Art Therapy for Autism, Dyslexia, ADHD and Other Neurodiversities

24/07/2025

24/07/2025

UNDERSTANDING ENZYME MUTATIONS AND MEDICATION IN AUTISM/ADHD AND BEYOND:

“WHEN LYNSEY GOT CHATTING TO A PAIN MANAGEMENT EXPERT…”

*DISCLAIMER:
I am not a medical professional and do not hold any relevant medical qualifications. The information provided is for general educational purposes only and should not be taken as medical advice. Always consult with qualified healthcare professionals or specialists regarding any medical concerns, diagnoses, or treatments. Individuals are encouraged to conduct their own research and seek personalised advice before making decisions about their health or medications.*

After speaking with a pain management expert, I learned more about how genetic variations in liver enzymes can significantly affect how people metabolise medications. This is especially important for those in the autistic community, where such variations appear to be more common than in the general population.

WHAT ARE THESE ENZYMES AND WHY DO THEY MATTER?

Our bodies rely on enzymes—special proteins in the liver—to break down and activate medications. One of the most important enzymes for processing many opioids (like tramadol and codeine), some antidepressants, and other drugs is called CYP2D6.

About 5–10% of Caucasian people have a variation in the CYP2D6 gene that makes them ultra-rapid metabolisers—meaning their bodies convert certain drugs into active forms too quickly. This rapid metabolism can cause:

Excessive amounts of the active drug in the bloodstream
Side effects like sedation, breathing difficulties, nausea, vomiting, hallucinations, or fainting
Overdose-like symptoms, even at normal doses
Unpredictable pain relief—sometimes the drug works too strongly, other times not effectively
These enzyme variations can influence medication effectiveness and safety (Preskorn et al., 2021; Hicks et al., 2020).

CYP2D6 MUTATIONS AND AUTISM

Emerging research indicates that genetic variations in CYP2D6 and other related enzymes are more common in autistic individuals. This means autistic people may have:

A higher likelihood of adverse drug reactions
Increased sensitivity to standard medication doses
Paradoxical or unpredictable responses to medications
A need for very personalised medication plans based on genetic testing
Other CYP enzymes such as CYP2C19, CYP3A4, and CYP1A2 also show variations in autistic populations. These enzymes influence how many commonly prescribed medications—like antidepressants, stimulants, antipsychotics, and anaesthetics—are metabolised (Ming et al., 2023; Braff et al., 2022).

WHY ARE THESE VARIATIONS MORE COMMON?

Several factors may explain this:

Genetic Overlap: Some genes involved in autism also regulate detoxification and liver enzyme activity.
Neuroimmune and Metabolic Differences: Many autistic individuals have immune or mitochondrial differences affecting drug absorption and breakdown.
Co-occurring Traits: Conditions like ADHD, Ehlers-Danlos Syndrome (EDS), mast cell disorders, and autoimmune tendencies often overlap with autism and are linked to altered drug metabolism (Mueller et al., 2022; Hannon et al., 2021).

MEDICATIONS AFFECTED BY CYP2D6

Common pain medications like codeine, tramadol, oxycodone, and hydrocodone require CYP2D6 to become active. For ultra-rapid metabolisers, these drugs can be too potent or dangerous. Safer alternatives include opioids like morphine, fentanyl, hydromorphone, and oxymorphone, which are processed through different enzymes (such as CYP3A4 and UGT2B7) and tend to work more predictably (Smith & Johnson, 2023; Australian Therapeutic Guidelines, 2024).

BEYOND PAIN MEDICATION: ANTIDEPRESSANTS AND ENZYMES

Antidepressants like citalopram and escitalopram are mainly metabolised by CYP2C19 and CYP3A4, with some involvement of CYP2D6. Genetic variations here can affect:

How quickly these drugs are cleared from the body
Side effect risk and severity
Drug effectiveness
People who are poor metabolisers of CYP2C19 may experience side effects and need lower doses, while ultra-rapid metabolisers might find these drugs ineffective unless doses are adjusted (Pirmohamed et al., 2022; Kennedy et al., 2021).

ALCOHOL METABOLISM AND GENETIC VARIATION

Alcohol is broken down mainly by ADH (Alcohol Dehydrogenase) and ALDH2 (Aldehyde Dehydrogenase 2) enzymes. Genetic differences, especially common in East Asian populations but also relevant elsewhere, can cause acetaldehyde (a toxic byproduct) to build up, leading to flushing, nausea, rapid heartbeat, and other unpleasant symptoms.

Neurodivergent people may have heightened sensitivity to alcohol due to enzyme differences, histamine intolerance, or neurotransmitter variations (Jones et al., 2022; Australian Alcohol Guidelines, 2023).

CONTRACEPTIVE PILLS AND ENZYME GENETICS

Contraceptive hormones are primarily metabolised by CYP3A4, with other enzymes like CYP2C9 and CYP2C19 playing supporting roles. Variations can lead to:

Faster hormone clearance and reduced contraceptive effectiveness
Slower metabolism causing stronger side effects such as mood changes or migraines
Many neurodivergent or sensitive individuals respond better to progestin-only pills or non-hormonal contraception because of these variations (Harman et al., 2023; British Association of Sexual Health & HIV, 2022).

THE BOTTOM LINE: WHY THIS MATTERS

Genetic enzyme variations can profoundly impact medication safety and effectiveness. For autistic individuals and others with overlapping conditions, pharmacogenetic testing can guide safer, more effective, and personalised medication choices.

Understanding these differences allows doctors and patients to avoid harmful side effects, choose appropriate medications, and optimise dosing — improving health outcomes and quality of life.

If you or someone you care for experiences unusual reactions to medications, or if you’re part of the autistic community, discussing pharmacogenetic testing with your healthcare provider could be an important step forward.

REFERENCES
Australian Alcohol Guidelines. (2023). National Health and Medical Research Council.

Australian Therapeutic Guidelines. (2024). Pain Management & Opioid Use. Therapeutic Guidelines Ltd.
Braff, D. L., et al. (2022). Genetic and metabolic contributors to autism spectrum disorder and medication response. Journal of Autism and Developmental Disorders, 52(1), 45-60.

Harman, J., et al. (2023). Genetic variation in steroid hormone metabolism and contraceptive efficacy. British Journal of Clinical Pharmacology, 89(3), 1105-1116.

Hicks, J. K., et al. (2020). Clinical pharmacogenetics implementation: CYP2D6 and opioid prescribing. Pharmacogenomics Journal, 20(5), 445-456.

Jones, S., et al. (2022). Genetic influences on alcohol metabolism and neurobehavioral effects. Addiction Biology, 27(2), e13015.

Kennedy, N., et al. (2021). CYP2C19 polymorphisms and SSRI response in depression: A systematic review. American Journal of Psychiatry, 178(12), 1132-1141.

Ming, X., et al. (2023). Cytochrome P450 polymorphisms in autism spectrum disorder. Translational Psychiatry, 13(1), 89.

Mueller, A. L., et al. (2022). Pharmacogenomics and comorbidities in autism: A clinical update. European Journal of Pediatrics, 181(10), 3801-3810.

Pirmohamed, M., et al. (2022). Genetic determinants of SSRI metabolism: Clinical implications. Clinical Pharmacology & Therapeutics, 112(6), 1460-1470.

Preskorn, S. H., et al. (2021). CYP2D6 genetic variation and opioid safety: Clinical considerations. Pain Medicine, 22(7), 1530-1537.

Smith, T. W., & Johnson, P. R. (2023). Opioid metabolism and safety in CYP2D6 ultra-rapid metabolisers. Australian Prescriber, 46(1), 25-30.

15/07/2025

Just came across this new Nature Genetics study that’s making the rounds — researchers have identified four biologically distinct subtypes of autism, each with different genetic patterns and clinical features.

They analysed data from over 5,000 people and found that certain kinds of genetic variants (common, inherited, de novo) were linked to different presentations of autism — for example, earlier developmental differences vs. social or psychiatric traits that show up later. Apparently the model held up when tested on another large dataset too.

There’s some suggestion this could eventually lead to more tailored support or even diagnosis pathways, rather than treating autism as one broad category.

🧬 Study: https://www.nature.com/articles/s41588-025-02224-z
📰 Summary article: https://medicalxpress.com/news/2025-07-major-autism-uncovers-biologically-distinct.html

Curious what others make of this — potential game-changer, or still a long way off from real-world relevance? What do we think?

Researchers at Princeton University and the Simons Foundation have identified four clinically and biologically distinct subtypes of autism, marking a transformative step in understanding the condition's genetic underpinnings and potential for personalized care.

15/07/2025

Adhd and menopause

09/07/2025

In South Portland, Maine, a group of parents sparked a quiet revolution by replacing smartphones with landlines for their kids. Concerned about the effects of constant screen time, they formed a “landline pod,” where children use home phones to call one another, plan playdates, and have real conversations—no texting, no apps, no distractions. The result? Kids building confidence, empathy, and stronger social skills through simple, meaningful connection. What began as one mother’s creative idea has grown into a neighborhood movement that’s bringing back the lost art of talking.

09/07/2025

SCHOOL TRANSITION MAT 🌈
Free download from my website

https://www.climbingtherainbow.org/product-page/school-transition-mat

A clear and informative mat that can help students with the upcoming transitions to a new class.

Simply download, print and fill in ☺️

08/07/2025

Virgin Australia and Adelaide Airport have launched an Australian-first accessibility program. ✈️

The 'Try Before You Buy' program is the first of its kind in Australia, offering a fully simulated travel experience.

Participants can book, check-in, board and sit on an aircraft - without the plane ever leaving the gate.

The initiative is designed to reduce anxiety and build confidence for individuals who may find flying challenging, including those with disabilities or sensory sensitivities.

Read more at 💻 https://ow.ly/LiSU50WkOkY

📷 Image: Virgin Australia

05/07/2025

Our new blog post explores how overlapping traits of autism and ADHD in girls can lead to vulnerability in relationships. Read the full piece over on our website to learn how we can better support and protect neurodivergent girls.

05/07/2025

Do you have experiences of HYPEREMESIS GRAVIDARUM (HG) yourself or have you noticed that it seems to occur more often in neurodivergent community? If you feel safe to do so I'd be interested to read comments from you below...

Okay so whats the deal?!

Recently, I've been listening curiously to several parents of clients tell me their experiences of HG during pregnancy.

And I'm intrigued…

Is there something linking up here?

HYPEREMESIS GRAVIDARUM (HG) is a severe, potentially life-threatening form of pregnancy sickness, marked by relentless nausea, vomiting, dehydration, and at times significant weight loss.

It affects approximately 1–3% of pregnancies in Australia and globally, though many cases are underdiagnosed or dismissed as ordinary morning sickness. For some, the impact is so devastating that termination or hospitalisation becomes necessary. In the UK, the tragic death of CHARLOTTE BRISLEY, a woman who died by su***de after suffering from HG, brought national attention to the condition’s psychological and physical toll.

Emerging research suggests HG is significantly more common in NEURODIVERGENT populations, particularly those with AUTISM or ADHD. A 2024 study by Brede et al. found that AUTISTIC women were 4.2 times more likely to experience HG, and ADHD has similarly been linked to heightened sensory sensitivity and emetophobia, which may exacerbate the condition (Brede et al., 2024; Chiappini et al., 2021).

Interestingly, HG was once hypothesised to CAUSE AUTISM in children due to in-utero stress. However, it’s now being reconsidered that this may reflect a misunderstanding of the genetic and neurodevelopmental underpinnings: it is increasingly likely that UNDIAGNOSED AUTISTIC MOTHERS were the common denominator. In this light, the apparent association between HG and AUTISM in offspring may be better explained by SHARED HERITABLE TRAITS, not environmental causation.

ALSO…

There is emerging evidence of a link between Hyperemesis Gravidarum (HG) and several complex conditions, including:

POTS (Postural Orthostatic Tachycardia Syndrome)

MCAS (Mast Cell Activation Syndrome)

Ehlers-Danlos Syndrome (EDS), particularly the hypermobile type (hEDS)

These conditions often overlap as part of a broader connective tissue disorder or autonomic dysfunction cluster, especially in neurodivergent and chronically ill populations. Below is an overview of what is known, why it happens, and where to find relevant research.

🔄 OVERLAPPING CONDITIONS & HYPEREMESIS GRAVIDARUM

1. HG and POTS

Link: POTS is a form of dysautonomia, where the autonomic nervous system (which regulates nausea, blood pressure, and digestion) malfunctions.
Why? Pregnancy puts extra strain on blood volume and cardiovascular regulation, which may worsen POTS symptoms, including nausea, dizziness, and vomiting. Women with undiagnosed POTS may experience more severe HG.

How it works:
Blood pooling and reduced perfusion to the brain or gut may worsen GI distress.
Delayed gastric emptying and reduced vagal tone heighten nausea and vomiting.

Research:
Blitshteyn, S., & Mehler, P. (2011). POTS and pregnancy: A review. Autonomic Neuroscience. https://doi.org/10.1016/j.autneu.2011.09.005

2. HG and MCAS

Link: MCAS is a dysregulation of mast cells, which release histamine and other inflammatory chemicals. These can increase nausea, vomiting, and hypersensitivity—especially during pregnancy when mast cell activity is altered.

Why?

Hormonal changes (especially rising oestrogen) during pregnancy can activate mast cells, worsening MCAS symptoms like vomiting, hives, and anaphylaxis.

Histamine is also linked to nausea and gut dysregulation.

How it works:
Mast cell mediators (histamine, prostaglandins) stimulate the vomiting centre in the brain.
Histamine can delay gastric emptying and irritate the GI lining.

Research:
Molderings, G. J., et al. (2011). Mast cell activation disease: A concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology, 4, 10. PMC link
A 2020 paper in Allergy, Asthma & Clinical Immunology explores pregnancy complications and MCAS.

Link
3. HG and Ehlers-Danlos Syndrome (hEDS)

Link: hEDS affects connective tissue, including that which supports the GI tract and autonomic nervous system. People with hEDS are more likely to also have POTS and MCAS, forming a “trifecta.”

Why?

hEDS can result in gastrointestinal motility disorders (e.g., gastroparesis), which contribute to severe nausea and vomiting.

Lax tissues can also impair vagal nerve tone, compounding autonomic instability.

How it works:
Connective tissue weakness in the gut + autonomic dysfunction + mast cell instability = increased risk for severe HG.

Research:
Chelimsky, G., et al. (2019). Joint hypermobility and autonomic disorders: A comprehensive review. Autonomic Neuroscience, 215, 102666. https://doi.org/10.1016/j.autneu.2018.10.005

🔄 PUTTING IT ALL TOGETHER
Many people with HG + POTS + MCAS + hEDS experience what's been informally called the “dysautonomia cluster” or “trifecta.”

These conditions are interconnected via:

Autonomic dysregulation
Connective tissue fragility
Histamine and inflammatory mediator dysregulation
Hormonal sensitivities (especially to oestrogen and progesterone)

📚 KEY ARTICLES TO START WITH
Blitshteyn, S. (2011). Postural tachycardia syndrome and pregnancy. Autonomic Neuroscience.
Link
Raj, S. R. (2013). The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management. Indian Pacing Electrophysiol J.
PMC Link
Mast Cell Activation in Pregnancy:
Allergy, Asthma & Clinical Immunology, 2020
Chelimsky, G. (2019). Joint Hypermobility and Autonomic Disorders.
DOI link

🌀 BONUS: Clinical Insight
Some specialists now suggest that HG might be a clinical clue to uncover:

Underlying dysautonomia
Undiagnosed hEDS
Histamine intolerance or MCAS
especially in women who also have:
Chronic fatigue
GI issues
Temperature sensitivity
Lightheadedness or fainting

If you're personally navigating this, it can be helpful to track:

Heart rate (e.g. via Apple Watch or Fitbit)
Histamine food reactions
Symptom changes with MCAS treatments (e.g. antihistamines, cromolyn, low histamine diet)