I sat down with Professor Edmund Sonuga-Barke, one of the world’s leading researchers in developmental psychopathology and ADHD. His work has shaped how the condition is understood, diagnosed, and treated across Europe and beyond.

The conversation covers a lot of ground: what is actually happening in the ADHD brain, why diagnosis rates have climbed so steeply in recent years, how social media fits into that picture, and what the evidence really says about medication. Professor Sonuga-Barke does not shy away from the contested questions, and the result is one of the more honest conversations about ADHD we have come across.

If you or someone you know has been diagnosed, is waiting for assessment, or is simply trying to make sense of what feels like an ADHD moment in culture, we think this is worth an hour of your time.

Watch the full episode on YouTube. Link below.

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How do we even compare them to humans?

What does studying animal minds teach us about AI models?

Will they destroy the planet?

Can we trust the CEOs in charge of AI?

We discuss this all in the latest episode of Bridging the Gap:

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The Science:

Avoidance is one of the most well-studied phenomena in behavioural neuroscience, and one of the most misunderstood in everyday life. Most people experience it as a failure of motivation. The research tells a different story.

When the brain anticipates something threatening, whether that is a difficult conversation, a medical appoin

tment, or an emotion it has learned to associate with pain, the amygdala flags it as a threat and the body begins preparing a stress response. Avoidance behaviour is the nervous system’s solution to that response: by not engaging with the trigger, the immediate discomfort drops. That drop in discomfort is experienced as relief, and relief is powerfully reinforcing. The brain logs the lesson: avoidance works (Craske et al., 2008).

The problem is that this relief is short-term and self-defeating. Every act of avoidance confirms to the amygdala that the threat was real and dangerous enough to escape. The threat pathway grows stronger. The avoided thing becomes more charged, not less. And the prefrontal cortex, which is responsible for evaluating threats accurately and overriding emotional responses, gets progressively less practice at doing so (Hartley and Phelps, 2010).

This is why avoidance tends to compound. The email not opened today becomes harder to open tomorrow. The conversation postponed once becomes the conversation that now carries a month’s worth of accumulated dread. The therapy session cancelled becomes the idea of therapy as something you will get to eventually. The nervous system is not being irrational. It is optimising for short-term comfort at the direct expense of long-term wellbeing.

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The Meaning:

Avoidance is often mistaken for a character flaw, procrastination, weakness, lack of discipline. In reality, it is a learned pattern that the brain has practised and refined over time, often starting in childhood when avoidance genuinely was the safest available response to an overwhelming environment.

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Is AI already smarter than us?

Or are the CEOs of frontier AI labs hyping up it’s capabilities to raise more funding?

I spoke with Konstantinos Voudoris (Kozzy), who evaluates AI models truthfully, with no commercial agenda. He has some shocking answers to these questions.

Watch or listen below:

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The Science

In January 2024, a man named Noland Arbaugh became the first human being to receive a Neuralink implant. Paralysed from the shoulders down following a diving accident, he had a chip the size of a small coin placed into his motor cortex by a surgical robot. Within weeks, he was using the device to move a computer cursor, browse the internet, play chess, and operate a smartphone. Using only his thoughts.

This is not science fiction presented as fact. It is the documented outcome of Neuralink’s PRIME Study, a clinical trial approved by the US Food and Drug Administration and currently in progress. By mid-2025, seven people with quadriplegia have received implants. Interim results report typing speeds of up to 40 words per minute using a virtual keyboard controlled entirely by neural signals, a rate comparable to able-bodied touchscreen typing. In November 2024, Neuralink launched a second trial called CONVOY, aimed at extending brain control to assistive robotic arms. In May 2025, the FDA granted the company breakthrough device designation for a speech restoration module, designed to help people with ALS, stroke, and cerebral palsy communicate again.

To understand what is actually happening inside the skull, it helps to understand the basic mechanism. The Neuralink device, called the N1, sits flush against the surface of the brain and deploys an array of electrode threads roughly four to six micrometres in diameter, thinner than a human hair. These threads detect the electrical firing patterns of individual neurons in the motor cortex, the brain region responsible for planning and initiating movement. A decoding algorithm then translates those patterns in real time into digital commands. The brain thinks about moving a cursor. The cursor moves.

Neuralink is technically ambitious but not without precedent. BrainGate, a research consortium involving Brown University and Massachusetts General Hospital, demonstrated cursor control via neural implant as early as 2004 using a device called BrainGate1, and has been refining the technology ever since (Hochberg et al., 2006). What Neuralink has added is miniaturisation, a fully wireless implant, robot-assisted surgery for greater precision, and, critically, the commercial infrastructure and funding to scale. In June 2025, the company closed a funding round of 650 million dollars, bringing total financing to over one billion dollars since its founding in 2016.

The technology is also expanding beyond movement. Neuralink’s Blindsight project, which received FDA breakthrough designation in September 2024, is developing a visual cortex implant designed to restore a form of vision to blind people whose optic nerves are damaged but whose visual cortex remains intact. The underlying principle draws on decades of research into cortical stimulation, including work by William Dobelle, who demonstrated rudimentary artificial vision via phosphene induction in blind patients as far back as the 1970s (Dobelle, 2000). What is new is the resolution and precision now achievable.

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The brain does not know the difference between a signal from a limb and a signal from a chip. It learns. It adapts. And that plasticity, the same property that allows recovery from stroke or injury, is the very thing that makes BCIs work at all.

The Meaning

The immediate applications of this technology are, by any measure, extraordinary. For someone who cannot move or speak, a device that restores the ability to communicate, to operate a computer, to control a robotic arm, is not a convenience. It is a fundamental restoration of autonomy and personhood. On those grounds alone, the development of BCIs deserves serious attention and serious support.

But the implications do not stop there, and Neuralink has never suggested they do. Elon Musk has spoken openly about the longer-term vision: a high-bandwidth interface between the human brain and artificial intelligence, designed not just to assist people with neurological conditions but eventually to augment the capabilities of healthy brains. To allow people to access information, communicate, and process data at speeds the unaided brain cannot match.

This is where the questions become genuinely difficult, and where we think it is worth slowing down.

The brain is not a static processor that inputs and outputs information neutrally. It is a living organ that physically reorganises itself in response to experience. The same neuroplasticity that makes BCIs therapeutically effective, the brain’s capacity to adapt to new input sources, also means that sustained use of a brain-computer interface would likely alter the brain itself in ways we cannot yet fully predict. We know from decades of research on sensory substitution and prosthetic limb use that the brain reassigns cortical territory to incorporate new tools (Merzenich et al., 1984). What happens to the brain that spends years co-processing with a chip is an open and genuinely important empirical question.

There are also questions about identity, consent, and power that neuroscience alone cannot answer. If a device mediates your thoughts, your communication, your memory, who owns that data? If the chip is manufactured, updated, and controlled by a private company, what happens to your cognitive autonomy when the company changes its terms of service? When the subscription lapses? When the company fails? These are not hypothetical edge cases. They are structural features of the model being proposed, and they deserve the same rigorous public debate as the clinical results.

The philosopher Thomas Metzinger, who has written extensively on consciousness and neural interfaces, has argued that BCI development requires what he calls a “neuroethics of the self”: a framework for thinking about what it means to alter, augment, or connect a brain in ways that change the fundamental processes by which a person experiences being who they are (Metzinger, 2003). We do not yet have that framework. We are building the technology faster than we are building the thinking needed to govern it.

The Practice

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Rosalind Picard is a professor at the MIT Media Lab and one of the leading researchers in affective computing, the science of building technology that understands and responds to human emotion. In a 2021 paper published in Communications of the ACM, she noted something that stopped us in our tracks.

After years of research drawing from psychiatry, neuroscience, and psychology, and after studying what people wish they had done differently at the end of their lives, the finding is consistent across cultures, education levels, income brackets, and professions. Almost nobody, looking back, wishes they had achieved more. What they wish, nearly universally, is that they had invested more deeply in their relationships.

Not the patents. Not the promotions. Not the presentations or the publications or the personal milestones. The relationships.

This is not a sentiment. It is a data pattern. And neuroscience has spent decades building an explanation for why it keeps appearing.

The brain is, at its core, a social organ. It did not evolve in isolation. It evolved in groups, and its regulatory systems are built around the assumption of connection with other people. Research by John Cacioppo at the University of Chicago, sustained over two decades, established that loneliness and social disconnection activate the same threat-response systems as physical danger. The isolated brain is a brain in a low-grade state of alarm, with elevated cortisol, increased inflammation, and disrupted sleep (Cacioppo and Hawkley, 2008). The effects are not metaphorical. Sustained loneliness is associated with a measurably higher risk of early mortality than obesity or physical inactivity.

The Harvard Study of Adult Development, one of the longest-running studies in the history of psychology, followed the same group of men across more than eighty years of their lives. Its conclusion, published across multiple decades of follow-up data, was unambiguous: the quality of a person’s close relationships was the strongest predictor of health, happiness, and longevity in later life. Not wealth. Not professional status. Not even physical health at midlife. Relationship quality (Waldinger and Schulz, 2010).

On the neurobiological side, close social bonds trigger the release of oxytocin, which reduces amygdala reactivity and lowers the physiological stress response. They activate the brain’s reward circuitry through dopamine and opioid pathways. They support the regulation of the autonomic nervous system through what Stephen Porges has described as the social engagement system, a set of neural circuits specifically evolved to allow humans to co-regulate each other’s physiological states (Porges, 2011). In short, other people are not just emotionally important to us. They are neurobiologically necessary. The brain uses relationships to regulate itself in ways it cannot fully achieve alone.

The brain did not evolve to function in isolation. It uses relationships to regulate itself in ways it cannot achieve alone. Loneliness is not just an emotional state. It is a physiological one.

The Meaning

There is a painful irony in the deathbed finding. The things most of us spend the majority of our waking hours pursuing, career progression, financial security, status, productivity, are rarely the things we end up feeling mattered most. And yet the reordering almost always happens too late, or at least later than it needed to.

Part of the reason for this is structural. Achievement is measurable. You can count the promotions, the salary increases, the projects completed. Relationships are harder to quantify and easier to deprioritise precisely because they do not announce their value in numbers. The deep conversation you did not have because you were busy, the friend you did not call back, the evening you did not put your phone away: none of these register as losses in the moment. They accumulate quietly.

There is also something worth naming about how modern life is organised. Many of the environments we spend the most time in, workplaces, commutes, screens, optimise for individual productivity rather than social connection. This is not a moral failing on anyone’s part. It is a structural mismatch between the conditions human brains evolved to thrive in and the conditions most of us actually inhabit.

Understanding that relationships are not a nice-to-have alongside a productive life, but are in fact the primary substrate of a healthy nervous system and a meaningful one, changes the calculation. It reframes time spent with people you care about not as time taken away from something more important, but as the thing that is most important, with everything else arranged around it.

The Practice

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There is a common assumption that stress, however unpleasant, is essentially temporary. The pressure lifts, the body resets, things return to normal. This assumption is understandable. It is also, for chronic stress, not what the research shows.

When the brain encounters a stressor, the hypothalamic-pituitary-adrenal axis triggers the release of cortisol, the body’s primary stress hormone. In short bursts, this is an adaptive and well-designed response. Cortisol sharpens attention, mobilises energy, and prepares the body to act. The problem emerges not from the response itself but from its duration. When cortisol remains elevated over weeks and months, the brain does not simply stay on high alert. It begins to change physically.

The region most consistently affected is the hippocampus, a structure central to memory formation, spatial navigation, and the regulation of the stress response itself. Research by Bruce McEwen at Rockefeller University, sustained over several decades, demonstrated that chronic stress exposure causes dendritic retraction in hippocampal neurons: the branching processes that allow neurons to communicate with one another physically shrink (McEwen, 1999). More recent work has confirmed that prolonged stress is also associated with reduced neurogenesis in the hippocampus, meaning the brain produces fewer new neurons in this region than it otherwise would (Bhagya et al., 2017). The hippocampus of someone under sustained stress is, in a measurable structural sense, different from what it was before.

The prefrontal cortex, responsible for planning, decision-making, impulse regulation, and perspective-taking, is similarly affected. Sustained cortisol exposure weakens the synaptic connections within this region and reduces its capacity to regulate the amygdala, the brain’s threat-detection centre (Liston et al., 2009). This creates a feedback loop that is worth understanding clearly: chronic stress impairs the very brain structures responsible for managing stress. The more overwhelmed you become, the less equipped the brain is to pull you back from that state.

The amygdala, by contrast, responds to chronic stress in the opposite direction. Rather than shrinking, it becomes more reactive. Studies using structural MRI have found that prolonged stress is associated with increased amygdala volume and heightened threat sensitivity, meaning the brain’s alarm system becomes louder and more easily triggered even as the structures designed to quieten it become less effective (Tottenham and Sheridan, 2009).

The brain under chronic stress is not simply a tired brain. It is a structurally reorganised brain: a shrinking hippocampus, a weakened prefrontal cortex, and a more reactive amygdala. These changes can be measured. They are also, importantly, reversible.

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The Meaning

If you have spent a sustained period under significant stress and noticed that your memory feels less reliable, your thinking less clear, your emotional reactions harder to manage, these are not signs that you are failing to cope. They are consistent with what the neuroscience would predict. The brain you are trying to function with has been operating under conditions that physically alter its structure. That deserves to be taken seriously, not dismissed as weakness or oversensitivity.

There is also something important in the directionality of these changes. The hippocampus, prefrontal cortex, and amygdala do not operate in isolation. They form an interconnected circuit that regulates how threat is detected, how memories are formed around it, and how the stress response is eventually switched off. Chronic stress disrupts all three nodes of this circuit simultaneously, and in ways that compound one another. A hyperreactive amygdala generates more threat signals. A weakened prefrontal cortex is less able to evaluate those signals accurately. A compromised hippocampus struggles to contextualise them against past experience. The result is a nervous system that is harder to reassure, even when the original stressors have passed.

This matters for how we understand recovery. People who have been under sustained stress for a long time often find that reducing the external stressor is not enough to restore how they feel. That is not a psychological failure. It reflects the fact that the brain has structurally adapted to an environment of threat, and structural change takes time and the right conditions to reverse.

The Practice

• Take the timescale seriously. If you have been chronically stressed for months or years, expecting to feel restored within days of the pressure lifting is not realistic, and the gap between expectation and experience tends to generate additional distress. Recovery from sustained stress is a neurobiological process that unfolds over weeks and months. Naming that honestly tends to reduce the secondary burden of believing something is wrong with you for not bouncing back faster.

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The Science

People-pleasing is rarely a quirk of character. For most people, it is a learned neurological adaptation, one that developed early, in conditions where it was genuinely necessary.

In childhood, the brain’s overriding biological priority is securing attachment. For children raised in environments where caregivers were unpredictable, critical, emotionally volatile, or consistently unavailable, the nervous system arrived at a conclusion that made complete sense at the time: the emotional states of other people are dangerous, and managing them is how you stay safe. The child who learned to read the room, to stay small, to smooth things over before conflict erupted, was not being overly sensitive. They were being adaptive.

This pattern becomes encoded in the brain’s threat-detection architecture. The anterior insula, which processes interoceptive signals and interpersonal cues, becomes highly calibrated to the emotional states of others. Research by Naomi Eisenberger and Matthew Lieberman at UCLA established that social rejection and disapproval activate overlapping neural circuits to those engaged by physical pain, including the dorsal anterior cingulate cortex and anterior insula (Eisenberger et al., 2003). When someone with a deep people-pleasing pattern senses another person’s displeasure, their brain is not being dramatic. It is registering something that, neurologically, resembles being hurt.

Alongside this heightened sensitivity to others, people-pleasers often show reduced activity in the ventromedial prefrontal cortex, the region associated with self-referential processing: knowing what you yourself want, feel, and need. Years of consistently deprioritising internal experience in favour of external demands can attenuate the very neural circuitry responsible for self-awareness (Denny et al., 2012). If you find it genuinely difficult to answer the question “what do I actually want right now?”, this is a plausible neurological reason why. The brain stopped practising that question because asking it did not feel safe.

The Meaning

People-pleasing is frequently misread, including by the person doing it, as generosity. And some of it genuinely is. But beneath the helpfulness, there is usually a quiet, effortful calculation running in the background: if I keep everyone comfortable, I will be safe. If I do not disappoint anyone, nothing bad will happen.

The cost is significant. Chronic suppression of one’s own needs and emotional responses activates the body’s stress systems in the same way external stressors do. Research on emotional suppression has consistently found associations with elevated physiological arousal, reduced immune function, and poorer psychological outcomes over time (Gross & Levenson, 1997). People-pleasers frequently report high rates of anxiety, resentment, burnout, and a persistent sense of not being truly known by the people around them. That last one makes sense: if you have spent years showing people a carefully managed version of yourself, genuine intimacy becomes structurally difficult.

Recognising people-pleasing as a nervous system adaptation, rather than a personality trait or a moral failing, makes both self-compassion and change more accessible. You are not too nice. Your nervous system concluded, based on early experience, that your own needs were a liability. That conclusion can be revised. It takes time, but it is not fixed.

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Anxiety is not a thinking problem. It is a wiring problem, and understanding that distinction changes everything.

When your brain registers a threat, whether real or perceived, the amygdala fires a stress signal before your prefrontal cortex has had any chance to assess what is actually happening. Neuroscientist Joseph LeDoux, whose work on fear circuitry remains foundational in the field, described this as the “low road” of emotional processing: a subcortical pathway so fast that conscious thought is completely bypassed (LeDoux, 1996). Your body is already in alarm mode before your rational mind has formed a single sentence.

By the time you are telling yourself you should not feel this way, cortisol and adrenaline are already circulating. Your heart rate has climbed. Your digestion has slowed. Your body is physiologically primed to run from a threat that, in most modern contexts, does not exist in any physical form.

Chronic anxiety makes this worse over time, not better. Repeated activation of the stress response strengthens amygdala reactivity while simultaneously impairing the prefrontal cortex’s regulatory capacity. Research by Amy Arnsten at Yale has shown that sustained stress exposure degrades the very neural architecture responsible for rational thought and emotional regulation (Arnsten, 1998). The more you have struggled with anxiety historically, the harder it becomes to reason your way out of it in the present. The prefrontal cortex, your inner voice of reason, gets progressively outgunned.

This is why telling someone who is anxious to think more positively is, neurologically speaking, like asking someone with a broken leg to run it off. The tool they are being told to use is the tool that has been compromised.

The Meaning

This is not weakness. It is not a character flaw. It is a nervous system doing exactly what it was built to do, in a world it was not built for.

The shame many anxious people carry, the quiet belief that they should be able to control this, that others manage fine, is built on a false premise. Anxiety is not a failure of willpower or intelligence. In fact, elevated anxiety has been associated with greater threat sensitivity and heightened vigilance, traits that would have been adaptive for much of human history (Stein et al., 2006). The same wiring that makes the anxious brain exhausting to inhabit is the wiring that makes it perceptive, conscientious, and attuned.

Reframing anxiety as a physiological state rather than a personal failure is not just compassionate. It is neurologically accurate, and it is the starting point for actually changing things.

The Practice

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Bridging The Gap is a new podcast series, produced by Red Cap Media, seeking to dive deeper into scientific topics, and bring forward discussions on a broad range of areas.

I recently interviewed Robert Plomin, Professor of Behavioural Genetics at King’s College London, whose research has quietly dismantled one of education’s most expensive assumptions.

The nature-nurture question nobody wants answered

Plomin has spent his career studying what actually makes us who we are, how much of our intelligence, personality, and academic performance is written into our DNA versus shaped by our environment. His findings, replicated across decades and tens of thousands of twins, have consistently pointed in one direction: genetics matters far more than we assumed, and environment far less.

Including the school environment.

To understand why, you need to know one word: heritability.

Heritability measures how much of the variation we see between people on any given trait - height, intelligence, school achievement - can be explained by differences in their DNA.

Imagine a room full of people of different heights. Heritability asks: how much of that variation is genetic versus environmental? For height, the answer is around 80%. We’ve known this for a while and accepted it comfortably.

Here’s where it gets uncomfortable.

For school achievement, heritability is approximately 60%.

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The Mental Health Program is now Grey Matters. Same writers. Same curiosity. But a name that finally fits what this publication has always been trying to do.

I want to tell you why.

Where this started

I started this newsletter because I thought mental health was misunderstood. Not clinically - there are excellent clinicians for that - but scientifically. The gap between what researchers actually know about the brain and what the rest of the world believes felt enormous to me, and it still does.

So I started writing. School visits. A podcast. Collaborations with other Cambridge researchers who felt the same pull toward making the science legible to people who hadn’t spent years inside a lab.

But something kept happening. The questions I found most compelling kept…

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These moments accumulate. Quietly, persistently, they build a narrative in your mind: that looks don’t just matter, they carry moral weight. That appearance is something close to value.

If the people around you seemed to like you more when you were attractive, stylish, slim - you inherited that equation. And once inherited, it embeds itself into your neural architecture and stays there, reshaping how you see yourself and everyone around you, until you do the slow, deliberate work of unlearning it.

That work is harder than it sounds. Because here’s the thing - they’re not entirely wrong.

We live in a world where attractiveness genuinely correlates with outcomes. Attractive people are less likely to receive criminal convictions for the same offences. They’re more likely to be hired, promoted, and paid more. The halo effect - a well-documented cognitive bias where we unconsciously attribute positive personality traits to physically attractive people - is one of the most replicated findings in social psychology. Society didn’t just tell you appearance matters. It built systems that confirm it.

And into this environment, we pipe a continuous stream of skincare products, gym supplements, and billboards featuring athletes who would look entirely average in bad lighting. The beauty standard isn’t just unrealistic - it’s engineered to stay that way.

But here’s what I keep coming back to.

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Drones are being exchanged overhead between Iran and Israel. I can’t fly back to Cambridge. I can’t connect to the supercomputer I need for my PhD. My collaborators in Israel are enduring air raid warnings and blackouts. Research, again, is on pause.

And sitting here, oddly idle, a question arrived that I haven’t been able to shake:

Has war been a net positive or negative for scientific discovery?

Hear me out.

When I finally got through to Dawn - Cambridge’s supercomputer, GPUs humming to life - the irony hit me immediately. This machine exists because of the genius assembled at Bletchley Park during WW2. Alan Turing and his team didn’t invent computing for curiosity. They built the Bombe to crack Germany’s Enigma cipher, or lose the war. The pressure was existential. The breakthrough was foundational.

The nuclear power plants keeping Dawn running? A downstream legacy of Oppenheimer’s Manhattan Project.

Supercomputers require immense amounts of power. Power we can increasingly meet because of nuclear energy - which traces back to Enrico Fermi running the world's first controlled nuclear reaction under a Chicago football stadium in 1942. A Manhattan Project experiment that terrified its creators, and eventually gave us the reactor.

The portable X-ray machines that changed battlefield medicine?

Marie Curie watched surgeons amputate limbs that could have been saved. She used her celebrity to bulldoze military bureaucracy, fund the machines herself, and deploy them to the front lines. The French called them Petites Curies. We still use versions of them today.

The counterargument.

War, it turns out, is a brutal accelerant. Necessity compresses decades into years.

But here’s where it gets uncomfortable.

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If you could do genuinely anything for the rest of your life, what would it be? What makes you intrinsically happy? Travel? Time with friends? Netflix? Exercise?

Now, how far away from that life are you?

One of the biggest things widening that gap between what we truly want and what makes us happy is the environment we grow up in and the narratives we teach ourselves early on.

Did the adults around you celebrate who you were, or what you achieved? Did they comment on the car your friends arrived in, the holidays other families took, the schools they got into?

Every time you saw your family, did they ask “what do you want to be when you’re older?” and light up when you said something socially approved - like going to uni or applying for finance internships? Or did they ask “what do you enjoy?” and “are you having fun?”

All of these scenarios quietly shape what we end up pursuing.

The risk is that if we’re exposed to certain environments when we’re young, we end up chasing careers and lives we never actually wanted.

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The debate over whether humans have free will has been raging for decades. Recent evidence has made the argument against free will particularly compelling. But please be reassured: this is a good thing.

The fact that we don’t have free will, and that our lives might even be determined from the outset, doesn’t mean we should give up because “it’s all pointless.”

Quite the opposite.

The Science: Both Sides of the Argument

The Case FOR Free Will

Proponents of free will argue that we experience genuine choice in every moment. When you decided to read this article, that felt like your decision, didn’t it?

Neuroscientist and philosopher Alva Noë suggests our subjective experience of making choices is evidence enough. Others point to quantum indeterminacy, the inherent randomness at the subatomic level, as leaving room for true free will to emerge. Still others argue that even if our brains operate deterministically, the complexity of human consciousness creates a form of agency that’s meaningful enough to call “free will.”

The strongest argument? We need to believe in free will for society to function. Without it, how do we justify holding people accountable for their actions?

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The Case AGAINST Free Will

The evidence against free will has been mounting for decades.

Benjamin Libet’s famous experiments in the 1980s showed that brain activity indicating a decision precedes our conscious awareness of making that decision by several hundred milliseconds. In other words, your brain has already “decided” before you think you’ve decided.

More recent neuroimaging studies have pushed this gap even further - researchers can predict simple decisions up to 7 seconds before subjects report being aware of their choice.

Then there’s the straightforward logical problem: every thought you have, every decision you make, emerges from brain states you didn’t choose. You didn’t select your genetics, your early childhood experiences, your neurochemistry, or the specific configuration of neurons firing in your brain right now. How can you have free will over outcomes when you had no control over the initial conditions?

Robert Sapolsky’s “Determined”: The Final Nail?

This is what swayed me toward the “no free will” camp.

Stanford neurobiologist Robert Sapolsky makes the most comprehensive scientific case against free will I’ve encountered. His book Determined doesn’t just attack free will from one angle - it systematically dismantles it from every level of biology.

It Starts Before You’re Even Born

Your genetics were determined at conception. Those genes influence your dopamine receptors, your serotonin production, your stress hormone regulation. None of this was your choice.

Then Comes Your Environment

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The nervous system prioritizes survival over insight. When safety cues are absent, cortisol remains elevated, heart rate variability decreases, and emotional range narrows. In this state, reflection and meaning-making are limited.

Repeated experiences of safety—predictable routines, regulated relationships, and gentle self-attunement—reshape neural pathways through neuroplasticity.

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