Stockholm – an autism diagnosis hotspot according to the
psychologist Sebastian Lundström
Nordic countries often lead the way and after
apparently over-diagnosing autism and ADHD they are now eager to de-diagnose
it.
I received an article from the British
Medical Journal which drew my attention.
Swedish authorities are considering requests for “de-diagnosis services” for autism and attention deficit/hyperactivity disorder (ADHD) from a new patient group: adults who no longer want their diagnosis.
The
proposals come against the backdrop of an ongoing study on around 100 patients,
all of whom joined the trial with the hope of getting their diagnostic labels
removed. It could see de-diagnosis services rolled out in several of Sweden’s
clinics in a matter of months, the study authors told The BMJ.
While
“de-diagnosis” is gaining traction in Sweden, clinicians and patient groups who
spoke to The BMJ were divided as to whether similar services
should be set up in the UK or the US.
What
is a de-diagnosis service?
The
psychologist Sebastian Lundström, one of the study’s researchers, told The
BMJ that his work on this new patient group was prompted by “the sheer
number of people with these diagnoses who now are turning into adult age and
being told that they can’t join the military services [or] the draft.”
Historically,
Swedish citizens with an ADHD or autism diagnosis have been barred from joining
the military or working as train drivers without a specific doctor’s note. They
must also provide a medical certificate when applying for a driving licence.
At
the Preventing Overdiagnosis Conference in Oxford earlier this month, Lundström
said that diagnoses had been “assigned by well meaning clinicians” to an
increasing number of Swedish children in recent years but that the label
could often be “sticky.”
Preventing
Overdiagnosis Conference in Oxford
In September 2025 there was a
conference about overdiagnosis across a wide range of conditions, it was not
just about autism and ADHD.
https://www.cebm.ox.ac.uk/preventing-overdiagnosis
But, it did have presentations like:
THE
TIDAL WAVE OF ADHD AND AUTISM: INSIGHTS FROM PATIENTS, PROFESSIONALS AND PUBLIC
HEALTH
Sebastian Lundström’s presentation is
available on YouTube. It is very interesting for anyone interested in the
skyrocketing level of autism diagnosis.
I have mentioned previously that since
in schools in many Western countries more than 20% of kids are now seen as
having special educational needs, do not be surprised if autism/ADHD rates
eventually hit 20%. ADHD does look like
autism-lite to me and the genetic studies also back this up. So, expect that
autism/ADHD reaches 20% of boys.
Now look at Stockholm.
It turns out that in Stockholm 5.9% of
teenage boys now have an autism diagnosis and 15% have an ADHD diagnosis. Some will
have both.
Here is the full video for those who
think this must be a mistake, or that doctors in Stockholm have gone insane.
Now, much to psychiatrists' surprise, adult Swedes are coming forward and trying to delete their autism/ADHD diagnosis from their records. Being Sweden, everything is recorded centrally. In the first 100 cases that were re-evaluated 90% were found to have no symptoms of autism/ADHD. In the video Professor Lundström gives the reasons for the misdiagnosis. It ranges from the parents insisting to have one, to the doctor giving one so that the child can access extra help at school. In many European countries the diagnosis qualifies the child/parents for various social security payments.
There are some downsides in Sweden to be an adult with an autism/ADHD diagnosis. It can affect employment, driving, or securing insurance.
The subject of ADHD leads to the
second half of this post. Here we reconnect with the theme of treatable ion
channel dysfunctions that have become somewhat a hallmark of this blog.
Calcium channel
blockers now considered for ADHD treatment
Repurposing amlodipine, a commonly used blood pressure medicine, could help manage attention-deficit/ hyperactivity disorder (ADHD) symptoms, according to an international study involving the University of Surrey.
Here is the full study
ADHD is a chronic neurodevelopmental disorder that significantly affects life outcomes, and current treatments often have adverse side effects, high abuse potential, and a 25% non-response rate, highlighting the need for new therapeutics. This study investigates amlodipine, an L-type calcium channel blocker, as a potential foundation for developing a novel ADHD treatment by integrating findings from animal models and human genetic data. Amlodipine reduced hyperactivity in SHR rats and decreased both hyperactivity and impulsivity in adgrl3.1−/− zebrafish. It also crosses the blood-brain barrier, reducing telencephalic activation. Crucially, Mendelian Randomization analysis linked ADHD to genetic variations in L-type calcium channel subunits (α1-C; CACNA1C, β1; CACNB1, α2δ3; CACNA2D3) targeted by amlodipine, while polygenic risk score analysis showed symptom mitigation in individuals with high ADHD genetic liability. With its well-tolerated profile and efficacy across species, supported by genetic evidence, amlodipine shows potential to be refined and developed into a novel treatment for ADHD.
This is not an entirely new finding,
but prior research shows that crossing the blood barrier is a key factor. Drugs
like Verapamil win over Amlodipine.
Calcium
channel blockers (CCBs) differ in their ability to penetrate into the brain.
Pharmacoepidemiological studies suggest that CCBs as a class may have
beneficial effects on the risks and outcomes of some psychiatric and
neurological disorders. It is plausible but unknown whether this effect relates
to their brain penetrance. To address this, we used the TriNetX electronic health records network to
identify people prescribed a brain-penetrant CCB (BP-CCB), or those given
amlodipine, a CCB with low brain penetrability. We created cohorts of
patients who, prior to first CCB exposure, either had to have, or could not
have had, a recorded ICD-10 diagnosis in any of the following categories:
psychotic disorder; affective disorder (including bipolar disorder and major
depressive disorder); anxiety disorder; substance use disorder; sleep disorder;
delirium; dementia, or movement disorder. Cohort pairs were propensity score
matched for age, sex, race, blood pressure, body mass index, and a range of
other variables. The outcomes were the incidence of these disorders measured
over a two-year exposure period. Matched cohort sizes ranged from 17,896 to
49,987. In people with no
prior history of psychiatric or neurodegenerative disorder, there was a
significantly lower incidence of most disorders with BP-CCBs compared to
amlodipine, with risk ratios ranging from 0.64 to 0.88 and an overall
risk ratio of 0.88, i.e. a risk reduction of 12%. In people who did have a
prior psychiatric or neurodegenerative diagnosis, differences were much
smaller, but again showed lower risks for several disorders with BP-CCBs
compared to amlodipine. The
differences were somewhat more marked in women and in people less than 60
years old. Results were similar when comparing BP-CCBs with verapamil
and diltiazem. We also compared BP-CCBs with angiotensin receptor blockers, and
found an overall risk ratio of 0.94 in favour of BP-CCBs, but with differential
effects across disorders including a higher risk of psychotic disorder and
dementia, but a lower risk for anxiety and sleep disorders. In some analyses,
there was evidence of residual confounding even after the extensive matching,
in that negative control outcomes showed a reduced incidence with BP-CCBs
relative to the comparator cohort. In summary, CCBs that readily penetrate the brain are associated with a
lower incidence of neuropsychiatric disorders, especially first diagnoses,
compared to CCBs which do not. This may reflect their blockade of
neuronal voltage-gated calcium channels. The findings encourage repurposing
trials using existing BP-CCBs, and suggest that novel BP-CCBs with enhanced and
more selective central actions might have greater therapeutic potential for
psychiatric and neurodegenerative disorders.
Conclusion
I do not think de-diagnosis of autism/ADHD will catch on in the UK or US. Few countries have a centralized register of who has autism/ADHD and in general there are few downsides to adults holding a diagnosis, unlike in Sweden. If it affected your rights to drive a car and what you pay for insurance, there would be a long queue for de-diagnosis.
In the Swedish military
conscription/assessment medical guidelines, autism spectrum disorders are
listed among psychiatric/neurological conditions that can lead to exemption
from service. Some patriotic young Swedes with autism/ADHD actually want to
serve.
As conscription may return to other less
patriotic European countries, you can expect an additional demand for adult
autism diagnosis to avoid the draft!
When it comes to calcium channels, I
think all bases have already been well covered in this blog.
I know of several different calcium and
other channel blockers being used by readers, the latest being Journavx/suzetrigine,
a new one approved in 2025, which blocks Nav1.8. Nicardipine is more likely to
block Nav1.8 in the brain. Journavx was developed specifically to have poor CNS
penetration to avoid central side effects. It targets acute pain situations
where short-term opioid use would normally be considered. It all depends which
Nav1.8 channels you want to block. But, if the blood brain barrier is impaired
(as we know it is in certain types of autism) then more of the drug will enter
the brain than expected.
An impaired blood brain barrier
would also help Amlodipine to cross.
Regular readers of this blog will
already know that calcium channels are dysfunctional across a wide range of
disorders from bipolar, schizophrenia, autism, intellectual disability to
epilepsy.
I was nonetheless surprised that a
university in the United Kingdom would propose repurposing Amlodipine (an L
type calcium channel blocker) to treat ADHD. Even if they are mistaken, at
least they are showing signs of curiosity!
There is no single perfect calcium
channel blocker for the brain.
If you want to target Cav1.2 you have
a great option in Verapamil, because it is relatively selective for this
channel and it crosses the blood brain barrier easily.
If you want to target Cav1.2 and
Cav1.3 then Amlodipine appears the best drug, but it does not cross the blood
brain barrier as well as Verapamil.
I think the ADHD researchers should
start with Cav1.2, because we know 100% it can be blocked in the brain using
Verapamil. Then compare the result with taking Amlodipine.
Pleiotropic
Association of CACNA1C Variants With Neuropsychiatric
Disorders
From this blog we know that both
verapamil and amlodipine can be safely used in autism. A small number of people
do have side effects and discontinue, but most do not have issues.
The effect of the two drugs overlap
but are not identical. This matches what we know about what channels they
block. Verapamil also has other effects:
· Verapamil partially blocks Cav1.3
· Verapamil partially blocks T-type channels (Cav3.1–3.3) particularly at higher doses.
· Verapamil partially blocks potassium Kv channels.
The big advantage of Amlodipine is
that it has a long half-life, so you take it once a day.
Verapamil needs to be taken 3 times a
day, or in the extended release version.
I did look on Reddit and plenty of
people with ADHD were commenting that taking Amlodipine for high blood pressure
had not improved their ADHD symptoms.
Note that ADHD is another umbrella
diagnosis and there will be many sub-types. For some people Amlodipine might
well help. For some people ADHD is just a consequence of being glued to a
smartphone all day, every day, for years on end. Guess what, 60% of adults with
ADHD report chronic sleep problems.
The over liberal diagnosis of autism
in Stockholm does look crazy. Maybe it is the Greta effect?
It is as if Stockholm has developed a
new version of the old “Stockholm syndrome” — an emotional loyalty to the very
diagnostic culture now being questioned. When 90% of adults seeking
de-diagnosis are found not to have autism or ADHD, it suggests that what began
as a well-meaning effort to help children may have trapped an entire system in
its own narrative. Fancy that.
(The term “Stockholm syndrome” comes
from a 1973 bank robbery in Stockholm, when hostages ended up sympathising with
their captors — a classic case of misplaced loyalty.)
