Infections by viruses and other pathogens are capable of altering the behavior of living beings.
Toxoplasma gondii is such a pathogen. T. gondii increases dopamine turnover in the brain of affected individuals, whereas in ADHD there is a dopamine (effect) deficiency in the PFC and striatum.
T. gondii should probably be considered more as a model for how pathogens influence behavior than as a direct influencing factor in relation to ADHD. However, it is conceivable that T. gondii (especially in ADHD-HI with hyperactivity) could cause unfavorable behavioral summations that could be dysfunctional to a particular degree as a result. At least for the differential diagnosis of ADHD-HI, T. gondii might play a role.
1. Toxoplasma gondii
1.1. Toxoplasma gondii alters behavior in humans and animals
It has been known for some time that the pathogen Toxoplasma gondii alters behavior in cats. However, a recent study shows that an infection with Toxoplasma gondii also significantly alters the behavior of humans. T. gondii causes changes in several thousand genes or proteins and considerable health risks.
People infected with Toxoplasma gondii showed
- 1.8 times more likely to aspire to be entrepreneurially self-employed
Toxoplasma gondii has infected an estimated 20% to 30% of the world’s human population. Regional prevalence varies from 9% in Norway to 60% in Brazil. The prevalence in females ranges from 50% to 63% in Germany. The prevalence in each population correlates
- Positively with neuroticism and
- Negatively with the institutional quality and economic performance of the respective countries
The parasite reproduces exclusively in wild and domestic cats.
In rodents, T. gondii infection causes
- An increased risk behavior in rats
- An attraction to cat urine
- A greater exploration of new areas in labyrinths
- A lower avoidance of open spaces
In humans, T. gondii is suspected to be the cause of an increased risk of
- Car accidents (2.65 times increased)
- Mental illness, such as schizophrenia (odds ratio 2.7)
- Drug addiction, especially alcohol
T. gondii causes changes in the production, metabolism, or synthesis of
- Testosterone increased
Elevated testosterone is a possible cause of risk-taking behavior, aggressiveness, and impulsivity in humans
Dopamine, where T. gondii increases dopamine turnover in the brain.
1.2. Toxoplasma gondii and ADHD
Studies on whether T. gondii increases or decreases the risk of ADHD are inconsistent.
Maternal infection during pregnancy has been associated with an increased risk of ADHD in the child.
However, it has not been proven that this is due to the specific effect of T. gondii. Other infections of the mother during pregnancy also increase the ADHD risk of the child, such as rubella, herpes simplex 2 or influenza.
Another study found no increased antibodies to T. gondii in ADHD sufferers. Another study found no statistical association between cat ownership by parents before the child’s birth and ADHD in the child at age 10. However, the same study found a 2.23-fold increased risk of ADHD in boys whose mother kept a dog before birth. Girls were not affected.
A larger study found that toxoplasmosis correlated with a 1.5-fold risk of ADHD (OR 2.5).
While Toxoplasma gondii increases dopamine metabolism in the brain, dopamine metabolism is typically decreased in ADHD. This may indicate that T. gondii is not a cause of ADHD.
It is theoretically conceivable that T. gondii could partially mask an existing ADHD, since T. gondii has a dopamine-increasing effect, whereas in ADHD there is (among other things) a dopamine (effect) deficiency. This hypothesis could be supported by results of a study that found T- gondii antibodies 25% less frequently in ADHD sufferers than in nonaffected individuals. In contrast, a metastudy of 7 studies did not reach a clear conclusion. A recent study found a 2.8-fold risk of ADHD in adults with T. gondii seropositivity, increased IgG titer (serointensity), and stronger anti-T. gondii IgG avidity. Symptom severity in affected individuals was increased. In particular, hyperactivity correlated with increased serointensity.
2. Lactobacillus rhamnosus (JB-1)
Lactobacillus rhamnosus (JB-1) given to healthy mice increased the level of glutamate and glutamine by 10% and the level of N-acetylaspartate and N-acetylaspartylglutamic acid by 37% within 2 weeks and the level of GABA by 25% within 4 weeks. Glutamate and glutamine levels remained elevated for 4 weeks after the end of treatment.
There were consistent changes in GABA-A and -B receptor subtypes in specific brain regions, which was associated with decreased anxiety and decreased depressive behavior.