Toxoplasmosis Increases Rage, Impulse, and Mental Health Issues

Toxoplasmosis Increases Rage, Impulse, and Mental Health Issues

When will mainstream medicine admit that Toxoplasma gondii chronic infections cause many different mental disorders? For how long do we continue to treat these infections with anti-depressants and anti-psychotic medication? I hope that, one day we will treat and reduce these mental health issues with medications that rid the brain of T. gondii and reduce the inflammation caused by the parasite.

Microbiologists have known for years that most medical conditions are caused by infections. There is plenty of information that links together toxoplasmosis and schizophrenia, now it is also linked to explosive anger disorders, suicidal behavior, and impulsivity. A recent study may provide clues in how this parasite causes multiple mental illnesses.

It does not surprise me that T. gondii causes similar mental issues with its other hosts. The parasite drives rats to commit suicide by causing them to show no fear to predators like cats and be easily consumed by them. T. gondii might have made cats more impulsive to trust humans, leading to domestication, increasing the parasite’s host capability. Too bad for T. gondii, humans have waste treatment plants, anti parasitical drugs, microbiology, and an more advanced immune system, so it takes a long time for the parasite to be able to infect the brain to control us so that it can attempt to propagate. We are an end host. 1

So what happens when this parasite wreaks havoc in our brain? Well depending on infection load, immune system status, age, brain health, and your biological sex may determine what mental illness you develop.

In this study, 358 subjects were psychological evaluated to determine impulse control, anxiety, and aggression. There was a healthy mental control group of 110 people, 138 people were suffering from psychiatric or personality disorder issues, and 110 suffered from borderline personality disorder. IgG antibodies to T. gondii were tested in everyone. There was an enormous difference between antibodies in people with personality disorders and mental issues than those that claimed to have healthy mental capabilities.

Positive IgG antibodies were found in 9% of the healthy control. The antibodies increased to 16.7% in people with mental issues or personality disorders and as high as 22% in individuals with the intermittent explosive disorder. Granted IgG antibody tests are not perfect in determining one’s current infection load and mainly marks one’s previous exposure to the pathogen. The results of the study are still interesting in that even in the bare minimum; exposure to the parasite increases the risk of one to develop these issues. Lifetime anxiety and depression reported issues were also increased in people that tested positive antibodies to prior parasite infection.

The following is from the study on why latent Toxoplasma gondii infections might be the cause of all these mental health issues:

“Several factors may account for these findings. First, chronic latent infection with T. gondii may lead to a low-grade chronic immune activation within the brain, with (or without) downstream effects on neurotransmitter systems involved in aggressive behavior. Second, chronic T. gondii infection may alter the structure and function of corticolimbic circuits that are known to modulate impulsive aggressive behavior. Specifically, persistent T. gondii infection in mice is associated with neuronal tissue lesions, altered neuronal function, ventricular dilation, and neuroinflammation. In addition, several, though not all, studies suggest that T. gondii–containing cysts localize primarily in the prefrontal cortex and amygdala and that latent infection with T. gondii induces dendritic retraction in the basolateral amygdala. Third, as shown experimentally in rats, T. gondii infection increases testicular expression of genes involved in the production of testosterone. In addition, there is evidence that T. gondii–infected males, though not females, have higher circulating levels of testosterone compared with controls. However, while a number of studies report a relationship between elevated levels of testosterone and aggression, the magnitude of this relationship is small. Thus, it is unlikely that testosterone plays any more than a modest role in this regard.” 2

“Neurotransmitter mechanisms by which T. gondii may affect behavior include effects on serotonergic and glutaminergic transmission, both of which have been shown to play a role in aggressive behavior in human studies. Relevant to serotonin, conversion of tryptophan to kynurenine is controlled by indoleamine 2,3-dioxygenase ([IDO]; IDO-1 and IDO-2). Since IDO can be activated by inflammatory cytokines, levels of kynurenine can rise while levels of serotonin decline. In addition, increased levels of kynurenine lead to increased levels of its active metabolite quinolinic acid, a potent N-methyl-d-aspartate receptor agonist, which may increase the risk for aggressive behavior in humans. While this hypothesis is partially supported by reported elevations of kynurenine and quinolinic acid levels in mice with chronic T. gondii infection, we did not find differences in circulating levels of proinflammatory cytokines (ie, IL-6) as a function of T. gondii seropositivity. It is possible that the proinflammatory processes that keep T. gondii in a latent state are confined to the brain and are not reflected in the periphery. It is also possible that impulsively aggressive individuals engage in behaviors that increase their own risk of infection with T. gondii or that latent toxoplasmosis changes behavior, as in felids, so that the expression of aggression is increased. In addition, T. gondii is known to increase risk-taking behavior in rodents, evolutionarily benefiting the parasite (ie, transforming natural aversion in cats to attraction). This is an example of the general phenomenon of host manipulation by parasites, documented in nature, and proposed as a model with some explanatory potential for alterations in human behavior associated with parasitic infections” 3

More research needs to be done to determine the extent of health issues that are caused by chronic toxoplasmosis and what can be done about this terrifying infectious disease.

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