This is one of the most fascinating topics he covers. In this brief discussion, Sapolsky comments on toxoplasmosis and reveals some startling research that suggests this parasite can not only invade your body but maybe can have effects on your decision making as a result.
As an analogy, I don't think the reader will struggle to relate to times when one simply could not help but pick at that zit, even though doing so would inflame it, rupture surrounding cell walls, and quite possibly result in a bigger outbreak. Try as one might, a persistent, unwanted thought would relentlessly pop into the mind. And the zit would be telling you the whole time not to worry, I'm one of those that you just pop, the system clears, all is well. Instead what's really happened is a thought in your mind - arising from we know not where - has convinced you to take the action most likely to spread the infection.
Perhaps a stretch? Nevertheless, it's an analogy to what may happen with toxoplasmosis infections.
As an analogy, I don't think the reader will struggle to relate to times when one simply could not help but pick at that zit, even though doing so would inflame it, rupture surrounding cell walls, and quite possibly result in a bigger outbreak. Try as one might, a persistent, unwanted thought would relentlessly pop into the mind. And the zit would be telling you the whole time not to worry, I'm one of those that you just pop, the system clears, all is well. Instead what's really happened is a thought in your mind - arising from we know not where - has convinced you to take the action most likely to spread the infection.
Perhaps a stretch? Nevertheless, it's an analogy to what may happen with toxoplasmosis infections.
Video from YouTube, original source here at Edge.org: http://edge.org/conversation/toxo
He opens the discussion by letting the viewer know his philosophical stance here - there's a whole lot less free will than we would like to believe. Here we are not talking about your pop psychology freshman philosophy course where determinism is argued through "I did what I did and could not have done differently" straw men, but rather through the subtle but substantial way in which biological underpinnings impact and even control behavior. A more apt framework would be the impact of heightened neural connections running from the amygdala to other brain centers. This is impacted by biology as well as environment and experience, but once it's unfolded the neural connections themselves will exert tremendous influence on the person's thoughts, emotions and behaviors independent of the person's desire to have such thoughts, emotions or behaviors so influenced.
Here the focus will be on parasites that are able to change the host's actions for their own benefit. As an opening example he mentions a barnacle parasite that can feminize male crabs, inducing them to burrow - and thus create a nice place for the barnacle to have its offspring.
Toxo comes into the picture by way of an old wives' tale forbidding mothers from having cats around during pregnancy. Basically the only spot that toxo can reproduce itself is within a cat's stomach. The toxo then goes out with the feces (which is where the caution comes from) and rodents eat the feces. Toxo's mission is to get that rodent back into the stomach of a cat.
Rodents themselves are genetically wired to fear cats. A rat that smells cat urine will go the other way. However, get that same rodent infected with toxo and it will suddenly be attracted to the scent. Thus it checks out cat urine and becomes more likely to find itself in the stomach of a cat.
So you'd think toxo is wreaking havoc with all sorts of elements within the rat, turning it into a deranged rat. Nope. Everything else remains and functions normally - olfaction, social behavior, learning and memory, and even fear behaviors all stay the same.
It takes about 6 weeks for toxo to migrate from the gut to the brain. In the brain it forms cysts in multiple locations, but mainly in the amygdala region. The amygdala is the brain's center for fear and anxiety. It is also the brain center for forming predator aversion pathways. Once in the amygdala toxo is able to take dendritic nerve cell endings and cause them to shrivel up.
Shrivel up the dendritic spine, shrivel up the fear pathway.
Taking the creepiness up several notches, recall that other fear/anxiety based behaviors remain constant. The parasite is actually locating and unwiring the very pathway it needs to destroy.
Amazingly, it does not stop there. Toxo wants to make cat urine attractive and it is able to do so by hijacking another well known pathway; sexual attraction. Part of the neural connection for sexual activity passes through the amygdala. This gets rewired and a rodent infected with toxo will no longer have a fear response to the urine but it will have activation of this sexual response pathway, resulting in attraction to the scent.
They are mapping out the toxo genome. One curious element discovered is that this protozoan parasite has two genes for tyrosine hydroxylase. This is responsible in part for the production of dopamine, which is all about rewards and the anticipation of rewards (really it's the thing that gets you to do the thing needed for the reward). It acts as a catalyst in the conversion of L-tyrosine into L-DOPA, which is in turn a precursor for dopamine.
So at the right moment, the parasite secretes the enzyme, thus driving the neurons to create dopamine at the time the toxo wants them to, thus associating dopamine with the neural pathway that toxo wants used!
Do other parasites that are closely related to toxo share this gene? No. Strangely it does not have genes for other common hormones - just this one that allows it to plug into the key for mammalian reward systems. And it starts generating it after it has penetrated into the brain and formed cysts, especially cysts in the amygdala.
For humans the current clinical dogma is that it's a disaster for a fetus but otherwise runs its course and goes latent. However, a small literature exists suggesting that males in particular become more impulsive after a toxo infection and that people who are toxo infected are 3-4 times more likely to be killed in car accidents that involve reckless speeding.
He quips that this is a protozoan parasite that knows more about the neurobiology of fear and motivation than 25,000 neuroscientists standing on each others' shoulders.
And it's not alone. The rabies virus knows how to control the neurobiology of aggression. It makes the animal more likely to bite and pass on the rabies infection.
So here's where the Pandora's Box opens. We know a little about a barnacle parasite. We know a little about toxo. We know a little about rabies. What else is out there that we don't know about but which has the same capacity to alter behavior? Do these three amount to the whole list? Or are there five more parasites, viruses or bacterial organisms that can alter behavior? 10? 100?
As a corollary, if toxo can do this, what other subconscious realms exist within us that influence our behavior every bit as much as toxo influences the rat's? Philosophically that may be a loaded, presumptive question since it implies its own conclusion, but it remains a very interesting question regardless.
As a completely unscientific anecdote, when I first picked up my dog he was, though from a good breeder, nevertheless attempting to eat wild cat poop that was in the vicinity. My current Malamute is significantly less risk aversive than the prior Malamute. And he plays with cats.
There's a high rate of toxo in the tropics - estimated that 50% of people have had a toxo infection (barefoot traveling). Another anecdote - a doctor from Stanford hospital remembered that during his residency one of the old surgeons had mentioned that he should check organs for toxo when examining people that had died in motorcycle accidents. The toxo was usually there.
On the scary side, Sapolsky mentions that the military is interested in toxo. Which makes sense because its core behavior is to induce behavior that the mammal would otherwise flee from. One would hypothesize that this would be an area of limited returns though, since volunteer military combatants would be expected to have a higher toxo infection rate than the population as a whole since the very act of volunteering requires a lower level of risk aversion.
There's a link between toxo and schizophrenia. Schizophrenics have higher than expected rates of having been infected with toxo, mothers with cats during pregnancy, etc. Interestingly, excessive dopamine release is connected with schizophrenia and is a hallmark of toxo. Additionally, if you take a toxo infected rat and introduce dopamine blockers - the same kind of drugs used to treat schizophrenia - the rats stop being attracted to cat urine.
Do other parasites that are closely related to toxo share this gene? No. Strangely it does not have genes for other common hormones - just this one that allows it to plug into the key for mammalian reward systems. And it starts generating it after it has penetrated into the brain and formed cysts, especially cysts in the amygdala.
For humans the current clinical dogma is that it's a disaster for a fetus but otherwise runs its course and goes latent. However, a small literature exists suggesting that males in particular become more impulsive after a toxo infection and that people who are toxo infected are 3-4 times more likely to be killed in car accidents that involve reckless speeding.
He quips that this is a protozoan parasite that knows more about the neurobiology of fear and motivation than 25,000 neuroscientists standing on each others' shoulders.
And it's not alone. The rabies virus knows how to control the neurobiology of aggression. It makes the animal more likely to bite and pass on the rabies infection.
So here's where the Pandora's Box opens. We know a little about a barnacle parasite. We know a little about toxo. We know a little about rabies. What else is out there that we don't know about but which has the same capacity to alter behavior? Do these three amount to the whole list? Or are there five more parasites, viruses or bacterial organisms that can alter behavior? 10? 100?
As a corollary, if toxo can do this, what other subconscious realms exist within us that influence our behavior every bit as much as toxo influences the rat's? Philosophically that may be a loaded, presumptive question since it implies its own conclusion, but it remains a very interesting question regardless.
As a completely unscientific anecdote, when I first picked up my dog he was, though from a good breeder, nevertheless attempting to eat wild cat poop that was in the vicinity. My current Malamute is significantly less risk aversive than the prior Malamute. And he plays with cats.
There's a high rate of toxo in the tropics - estimated that 50% of people have had a toxo infection (barefoot traveling). Another anecdote - a doctor from Stanford hospital remembered that during his residency one of the old surgeons had mentioned that he should check organs for toxo when examining people that had died in motorcycle accidents. The toxo was usually there.
On the scary side, Sapolsky mentions that the military is interested in toxo. Which makes sense because its core behavior is to induce behavior that the mammal would otherwise flee from. One would hypothesize that this would be an area of limited returns though, since volunteer military combatants would be expected to have a higher toxo infection rate than the population as a whole since the very act of volunteering requires a lower level of risk aversion.
There's a link between toxo and schizophrenia. Schizophrenics have higher than expected rates of having been infected with toxo, mothers with cats during pregnancy, etc. Interestingly, excessive dopamine release is connected with schizophrenia and is a hallmark of toxo. Additionally, if you take a toxo infected rat and introduce dopamine blockers - the same kind of drugs used to treat schizophrenia - the rats stop being attracted to cat urine.
He next touches on some recent research on stress related disease. Telomeres are at the end of the chromosome and, much like the plastic end of a shoelace, function to keep the DNA wrapped tightly, and correctly, together. They grow shorter with each division until they hit a point were they become senescent (no longer capable of dividing but still alive and metabolically active).
From Nature (http://www.nature.com/nature/journal/v509/n7501/full/nature13193.html):
Relatively little is known about the basic biology of senescent cells, particularly in vivo, but mounting evidence that cell senescence plays a role in ageing and age-related disease has stimulated interest in the topic. Here Jan van Deursen reviews recent work on the role of senescent cells in ageing. New findings suggest that senescence is not a static cellular endpoint. Rather, it is a dynamic series of cellular states linked to tissue repair and cancer as well as to ageing. van Deursen goes on to discuss how the new information that is emerging could be exploited to clear detrimental senescent cell populations selectively to improve healthy lifespan.
A study on telomere length in mothers of chronically disabled children found that their telomeres were significantly shorter than the length that would be expected of someone of the same age in the population.
Major long term clinical depression results in shortened telomeres in white blood cells.
Next up, what about the chromosomes in those baboons?
From Nature (http://www.nature.com/nature/journal/v509/n7501/full/nature13193.html):
Relatively little is known about the basic biology of senescent cells, particularly in vivo, but mounting evidence that cell senescence plays a role in ageing and age-related disease has stimulated interest in the topic. Here Jan van Deursen reviews recent work on the role of senescent cells in ageing. New findings suggest that senescence is not a static cellular endpoint. Rather, it is a dynamic series of cellular states linked to tissue repair and cancer as well as to ageing. van Deursen goes on to discuss how the new information that is emerging could be exploited to clear detrimental senescent cell populations selectively to improve healthy lifespan.
A study on telomere length in mothers of chronically disabled children found that their telomeres were significantly shorter than the length that would be expected of someone of the same age in the population.
Major long term clinical depression results in shortened telomeres in white blood cells.
Next up, what about the chromosomes in those baboons?