she first saw this behavioral phenomenon. And I believe she's now at University College London. And the other is Glenn McConkey at University of Leeds. And they're on this. She's more of a behaviorist, he's more of an enzyme biochemist guy. We're doing the neurobiology end of it. We're all talking lots. (I'm not quite sure what the previous paragraph adds, so I'd be happy to see it cut, if you're looking to save some space).

There's a long-standing literature that absolutely shows there's a statistical link between Toxo infection and schizophrenia. It's not a big link, but it's solidly there. Schizophrenics have higher than expected rates of having been infected with Toxo, and not particularly the case for other related parasites. Links between schizophrenia and mothers who had house cats during pregnancy. There's a whole literature on that. So where does this fit in?

Two really interesting things. Back to dopamine and the tyrosine hydroxylase gene that Toxo somehow ripped off from mammals, which allows it to make more dopamine. Dopamine levels are too high in schizophrenia. That's the leading suggestion of what schizophrenia is about neurochemically. You take Toxo-infected rodents and their brains have elevated levels of dopamine. Final deal is, and this came from Webster's group, you take a rat who's been Toxo-infected and is now at the state where it would find cat urine to be attractive, and you give it drugs that block dopamine receptors, the drugs that are used to treat schizophrenics, and it stops being attracted to the cat urine. There is some schizophrenia connection here with this.

Any time Toxo's picked up in the media, and this schizophrenia angle is brought in, the irresistible angle is the generic crazy cat lady, you know, living in the apartment with 43 cats and their detritus. And that's an irresistible one in terms of Toxo psychiatric status: cats. But God knows what stuff is lurking there.

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