Infections caused by viruses and other pathogens are capable of changing the behavior of living organisms.
Toxoplasma gondii is one such pathogen. T. gondii increases dopamine turnover in the brains of those affected, whereas ADHD is characterized by a dopamine (action) deficiency in the PFC and striatum.
T. gondii should probably be considered more as a model for the influence of pathogens on behavior than as a direct influencing factor in relation to ADHD. At the very least, T. gondii may play a role in the differential diagnosis of ADHD-HI. Infected humans show an increased entrepreneurial drive, infected rodents an increased risk-taking behavior and an attraction to cat urine.
T. gondii is thought to be linked to an increased risk of car accidents, mental illness, drug addiction and other behavioral disorders in humans.
T. gondii is found in 50 to 60 % of the population in Germany. The parasite reproduces exclusively in cats.
A T. gondii infection in the mother during pregnancy can increase the child’s risk of ADHD.
1. Toxoplasma gondii¶
1.1. Toxoplasma gondii alters behavior in humans and animals¶
It has long been known that the Toxoplasma gondii pathogen alters behavior in cats. However, a more recent study shows that an infection with Toxoplasma gondii also significantly alters the behavior of humans. T. gondii causes changes in several thousand genes and proteins and poses considerable health risks.
People who are infected with Toxoplasma gondii showed
- 1.8 times more likely to want to be self-employed as an entrepreneur
Toxoplasma gondii has infected an estimated 20 to 30 % of the world’s human population. The regional prevalence varies between 9 % in Norway and 60 % in Brazil. The prevalence in women in Germany is 50 to 63 %. The prevalence in the respective 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, a T. gondii infection causes
- Increased risk behavior in rats
- An attraction to cat urine
- Greater exploration of new areas in labyrinths
- Less avoidance of open spaces
In humans, T. gondii is suspected of being the cause of an increased risk of
- Car accidents (2.65 times higher)
- Mental illnesses, such as schizophrenia (odds ratio 2.7)
-
Neuroticism
- Drug addiction, especially alcohol
- Impulsiveness
- Aggression
- Suicide
T. gondii causes changes in the production, metabolism or synthesis of
- Hormones
- Increased testosterone
Increased testosterone is a possible cause of risk-taking behavior, aggressiveness and impulsivity in humans
- Neurotransmitters
- Serotonin
-
Dopamine, whereby T. gondii increases dopamine turnover in the brain.
- Noradrenaline
1.2. Toxoplasma gondii and ADHD¶
The study situation on the question of whether T. gondii increases or decreases the risk of ADHD is inconsistent.
Infection of the mother during pregnancy has been associated with an increased risk of ADHD in the child.
However, there is no evidence that this is due to the specific effect of T. gondii. Other infections of the mother during pregnancy also increase the child’s risk of ADHD, such as rubella, herpes simplex 2 or influenza.
Another study found no increased antibodies against T. gondii in ADHD sufferers. Another study found no statistical association between cat ownership by the parents before the birth of the child and ADHD in the child at the age of 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 reduced in ADHD. This could indicate that T. gondii is not a cause of ADHD.
It is theoretically conceivable that T. gondii could partially conceal existing ADHD, as T. gondii has a dopamine-increasing effect, whereas ADHD is characterized by a dopamine (effect) deficiency (among other things). This hypothesis could be supported by the results of a study according to which T gondii antibodies were found 25 % less frequently in ADHD sufferers than in non-affected persons. However, a meta-study of 7 studies came to no clear conclusion. A more recent study found a 2.8-fold risk of ADHD in adults with T. gondii seropositivity, increased IgG titer (serointensity) and higher anti-T. gondii IgG avidity. The severity of symptoms in those affected 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 % within 2 weeks, the level of N-acetylaspartate and N-acetylaspartylglutamic acid by 37 % 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 certain brain regions, which was associated with reduced anxiety and depression behavior.
