Serotonin Research

Serotonin is one of the most well-known neurotransmitters (made from the amino acid tryptophan) and has multiple effects on the brain. According to research, it is key in mood stabilisation, and it is also known for being the happy hormone. It aids in feelings of happiness you may have throughout your day. It functions as a neurotransmitter in your central nervous system, and a hormone in your peripheral nervous system.

The chemical form of Serotonin.

Serotonin also helps in:

• Sleeping.

• Digestion/eating.

• Healing wounds.

Serotonin levels affect your mood and other bodily functions. Normal levels of serotonin usually mean that you will feel relaxed, relatively happy and calm, and more focused. You will generally feel comfortable.

Depending on how drastically and how long serotonin levels change, problems can begin to arise. Simply having fluctuating levels is normal. Increases and decreases occur naturally, and they are why we can react to certain situations appropriately.

Serotonin and aggression

As you can see, research on serotonin indicates it plays an important role in mood regulation.

The orbitofrontal cortex (OFC) is associated with self-control and higher cognitive functions. Normal levels of serotonin in the OFC are a large part of the reason why you can inhibit impulsive behaviours. The OFC sends important messages to other areas of the brain, notably the amygdala, for emotional processing.

If we connect all of this information, we can see that:

• Serotonin is a mood regulator: it inhibits or dampens certain moods, in this case, aggression.

• If serotonin levels are low in the OFC, impulsive behaviours are not regulated or inhibited.

• In some cases, the amygdala may have been stimulated, and it will send aggressive impulses to the OFC.

• If serotonin levels are indeed low, these impulses ARE NOT inhibited, and the person will act on these impulses.

This is the serotonin-deficiency hypothesis. According to it, the causes for serotonin deficiency can vary. The OFC is unable to control these aggressive impulses coming from the limbic system.

A happy brain and sad brain, flaticon.com.

Consider the following studies:

Coccaro et al. (2007)

In this study, ten people suffering from intermittent explosive disorder (IED, a disorder associated with reactive aggressive behaviour where people are known to perform poorly on facial emotion recognition tasks) were compared with ten healthy individuals (the control group). They were asked to react to emotional faces whilst being measured by an fMRI. The researchers measured and compared amygdala and OFC reactivity to faces.

• The activation levels were then also measured against previous aggressive behaviours from the individuals.

• Those with IED had exaggerated amygdala reactivity and diminished OFC activation to angry faces, compared to the controls. The findings show an amygdala-OFC dysfunction in response to processing angry faces, supporting the connection between the OFC and the amygdala.

Mann et al. (1990)

In this study, 35 participants were given a questionnaire that assessed their aggression levels. They were also given the drug dexfenfluramine, which lowers serotonin levels in the brain. As we know, serotonin is important in mood regulation.

• Aggression levels rose in males but not in females following the administration of dexfenfluramine.

• This shows there is a difference in how serotonin and aggression work within the different sexes (an issue with beta bias, something which should be acknowledged in other studies!)

Brown et al. (1979)

In this study, military men who were struggling to settle into military life had their cerebrospinal fluid levels measured for certain factors, notably serotonin (5HIAA, where serotonin has been broken down).

• 5HIAA levels had a significantly negative correlation with a history of aggressive behaviours in these men. To put it simply, they had lower levels of this byproduct of serotonin being broken down.

• These low levels indicate that there’s less serotonin in the brain, which, as previously established, could explain why they had a history of aggression.

Deneris et al. (2003)

In this study, the PET-1 gene was found to be associated with the neurone development of serotonin.

• Mice lacking in the PET-1 gene had serotonin neurones that failed to differentiate, and any remaining neurones had issues with serotonin synthesis, uptake, and storage.

• This resulted in the mice having anxious and aggressive behaviours, suggesting insufficient systems for serotonin production and function are key aspects of aggressive behaviours, at least in mice.

Delville et al. (1997)

In this study, they tested the effects of fluoxetine (a drug that inhibits serotonin reuptake) on mice, assessing aggressive behaviours such as biting.

• They found that after taking fluoxetine, the mice took a longer time to bite or act aggressively.

• This suggests that when serotonin remains in the synaptic cleft for longer, it allows for a heightened mood regulation. Specifically, it reduced aggressive behaviours.

It is important to evaluate the research on the relationship between serotonin and aggression to establish how reliable and valid it is to make assumptions.

Crockett et al. (2012)

In this study, the diets of 30 random, healthy individuals were manipulated. This altered their serotonin levels.

• This was done by giving them amino acid mixtures with low levels of tryptophan, the building blocks of serotonin, on the serotonin depletion day. They were given the same mixture but with normal levels of tryptophan on the control day.

• They were then asked to view emotional faces (angry, neutral, sad) whilst being scanned using an fMRI. This allowed them to see how different regions of the brain communicate with each other in reaction to the stimulus.

• Researchers found that on serotonin depletion days, the low levels of serotonin resulted in weakened communication between the amygdala and frontal cortex.

• Those who were naturally more aggressive (established through a personality questionnaire) had an even weaker communication problem between these two areas.

• Researchers suggest that these low serotonin levels are the reason why the frontal cortex struggles to inhibit and control the amygdala’s aggressive impulses. Without serotonin inhibiting the impulsive responses being sent, they reacted more aggressively to stimuli.

• This study has high validity, as it used randomised participants and was a double-blind study.

Krakowski (2003)

Krakowski argued that it is difficult to establish a causal relationship between serotonin and aggression.

• Overall, he suggested that the influence of serotonin in aggression depends on multiple factors, namely the individual's own self-control on their impulses, their emotional regulation, and the social situation at hand.

• When dysfunction in serotonin occurs in aggressive individuals, whether this results in aggressive behaviours depends on individual differences and the social context the individual is in.