Nerve cells in your brain do not touch each other. Your conscious and unconscious thoughts have to be transmitted from neuron to neuron. Instead of using radio signals like your home Wi-Fi, your brain uses chemicals called neurotransmitters. Dopamine is one of these neurotransmitters, and abnormalities in reception and production have been implicated in positive schizophrenia symptoms.
Scientists do not believe that an overabundance of dopamine causes true schizophrenia-related psychotic symptoms, but rather an overabundance or abnormality in the distribution of D2 receptors. These receptors are the part of the neuron that picks up these chemical signals. Scientists have some compelling evidence for this hypothesis surrounding schizophrenia and dopamine.
Evidence That Dopamine Reception Abnormalities Cause Positive Schizophrenia Symptoms
- Receptor antagonists: Many effective anti-psychotic drugs are called receptor antagonists because they limit dopamine transmission. This is because they bind themselves to the receptors, inhibiting dopamine reception.
- Psychostimulant drugs that cause increased levels of dopamine: Cocaine, amphetamines, and similar drugs increase dopamine production, and these psychostimulant drugs can mimic psychosis if used in large amounts of over long periods of time. This is true of recreational drugs, but also prescription drugs with established medical uses.
- Genetic Evidence: Genes that affect dopamine function might be more prevalent in people who suffer from the positive psychosis symptoms of schizophrenia. This might explain why some people are more vulnerable to other causes of this disease than others.
First note that common anti-psychotic medication works by inhibiting dopamine reception. Consider that both medicinal and illegal drugs that increase dopamine production can produce psychotic-like states in long-term and heavy users. Finally, geneticists have managed to establish a possible link between the overabundance of dopamine-related genes in people afflicted with psychotic episodes. It seems clear that there is a link between dopamine and psychosis.
Evidence against the Direct Dopamine and Schizophrenia Link
There is compelling evidence that the dopamine and schizophrenia link is not that simple. Positron Emission Technology (PET) scans let scientist safely watch what is going on in the brains or living test subjects. Scientists have used these scans to see that some patients do not respond to receptor antagonist drug therapy. This is true even though the drugs are doing exactly what they are supposed to do.
- The patients who do not respond have had 90% of their D2 receptors blocked by antipsychotics and still suffered from positive schizophrenia symptoms.
- This type of patient tends to have suffered from positive symptoms longer. This typically occurs in patients who have been afflicted with symptoms for 10 to 30 years.
- The scans show that these drugs work within minutes, but it sometimes takes days of regular medication for them to be effective.
- Over 90% of first-episode patients did respond to the medication within minutes, and that was only after about 60% to 70% of D2 receptors were blocked.
This led some scientists to conclude that dopamine might only be indirectly responsible for positive symptoms. Other drug studies suggest that serotonin abnormalities might also be responsible for the psychotic episodes. Serotonin is another neurotransmitter. It might also be possible to conclude that somehow the link between serotonin, dopamine, and schizophrenia is self-reinforcing over time.
The Dopamine and Schizophrenia Link Is Not That Simple
David Healy, a psychiatry professor at Bangor University, says that drug companies have over-simplified the link between dopamine and schizophrenia. He contends that the pharmaceutical industry has a pervasive effect on medical literature. He believes this deliberate oversimplification is simply a drug marketing tool.
Medication works, but it might not be that simple to select the right medication for an individual sufferer. The right choice of medication may also change over time for each individual.
Schizophrenia symptoms are probably caused by combinations of factors in each individual, and these can even vary over time. These factors can include genetics, pre-natal exposure to toxins, early childhood environment, stress, drug use, and social support systems. Some people’s brains seem more vulnerable to each factor than others, and also more responsive to different types of therapy.
Is Schizophrenia Just Caused By Chemicals?
Most scientists do accept the fact that positive symptoms result from brain vulnerabilities and life-events. The vulnerabilities, like dopamine-receptor abnormalities, could be either inherited or acquired. It also seems reasonable to conclude that the onset of positive symptoms makes the brain even more vulnerable to more psychotic events. This theory led to the development of a new brain-vulnerability model for schizophrenia.
Traumatic events can trigger positive symptoms in vulnerable people too. On the other hand, positive events like a close social and family circle seem to have some protective power. But it might be the very onset of this mental disease that hurts those social associations, and that makes the problem worse. That could mean that psychological therapy and medications must both be used to get the best chance of a positive outcome. This might also mean that friends and family of the afflicted person could also benefit from counseling.