ASD, Oxytocin, & Serotonin Differences
We're going to go over three parts in this article:
- Proposed Baseline Traits of Neurotype I / Neurodivergence (from Part 7)
- Social Communication & Interaction (The Oxytocin Difference)
- Restricted, Repetitive Behaviors (The Serotonin Difference)
Please note that the mind is complex. Beyond biological factors, an individual has a lifetime of experiences and coping mechanisms (including possible underdeveloped ones) that may affect how their diagnosis presents. So the following sections will include some of the current research around these main topics. My hope in compiling this information is that it can help facilitate future research too.
Proposed Baseline Traits of Neurodivergence
These are the proposed baseline traits of Neurotype I from Part 7. After this, I'll outline the possible contributing factors for 1) social communication and interaction and 2) restricted, repetitive behaviors criteria from the DSM-5.
- Higher cortical arousal: Mind is stimulated more naturally by acetylcholine, may process stimuli faster, thoughts may race, can get overstimulated or have trouble shaking hyper-focus in times of stress (as cortisol suppresses serotonin, which normally modulates acetylcholine.)
- Prefers concrete details over abstracts in conversations: Likes less ambiguity, more straightforward approaches, when someone says outright what they want or how they feel, and gives more consideration to facts over interpretations.
- Sensitive to polychronic time: Minutes and hours feel untrackable without a timer, can get lost in a task, prefers to multitask.
- More motivated by tangible rewards: Needs to know or see end results, may have trouble motivating themselves with abstract rewards (including social validation), may feel dread instead of excitement while anticipating something, have trouble accomplishing long-term goals without milestone rewards.
- Lean more toward serotonergic traits versus dopaminergic ones: Per Fisher's Builder personality: cautious, persistent, loyal, fond of rules and facts, and orderly.
- Overly sensitive to negative outcomes: May be less impulsive and may rely more on aversive motivation to avoid punishments, negative situations, and feeling bored.
- Struggles more in the absence of serotonin versus the absence of dopamine: May experience anxious depressive episodes, have trouble controlling emotions, and struggle with stepping away from a hyper-focus.
Social Communication & Interaction
(The Oxytocin Difference)
Oxytocin is a key component in human bonding. Uvnas-Moberg and Petersson note that not only does it "induce anti-stress-like effects such as reduction of blood pressure and cortisol levels", but it also "stimulates various types of positive social interaction." (Source) HE Fisher notes that it is associated with attachment (as well as vasopressin), which she says is "characterized by feelings of calm, security, social comfort, and emotional union" to name a few. (Source) And CS Carter discusses how the oxytocin pathway promotes social engagement and reward. (Source)
Without discussing the specific interactions of oxytocin and vasopressin in human bonding (we'll do so in another section), let's look at how oxytocin differences in autistic people can lead to a diagnosis. First off, oxytocin can induce serotonergic responses in several brain regions for most individuals, which can help boost those feelings of calm, security, social comfort, and emotional union. In a study by Lefevre et al, nasal administration of OT didn't recruit that serotonergic response in their ASD group. (Source) This may help explain why autistic individuals may not engage in efforts like joint-attention seeking as oxytocin doesn't induce the same feel-good response it may in others.
It's important to keep in mind two things here:
- The effects of long-term oxytocin administration have not been fully documented, and the possibility for oxytocin to bind to vasopressin receptors shows a potential risk of inducing further anxiety. (Source) Studies are currently assessing intranasal administration of OT in ASD. But an autistic person should not be pushed into treatment just because someone else says they're not as interactive as they "should be." Instead, if oxytocin is a viable option for treatment, it can be used if the autistic person seeks help for symptoms like anxiety. The goal of medicine and treatment should not be to alter someone's personality to fit others' ideals, but to help the individual with self-reported concerns.
- I cannot stress this enough: an autistic individual has the say in what they do and do not struggle with. There is an overarching issue in social circles to pressure people into being something they're not. While a non-autistic person — especially E Neurotypes — may enjoy posturing to boost reputation, the concept may feel so foreign and unnecessary to an autistic individual that they consider it to be uncomfortable and demeaning. (When an autistic person is forced to act non-autistic or hide things about themselves, it's considered "masking.") Those negative experiences can lead to anxiety and deter the person from engaging in those situations in the future. (This may or may not be related to the behavioral inhibition system.) And extreme situations can lead to long-term stress and/or trauma.
In a separate series, I'm going to also talk about the empathy spectrum. Empathy has been skewed in autism research due to the belief that a person either has empathy or doesn't. However, we have other human behavior research to show that there are different levels of empathy. And that the spectrum allows for different types of mindsets, that can facilitate innovation and relationship bonding in a variety of ways. (This is part of what I meant in Part 7 about preserving the term "neurodiversity" for the autistic community. Not being as heavily preoccupied with things like posturing can lead to a different approach to everything from problem-solving to relationships.) But the most important part of this mention is that our language around empathy in past ASD research needs to be reassessed.
Restricted, Repetitive Behaviors
(The Serotonin Difference)
The general consensus in research is that too little serotonin in the brain can lead to the repetitive and compulsive behaviors in autistic persons. Veenstra-VanderWeele et al specifically noted how serotonin transporter variants could lead to “ alterations in social function, communication, and repetitive behavior.” (Source) This difference is also seen in research on OCD, which I want to talk about more in a moment to give some general perspective. (Source)
It's understandable the power that serotonin has. As Berger et al mentioned, “Serotonin and serotonin receptors are important in the regulation of virtually all brain functions.” (Source) This includes the “behavioral and neuropsychological processes modulated by serotonin [including] mood, perception, reward, anger, aggression, appetite, memory, sexuality, and attention, among others.” (Source) Another note from their work is that serotonin has roles in cardiovascular function, bowel motility, bladder control, regulation of energy balance and food intake, GI and endocrine function, and pulmonary physiology as well. (Source)
Some of this may sound odd if you've ever heard of the term hyperserotonemia (high serotonin plasma levels), which has been seen in about 25% of autistic individuals. (Source) This is separate from serotonin levels in the brain. As mentioned, serotonin helps with a multitude of functions in the body, and most of it resides outside of the mind. (Lefevre et al noted that hyperserotonemia may in fact be tied more to gut disturbances where a majority of serotonin is synthesized. Source) The same way we can’t just give a person a serotonin supplement to treat depression — as it cannot cross the blood-brain barrier — serotonin in the blood may not be able to reach the brain either. (Throwing in a little caveat here that mixing medications or having exposure to too much serotonin can lead to severe or even fatal symptoms of serotonin syndrome. Do not take medications or supplements without a doctor’s input. Balance is key with any neurotransmitter and hormone.)
Too little serotonin in the brain can lead to the repetitive and compulsive behaviors in ASD. Repetition is not necessarily a bad thing, as it can have a soothing effect for people with ASD — the way fidgeting can help those with ADHD. (Source) Again, we should never assume what someone is struggling with. Often what others would call disruptive in ASD is not what an autistic person would consider disruptive for themselves. For example, someone without ASD might call stimming “disruptive.” Meanwhile, someone with ASD would consider things like overstimulation and anxiety to be disruptive.
I don’t want to assume what repetitive and compulsive behaviors in ASD is like. As mentioned above though, I do have personal experience with a diagnosis that involves repetition and compulsion (OCD.) This is not based on research, just purely observational. And it’s to provide some context around other forms of repetition and compulsions due to a serotonin-deficit:
- My compulsions would usually hit when I was stressed. (We also know that cortisol, the biomarker for stress, suppresses serotonin which may have made the situations worse.)
- My mind felt like it was going wild with all that could happen. It would land on one thing and then hyper-focus.
- In trying to prevent something terrifying from happening, I’d end up in a problem-solving loop.
- I’d feel compelled to do something to mitigate that risk. Because the fear was usually based on something obscure or abstract, at times I had no way of knowing whether that risk was deterred by my actions.
- But I had no idea if it would work, so it didn’t necessarily calm me down. Then I’d feel compelled to do it again.
- Sometimes it would take 45 minutes for me to break the cycle or something else would catch my attention and it would start all over again.
I want to make it clear that in no way am I trying to imply that this is what an autistic experience is like. And it’s important to note that OCD usually stems from fear, while there are other conditions that can have similar reactions to general stress, frustration, or being overstimulated. It may be because 1) we need serotonin to modulate acetylcholine and 2) how we’ve seen evidence in task analysis that serotonin can help inhibit dopamine while we’re dealing with uncertainty and also after the task is done. (Source)
I also wanted to include these notes from Chugani et al:
- “For nonautistic children, serotonin synthesis capacity was more than 200% of adult values until the age of 5 years and then declined toward adult values.”
- “In autistic children, serotonin synthesis capacity increased gradually between the ages of 2 years and 15 years to values 1.5 times adult normal values.” (Source)
As well as this note from Carhart-Harris and Nutt whose paper “proposes that the principal function of brain serotonin is to enhance adaptive responses to adverse conditions via two distinct pathways: (1) a passive coping pathway which improves stress tolerability; and (2) an active coping pathway associated with heightened plasticity, which, with support, can improve an organism’s ability to identify and overcome source(s) of stress by changing outlook and/or behaviour.” (Source)