Metabolites and Misinterpretations: Debunking the Latest Autism 'Risk Factor' Research
In a recent study published in Psychiatry and Clinical Neurosciences, researchers claim to have found a link between arachidonic acid-derived dihydroxy fatty acids in neonatal cord blood and subsequent ‘autism spectrum disorder (ASD) symptoms’ and ‘adaptive functioning.’ As an autistic adult, researcher, and advocate for neurodiversity, I find these claims deeply troubling. They exemplify a dangerous trend towards biological determinism in autism research—a perspective with historical ties to the abhorrent practice of eugenics (aka, “race science”) and one that fundamentally opposes the lived experiences of autistic individuals. This study, whilst scientifically rigorous within its paradigm, fails to consider crucial alternative interpretations and broader ethical implications. By examining this research through the lens of the Power Threat Meaning Framework (PTMF), we can unveil the societal power structures and potential threats to autistic wellbeing that underpin such biological reductionist approaches. Today’s article aims to challenge the study’s assumptions, highlight its overlooked genetic factors, and emphasise the urgent need for autistic voices in autism research.
The Pathologising Perspective
The study’s approach, rooted firmly in the medical model, exemplifies a pervasive issue in autism research. I first encountered this study via a sensationalist headline in my spam folder: “Umbilical Cord Blood Test Could Predict Autism Risk,” courtesy of a dubious click-bait operation masquerading as a neuroscience news service. Such framing immediately sets off alarm bells for those of us in the autistic community.
This medical model perspective fundamentally mischaracterises autism as a disorder to be predicted, prevented, or cured, rather than a natural variation in human neurology. It stands in stark contrast to the neurodiversity paradigm, which recognises autism as a valid and valuable form of human diversity. The researchers’ focus on “ASD symptoms” and “adaptive functioning impairment” reveals an implicit bias towards neurotypical standards of behaviour and development.
The interpretation of biological markers through this pathologising lens is particularly problematic. By framing certain metabolite levels as “risk factors” for autism, the study implicitly suggests that autism itself is a negative outcome to be avoided. This perspective not only disregards the potential strengths and unique contributions of autistic individuals but also paves the way for harmful interventions aimed at “preventing” or “treating” autism.
Moreover, this approach fails to consider how societal structures and expectations might influence the expression and perception of “autistic traits.” The PTMF would encourage us to examine how power dynamics in society might be shaping these “symptoms” and “impairments,” rather than assuming they are inherent deficits. By pathologising autism, such research risks reinforcing societal stigma and discrimination against autistic individuals, perpetuating a cycle of marginalisation and misunderstanding.
Overlooking Genetic Factors
In their eager pursuit of biological markers, the researchers seem to have overlooked a rather obvious fact: autistic parents tend to make autistic children. Shocking, I know. It’s almost as if there might be some genetic component at play. This oversight is not merely amusing; it’s a significant flaw in their interpretation of the data.
Autism’s strong genetic basis is well-established in scientific literature. Twin studies, family studies, and genomic research have consistently demonstrated that autism is one of the most heritable ‘neurodevelopmental conditions.’ Yet, this study appears to treat the presence of certain metabolites in cord blood as potential causative factors, rather than considering them as possible expressions of underlying genetic variations.
From an evolutionary perspective, autism has been a part of human diversity for at least 50,000 years (Hoerricks, 2023). The persistence of ‘autistic traits’ in the human genome suggests that these characteristics have played a valuable role in our species’ survival and development. Some researchers (myself included) have even proposed that certain ‘autistic traits,’ such as attention to detail and pattern recognition, may have been advantageous in our ancestral environment.
Given this context, it’s high time we reframed these so-called “risk factors” as what they truly are: natural genetic variations. The presence of certain metabolites in cord blood isn’t a harbinger of doom, but rather a potential indicator of neurological diversity. It’s akin to treating the presence of genes for red hair as a “risk factor” for gingerness.
By failing to adequately consider these genetic factors, the study perpetuates a narrative of autism as a random occurrence or unfortunate accident, rather than a natural and valuable form of human diversity. This oversight not only undermines the validity of their conclusions but also contributes to the harmful notion that autism is something to be prevented or cured, rather than understood and accepted.
Correlation vs. Causation: A Critical Distinction
The study’s implications hinge on a classic scientific pitfall: confusing correlation with causation. Whilst the researchers have identified an association between certain metabolites and ‘autistic traits,’ they’ve taken a leap worthy of Olympic long-jumpers in suggesting a causal relationship. This isn’t just academic nitpicking; it’s a crucial distinction with real-world consequences.
The ‘cures movement,’ a group as helpful to autistic individuals as a chocolate teapot, often pounces on such correlational findings, twisting them into sensationalist headlines and fear-mongering propaganda. “Umbilical cord blood predicts autism!” they’ll cry, conveniently ignoring the nuances of scientific research. Whilst I’m not suggesting the researchers are card-carrying members of this movement, their framing of the results certainly provides ample fodder for such misinterpretations.
This conflation of correlation and causation can lead parents down a rabbit hole of unproven interventions and ‘treatments,’ potentially causing harm to autistic children in the process. It can also fuel prenatal testing aimed at ‘preventing’ autism, a horrifying prospect that echoes the darkest chapters of eugenic history.
In autism research, cautious interpretation isn’t just good science; it’s an ethical imperative. We must be vigilant against oversimplification and misrepresentation of findings. Correlation may indeed hint at underlying relationships, but it’s a far cry from proving causation. Until we have robust, replicated evidence of causal mechanisms – and even then, we must question the ethical implications – we should treat such findings as what they are: interesting observations that warrant further investigation, not a blueprint for ‘prevention’ or ‘treatment’ of a natural neurological variation.
Challenging the Linear Neurodevelopmental Narrative
The study’s underlying assumption of a single, “typical” developmental trajectory is about as useful as a chocolate fireguard (I think the oestrogen has me fixated on chocolate, though I can’t even eat it). This binary thinking of “typical” versus “atypical” development is not just oversimplified; it’s downright harmful. It’s high time we recognised that neurodevelopment is as diverse as humanity itself.
Take my own journey, for instance. I didn’t gain functional literacy until my late 30s. Was this due to my autism or being a gestalt language processor? Hardly. It was the result of growing up in a time and place that was about as supportive of neurodiversity as a fish is of cycling. The PTMF helps us understand that my delayed literacy wasn’t an inherent deficit, but a consequence of societal structures ill-equipped to support diverse learning styles.
Neurodevelopmental diversity isn’t a bug; it’s a feature. Our species has thrived precisely because of our neurological variations, not in spite of them. Autistic ‘traits’ like pattern recognition, intense focus, and unique problem-solving approaches have likely been crucial in human innovation throughout history. From the first person to notice that seeds grow into plants (probably an autistic person obsessing over a patch of ground) to modern-day coders creating complex algorithms, autistic ‘traits’ have shaped our world.
By clinging to a narrow, linear view of development, we not only miss the rich tapestry of human neurodiversity but also risk pathologising natural variations. It’s time we ditched this outdated narrative and embraced a more nuanced, diverse understanding of neurodevelopment. After all, in the grand symphony of human cognition, we autistics aren’t playing out of tune – we’re playing Mushroom Jazz in a world expecting classical.
The Absence of Autistic Voices
The glaring absence of autistic voices in this study is about as surprising as finding out that water is wet. It’s a classic case of “Nothing About Us Without Us” being interpreted as “Everything About You Without You.” The researchers seem to have forgotten that autistic people aren’t merely subjects to be studied under a microscope, but living, breathing, thinking individuals with valuable insights into our own experiences.
This oversight isn’t just a minor faux pas; it’s a fundamental flaw that permeates the entire study. Without autistic input, the researchers are like colourblind art critics trying to analyse a Monet - they’re missing crucial perspectives that could dramatically alter their interpretations. They’re measuring “impairments” and “symptoms” based on the neuro-majority’s standards, without considering that what they see as deficits might actually be adaptive strategies in a world not designed for autistic minds.
The lack of autistic involvement affects everything from study design to data interpretation. Are they measuring what’s actually important to autistic quality of life, or just what neurotypical researchers think should be important? It’s like trying to understand French cuisine by only interviewing English chefs - you might get some insights, but you’re missing the essence.
It’s high time for a revolution in autism research. We need participatory methods that include autistic individuals at every stage - from conceptualisation to publication. We’re not just data points; we’re experts in our own experiences. Including our perspectives isn’t just ethically right; it’s scientifically necessary for truly understanding autism. After all, if you want to know what it’s like to be a fish, you don’t ask the fisherman - you ask the fish.
Potential Harms and Ethical Concerns
The potential harms stemming from this study are about as subtle as a sledgehammer to a glass house. By framing certain metabolites as “risk factors” for autism, the researchers are unwittingly (or perhaps wittingly) paving the way for a new wave of eugenic practices that would make Francis Galton proud.
Let’s not mince words: the goal of eugenics has always been the “perfection of mankind,” with “perfection” conveniently defined by white, affluent, Protestant folks from the Global North. Now, it seems the neuro-majority has no qualms about adding “neurotypical” to that list of desirable traits. The quest to exterminate our genome is apparently just business as usual.
The risks of prenatal testing based on these findings are chilling. Imagine a world where the presence of certain metabolites in cord blood leads to the termination of pregnancies or invasive prenatal interventions. It’s not science fiction; it’s a very real threat to neurodiversity. We’re not talking about preventing suffering here; we’re talking about preventing autistic people from existing.
The ethical implications of “treating” autism are about as murky as a swamp in fog. Autism isn’t a disease to be cured; it’s a fundamental aspect of who we are. Attempts to “treat” autism are often just thinly veiled efforts to make us conform to the standards of the neuro-majority. It’s like trying to “cure” left-handedness or red hair - not only is it impossible, but it’s also deeply unethical (but they did try with the left handers).
This kind of research, however ‘well-intentioned,’ feeds into a dangerous narrative that autistic people are problems to be solved rather than human beings to be accepted and supported. It’s high time we recognised that the real problem isn’t autism; it’s a society that refuses to accommodate and celebrate neurodiversity.
Final thoughts …
To wrap up, this study is about as helpful in understanding autism as a fish is in understanding mountain climbing. From its pathologising perspective to its genetic oversight, from its correlation-causation confusion to its linear developmental fairy tales, it’s a masterclass in how not to do autism research. It’s high time we ditched these neuro-majority-centric, potentially eugenic approaches and embraced research that actually includes autistic voices. We need studies that celebrate neurodiversity, not ones that treat us like puzzles to be solved or problems to be fixed (can we focus on secure housing?). Let’s aim for research that's as diverse and vibrant as the autistic community itself. After all, if you’re going to study jazz, you’d better be ready to improvise.