Improving Learning by Consolidation? Perhaps Vagal Nerve Stimulation? Perhaps Exercise?

 

This is today’s paper: 

Vagal nerve stimulation induces vascular oscillations and enhances long-term learning

I have a longstanding interest in what you might call improving cognitive function or treating intellectual disability.

Having a strong intellect does not guarantee that you can function well in society, but a basic level of intellectual ability is clearly a prerequisite for many aspects of independent living.

Adaptive function is the term used to describe all the basic skills that most of us take for granted.

My particular interest has been whether it is possible to fast-track skill acquisition in previously slow learners using biology and chemistry.

More broadly, many people with average IQ struggle to retain skills that are being taught to them. Here, the problem may lie at a later stage of learning: consolidation. Without successful consolidation, you do not retain what you have been taught and therefore cannot apply it later. It is not necessarily that you could not understand it in the first place.

A learner needs to be able to:

acquire → consolidate → retain → generalize

new skills.

In many respects, this may be more important than IQ itself.

Acquisition — Can you learn it initially?
Consolidation — Does the new learning become biologically stabilised?
Retention — Can you still remember or perform it later?
Generalization — Can you use it in different situations?
Adaptive function — Does it help you function independently in real life?

After all, what determines whether a person can function independently is not simply how many points they score on an intelligence test. It is whether they can learn to communicate, read, calculate, cook, travel independently, use a computer, perform a job, manage money, and acquire whatever other skills their particular life requires.

For those with classic autism, the initial barrier of skill acquisition can often prove insurmountable.

For children who are above the modern threshold for intellectual disability, the problem may occur at a later hurdle.

Historically, the threshold used to define intellectual disability was much less strict. As a result, perhaps 18% of children could fall below the threshold. Today, the definition is much narrower, with intellectual disability affecting approximately 2.5% of the population. That means that a large group of children who might once have been recognised as having significant learning limitations are now expected to succeed within mainstream education.

They may have sufficient intellectual ability to understand and initially acquire what they are taught, but struggle to consolidate, retain and apply it sufficiently well, ultimately falling behind at school.

Today's post is primarily about these people, although many of the same ideas may still be relevant to improving adaptive function in classic autism.

 

The problem in schools

The scale of the educational problem is striking.

In England, the 2026 high school results (called GCSEs) showed that 28.2% of 16-year-olds did not achieve a pass grade (grade 4 or above) in maths and 28.6% did not achieve grade 4 or above in English.

If you fail you have to resit the exam.

The same analysis reported that 84.7% of maths resit candidates and 80.2% of English-language resit candidates again failed to achieve a pass grade in 2026.

If someone fails an examination, there are many possible explanations.

Perhaps they were not taught the material effectively.

Perhaps attendance, poverty, anxiety, motivation, language, sensory problems, attention or working memory are involved.

But in at least some individuals, there may also be a problem with acquiring, consolidating or retaining the required skills.

If repeating the educational process produces another failure in four out of five resit candidates, simply providing more of the same may not be enough.

And the consequences extend far beyond an examination.

Failure to acquire foundational literacy and numeracy can restrict access to further education, apprenticeships and employment. Young people without qualifications are at substantially greater risk of becoming NEET — not in education, employment or training.

There are 1 million NEETs in the UK aged 16 to 24 years old.

The ability to acquire foundational skills is a major determinant of life opportunities.

 

Autism provides another way of looking at the problem

This is one reason I have become increasingly interested in the concept of adaptive behaviour.

Someone with autism or intellectual disability may not need to become more intelligent in some abstract sense.

They may need to become better able to learn a particular set of useful skills.

That could mean:

• communicating wants and needs
• dressing and personal hygiene
• preparing food
• following a sequence of instructions
• travelling independently
• learning a vocational task
• using money
• learning academic skills
• coping with a new environment
• transferring a learned skill from one situation to another.

These are adaptive skills.

And there is an important distinction between diagnosis and learning capacity.

Monty has classic autism. Yet, with his pharmacotherapy and sustained educational support, he was able to pass GCSE-level maths and English, albeit at the age of 18 and on the first attempt.

That does not mean autism does not affect learning. It very much does.

It means that a diagnostic label does not tell us how much an individual can ultimately learn.

The useful question is:

What is preventing this particular person from learning, and can we change it?

In Monty's case, years of teaching and behavioural support had already been trying to give him these skills. What changed, alongside the Polypill, was his ability to consolidate what that support was providing. That is one individual's trajectory, not proof that the Polypill was the active ingredient — but it is the observation that started me asking the question this article is built around.

 

ABA: an application of "practice makes perfect"

One reason behavioural interventions such as applied behaviour analysis are interesting is that they attack the problem directly.

·        Break a complicated behaviour into components.

·        Teach one component.

·        Practice it repeatedly.

·        Reinforce successful performance.

·        Gradually increase the difficulty.

·        Combine the components.

·        Repeat until the behaviour becomes reliable.

 

In that sense, ABA can be viewed as a highly structured application of a very old idea:

Practice makes perfect.

Of course, modern behavioural intervention is considerably more sophisticated (when done correctly!!) than simply making someone repeat something. It involves task analysis, prompting, shaping, reinforcement, generalization and measurement.

The evidence is also more complicated than either its strongest advocates or its strongest critics sometimes suggest. Studies and meta-analyses report improvements in some adaptive and developmental outcomes, but the evidence varies in quality and effects are not uniform.

The important point here is not whether ABA is the perfect treatment for autism.

It is that:

Intensive, structured practice can produce measurable changes in what a person can do.

That raises a fascinating biological question.

What if the effectiveness of intensive practice partly depends on something happening inside the brain?

The therapy provides the enormous amount of structured practice.

But the brain still has to change in response to that practice.

 

The brain has to be plastic

Learning requires plasticity.

A new skill involves changes in neural circuits. Some of those changes are temporary. Others become consolidated and eventually become relatively automatic.

So perhaps there are two ways to improve learning:

Increase the quality and quantity of practice.

Or:

Make the brain more receptive to the practice.

Behavioural intervention primarily attacks the first problem.

Pharmacology attacks the second.

Neuromodulation might provide another route.

 

There is already a large cognitive-enhancement industry

The idea of modifying the brain to improve cognition is hardly new.

There is already a huge industry devoted to it, ranging from prescription stimulants to old-fashioned nootropics, metabolic interventions and nutritional supplements.

 

Prescription stimulants

The clearest examples are methylphenidate and the amphetamine-based drugs used to treat ADHD.

In people with ADHD, these drugs can improve attention and several neurocognitive functions. A meta-analysis of randomized trials found small improvements in working memory, vigilance and response inhibition with methylphenidate.

Interestingly, the effects are not necessarily confined to people with ADHD. In healthy adults, meta-analyses find small effects on particular cognitive domains rather than a general increase in intelligence.

And there is an especially relevant finding for the argument of this article: a controlled experiment found that methylphenidate enhanced declarative memory consolidation in healthy volunteers.

That is much more interesting than simply saying that stimulants make people more alert.

It suggests that at least some pharmacological cognitive enhancement may operate at the level we are interested in - not simply performing better during learning, but retaining more of what was learned afterwards.

 

Piracetam, vinpocetine and the nootropics

Then there are the classic nootropics such as piracetam and vinpocetine.

Piracetam has been investigated for decades, but the modern evidence is considerably less impressive than its reputation might suggest. Recent systematic review evidence has not established a clear memory benefit over placebo.

Vinpocetine is particularly interesting because its proposed mechanisms include effects on cerebral circulation and neuronal metabolism. But again, mechanistic plausibility is not the same as clinical efficacy. A Cochrane review concluded that the evidence was insufficient to establish vinpocetine as an effective treatment for cognitive impairment.

Nevertheless, these drugs introduce another important idea.

 

Blood flow and brain metabolism

Some compounds marketed or investigated as cognitive enhancers work partly by altering cerebral blood flow, oxygen delivery or brain metabolism.

This does not mean that simply increasing cerebral blood flow makes someone more intelligent. Cerebral perfusion is tightly regulated, and more is not necessarily better.

But neurons require oxygen and metabolic substrates, and vascular responses are closely coupled to neural activity.

This makes the vascular finding in the new Tohoku VNS study particularly intriguing.

The researchers found rhythmic changes in cerebellar blood volume following VNS, and the magnitude of these oscillations was associated with subsequent long-term learning.

Perhaps vascular and metabolic changes are not merely passive consequences of neural activity.

Perhaps, under some circumstances, the vascular/metabolic state of the brain helps determine how effectively learning is consolidated.

 

Ketones and omega-3s

The same logic has inspired very different approaches.

Ketone esters are being investigated as a way of changing the brain's fuel supply by rapidly increasing beta-hydroxybutyrate (BHB). Omega-3 supplements, particularly EPA and DHA, are marketed extensively for "brain health" and sometimes even for increasing intelligence.

There are interesting biological mechanisms and some encouraging findings in particular populations.

But neither should currently be described as a proven way of raising IQ.

Again, the distinction matters:

changing a biological variable → changing a cognitive measure → improving learning → improving real-world function

are four different claims.

And that distinction is central to what I am proposing here.

 

An older hypothesis: TRH and "retuning" the brain

There is another thread in my own thinking that now looks unexpectedly relevant.

More than a decade ago, I was trying to understand something particularly striking about Monty.

Why did certain forms of intense sensory stimulation sometimes seem to produce such dramatic changes in his behaviour?

Being on the upper deck of a ferry in the wind, sitting on an open-top bus or experiencing similar forms of strong sensory stimulation appeared to have effects that seemed disproportionate to the stimulus itself.

I began looking for physiological situations that might produce a similar state change.

This led me to thyrotropin-releasing hormone (TRH).

TRH is best known for its role in the hypothalamic-pituitary-thyroid axis, but it is also a neuropeptide with effects on neural activity, arousal and neurotransmitter systems.

I eventually proposed what I called the Peter Hypothesis of TRH-induced behavioural homeostasis in autism.

The idea was that abnormal TRH signalling might contribute to some aspects of sensory and behavioural dysregulation in some autistic individuals, and that increasing TRH activity might potentially "retune" aspects of brain function.

This was — and remains — a hypothesis, not an established explanation of autism.

But it led to a practical question.

Native TRH has a very short half-life and is not particularly convenient as a therapeutic agent.

I therefore became interested in taltirelin (Ceredist), an orally active TRH analogue developed in Japan for spinocerebellar degeneration.

My own subsequent experience with Ceredist was striking, but it is important to be clear about what that means and what it does not mean.

The TRH literature provides another reason for investigating the hypothesis: experimental studies of TRH and TRH-like peptides have reported effects on memory and memory consolidation, particularly in animal models.

That brings us surprisingly close to the question we are now asking about VNS.

 

The gut–vagus–TRH connection

More recently, another piece of the puzzle appeared.

I wrote about research involving rifaximin, the gut microbiome, the vagus nerve and TRH.

Rifaximin is particularly interesting because it acts largely within the gut rather than penetrating the brain in significant amounts.

Yet experimental work has suggested that rifaximin-induced changes in the gut can influence brain and peripheral TRH/TRH-like peptide systems.

The proposed pathway was:

rifaximin → gut microbiota → vagal signalling → brainstem/hypothalamic signalling → TRH

This was based on animal research and remains a hypothesis rather than an established human mechanism.

But conceptually it is fascinating.

Perhaps we do not always need to administer a brain-active molecule directly.

Perhaps we can sometimes influence the body's own signalling system that causes the brain to change.

That gives us an interesting contrast:

Direct pharmacological route

taltirelin/Ceredist → TRH receptors

versus

Indirect brain-body route

gut → vagus → brain → endogenous TRH signalling.

And now there is a third possibility.

 

The vagus nerve enters the learning story

This brings us to vagus nerve stimulation (VNS).

I actually wrote about transcutaneous VNS back in 2018, so the technology itself is not new to me.

What has changed is the question we can now ask of it.

VNS has been used clinically for years, particularly in epilepsy, and is also used in some forms of depression and stroke rehabilitation.

The new question is whether VNS can be used not merely to treat a neurological disorder, but to enhance learning itself.

There is now preliminary human evidence that it can influence neuroplasticity and learning.

Recent human studies of transcutaneous VNS have reported effects on motor learning and neural plasticity, although results are not uniformly positive.

Some studies have found improved learning under particular stimulation conditions, while others have found no benefit.

This is important.

It means that VNS should not be thought of as a generic "brain booster."

The timing, location, intensity and type of stimulation may matter.

Then came the Tohoku experiment:

Vagal nerve stimulation induces vascular oscillations and enhances long-term learning

A recent study from Tohoku University has made the idea considerably more interesting.

Researchers trained mice on a cerebellar motor-learning task and then delivered VNS after the training session.

The stimulation did not simply make the animals perform better immediately.

Instead, the improvement emerged later.

The researchers interpreted this as evidence that VNS was affecting post-training processes involved in long-term consolidation.

They also observed rhythmic changes in blood volume around the cerebellar flocculus after VNS.

Animals with larger VNS-induced vascular oscillations tended to show better learning several days later.

The important point is therefore not simply:

"VNS improves learning."

It is:

VNS delivered after learning may alter the biological environment in which learning becomes a lasting memory.

This is still an animal experiment.

It does not establish that the same thing happens in humans.

And the vascular oscillations are associated with the learning effect; the experiment does not prove that they are themselves the causal mechanism.

But it introduces a very interesting concept:

Perhaps the period immediately after learning is a therapeutic window.

The vagus may have several routes to memory consolidation

This is where the new finding connects unexpectedly well with my earlier TRH work.

We now have two very different ideas involving the vagus and memory consolidation.

The Tohoku study suggests:

electrical vagal stimulation → vascular/metabolic changes → enhanced post-training consolidation

My earlier gut-brain hypothesis suggests:

gut manipulation → vagal signalling → TRH → effects on neural state and memory

These are obviously not the same mechanism, and the evidence supporting them is at very different stages.

But they share an important feature:

The vagus may provide a route through which signals from outside the brain influence the biological processes that determine whether learning becomes a lasting memory.

This makes the vagus more interesting than simply another way of increasing alertness.

It raises the possibility that the vagus forms part of a broader brain-body learning system, in which neural, hormonal, metabolic and vascular signals influence what happens after a learning experience.

And there may be several ways of accessing that system.

We might stimulate it electrically.

We might influence the gut signals reaching it.

We might alter downstream cholinergic or noradrenergic systems.

Or we might influence hormones such as TRH.

These approaches are not equivalent.

But they point towards the same broad question:

Can we manipulate the biological state of the learner so that practice produces a larger or more durable change?

 

Which VNS are we actually talking about?

Once we start talking about vagus nerve stimulation as a possible way of enhancing learning, another problem immediately appears.

There are now many devices being sold as "vagus nerve stimulators."

They are not all the same.

Some are well-characterized medical or research devices that have been used in peer-reviewed human studies.

Others are consumer wellness products for which the evidence is much thinner.

Some use completely different stimulation parameters or stimulate different parts of the body.

Putting two electrodes on the ear and calling the resulting device a "vagus nerve stimulator" does not demonstrate that it is producing the biological effect seen in a research study.

The question should therefore not simply be:

Does this gadget stimulate the vagus nerve?

It should be:

Has this particular technology, at this particular anatomical site and with these particular stimulation parameters, actually produced a reproducible biological or clinical effect in controlled human research?

That is a much higher standard.

 

NEMOS and research-grade auricular VNS (it fits to your ear)

 

The NEMOS/tVNS system is one of the best-established research platforms for auricular VNS.

Studies have commonly used stimulation at the cymba conchae, often around 25 Hz with pulse widths around 200 microseconds and intensity individually adjusted for tolerability.

The important point is not that every NEMOS study has been positive.

It hasn't.

The important point is that the device and stimulation approach have a substantial peer-reviewed research history.

That makes it very different from an anonymous electrical stimulator bought online.

 

Parasym/Nurosym

 

 

Another interesting example is the Parasym technology now marketed as Nurosym.

The technology has been used in peer-reviewed human research, including randomized studies.

That doesn't mean Nurosym has been proven to enhance learning.

It hasn't.

Nor should manufacturer-reported numbers of clinical studies be confused with the number of independent positive randomized trials.

But it does mean that the technology has considerably more research provenance than a generic "vagus nerve" gadget.

If I were interested in testing this hypothesis experimentally, I would therefore prefer a device with a documented research history rather than simply the cheapest device advertised as VNS.

 

Cervical VNS is another category (it attaches to your neck)

Devices such as gammaCore provide non-invasive cervical VNS rather than auricular stimulation. Round your neck and not in your ear.

 

gammaCore has a substantial clinical research base and is used medically for headache disorders.

But cervical VNS and auricular VNS should not automatically be treated as equivalent.

A result obtained with one should not simply be transferred to the other.

 

And the cheap devices?

This is where I would be most cautious.

A cheap electrical stimulator may genuinely produce physiological effects.

It may even stimulate some vagal afferents.

But unless we know:

• where the electrodes are positioned
• the current being delivered
• frequency
• pulse width
• waveform
• intensity
• duration
• and timing

we cannot assume that it reproduces the intervention used in a research study.

Cheap does not necessarily mean ineffective.

But:

cheap + no parameter transparency + no independent human evidence = unknown.

I would not describe such a device as a scientifically validated VNS intervention.

 

The timing problem may be even more important than the device

There is another reason not to think of VNS as a simple wellness treatment.

The stimulation may need to be appropriately timed.

Some human experiments have found benefits when stimulation is paired with particular phases of learning or movement.

Other studies have found no effect.

And some have found evidence that poorly timed or nonspecific stimulation can actually interfere with learning.

The Tohoku experiment therefore makes the question of timing particularly interesting.

Perhaps the optimal sequence will eventually turn out to be:

high-quality training → VNS → consolidation

rather than:

VNS → training

We simply don't know yet.

 

There may also be a pharmacological version of VNS

This brings us back to the earlier TRH hypothesis.

Perhaps the vagal system does not always have to be stimulated electrically.

The vagus is intimately connected with cholinergic signalling and the so-called inflammatory reflex.

And the gut can influence the brain partly through vagal signalling.

TRH provides another possible downstream pathway.

This gives us several conceptually different ways of modifying the brain-body system:

Electrical neuromodulation

VNS → brainstem/autonomic pathways → neuromodulation

Gut-mediated signalling

microbiome → vagus → brain → endogenous signalling

Pharmacological modulation

taltirelin/Ceredist or another drug → specific neural/hormonal pathway

These are not interchangeable.

But perhaps the future will involve identifying which biological bottleneck is relevant in an individual and choosing the intervention accordingly.

 

Exercise: another route to a plasticity-permissive brain?

There may be another route into this broader brain-body learning system: exercise.

We have known for decades that physical activity is good for the brain. Exercise is associated with improved cognitive health and, in animal studies, changes in neurotrophic signalling and hippocampal neurogenesis.

But a fascinating new line of research suggests that we may be missing part of the story.

Perhaps contracting muscle does not merely improve the brain indirectly through better cardiovascular health.

Perhaps muscle actively sends signals that change the biological state of the brain.

Recent experiments in mice and cell cultures have suggested a possible pathway involving astrocytes. Exercise was associated with a mechanically activated, contractile state in hippocampal astrocytes, while factors released from contracting skeletal muscle could induce changes in astrocyte behaviour in laboratory experiments.

Exercise engages a mechanically activated astrocyte state linking muscle activity to hippocampal plasticity

Read the full paper on bioRxiv

 

This is still early science. The mechanism has not been established in humans, and it would be premature to claim that exercise improves learning through astrocyte contraction.

But the hypothesis is intriguing.

The possible sequence is:

muscle contraction → peripheral signals → astrocyte state change → altered neural environment → increased capacity for plasticity

That may be more important than the simplistic idea that exercise merely "creates more neurons".

 

Exercise after learning

There is already evidence that exercise performed after learning can influence later memory.

This is particularly interesting because the exercise occurs after the information has already been acquired.

In some experiments, timing appears to matter. Exercise immediately after learning is not always optimal; exercise performed later during the consolidation period may sometimes produce stronger effects.

That raises a different question from the usual one:

Does exercise make us more alert while we are learning?

Perhaps the more interesting question is:

Can exercise alter the biological processes that determine whether recently acquired information becomes a lasting memory?

One possible model is that learning creates a temporary neural trace.

Exercise then generates a complex physiological signal involving muscle-derived molecules, metabolism, autonomic activity and perhaps astrocyte responses.

These signals may alter the biological environment in which recently activated neural circuits are attempting to consolidate.

In other words, learning provides the information while exercise may help provide the conditions for lasting plastic change.

 

A possible parallel with VNS

This creates an interesting parallel with vagus nerve stimulation.

The Tohoku experiment discussed earlier suggested:

training → VNS → altered post-training biological state → enhanced long-term learning

The exercise hypothesis might be:

training → exercise → peripheral and brain signalling → altered plasticity/consolidation state

These mechanisms are clearly not identical.

VNS primarily accesses the brain through vagal and brainstem pathways.

Exercise produces a much broader physiological response involving muscle, metabolism, circulation, autonomic activity and potentially muscle-to-brain signalling.

But they may share an important conceptual feature.

Both could potentially influence the period after learning when neural changes are being stabilized.

 

Practice plus biology

This brings us back to the central question of this article.

Perhaps learning interventions have two components.

The first is what does the person need to practise?

The second is what biological conditions allow the brain to respond most effectively to that practice?

Behavioural intervention, education and rehabilitation primarily provide the first.

Pharmacology, sleep, exercise and neuromodulation may influence the second.

The future may therefore involve deliberately combining them.

For example:

   

This could connect several apparently unrelated problems

A child struggling with literacy, an autistic child learning a functional behaviour, a person with intellectual disability learning independent-living skills, an adult struggling to learn a new job and an older person with mild cognitive impairment are obviously not experiencing the same neurological condition.

But they can all face a common functional problem:

Can the brain acquire, consolidate, retain and generalize the skills needed for that person's life?

That may be a more useful target for cognitive enhancement than simply trying to increase IQ.

The real endpoint should be adaptive function

A treatment might improve a score on a computerized memory test by 8%. Interesting.

But it would be far more meaningful if it allowed someone to learn a new vocational procedure with fewer repetitions, prepare a meal independently, retain mathematics they have repeatedly been taught or learn strategies that help them remain independent.

We can measure this progression:

Acquisition — How much practice is required?

Consolidation — Does the new learning become stabilised?

Retention — What remains after a week or a month?

Generalization — Can the skill be used in different situations?

Adaptive function — Does it actually make the person more independent?

Conclusion

Perhaps the future is not a single cognitive enhancer, but a personalized combination of:

• Pharmacotherapy — to address a specific biological bottleneck.
• Structured practice — to provide the information and repetitions needed to learn.
• Exercise — potentially to support plasticity and consolidation.
• Perhaps neuromodulation, including VNS — to influence plasticity or post-learning consolidation.

Different people will have different bottlenecks, so not everyone will need the same combination.

The goal is not simply to increase IQ, but to help each person acquire, retain, generalize and use the skills their life requires.