ADHD is not a neurological condition

ADHD is commonly said to be a neurological developmental disorder. The difficulty I have with this statement is that it implies ADHD is a brain disorder. I have no problem with people seeking environmental adjustments, for example at work or in education, because of the kind of person they are. But to justify these adjustments because of a brain disorder is misleading.

Development is neither predestined by our genes nor completely malleable to shaping by the environment. To suggest that ADHD and other neurodevelopmental conditions cannot be “cured” may underestimate the extent to which people can change. It’s all very well to encourage training and education about ADHD, but people do need to be taught facts rather than speculation.

Psychiatry commonly justifies its speculation that ADHD and other functional mental disorders have a biological cause by suggesting it takes a biopsychosocial position, properly taking into account psychosocial as well as biological factors. But it fails to allow for the extent to which the brain is socially constructed by our experiences. Genes set the boundaries of the possible but environments define the actuality of what happens. It doesn’t make sense to reduce mental conditions such as ADHD to a brain disorder. Brain connections in ADHD may be no different from our ‘normal’ experiences. Certainly they have not been proven to be different and even academic reviews of the biological basis of ADHD will caution that no biological markers for ADHD have been found.

Doctors irresponsibly minimising antidepressant withdrawal

Doctors have always minimised the significance of antidepressant discontinuation problems (see eg. previous post). It doesn’t seem to concern them that they have made so many people dependent on antidepressants (see eg. another previous post).

In a systematic review and meta-analysis, Kalfas et el (2025) conclude that the mean number of discontinuation symptoms at week 1 after stopping antidepressants was below the threshold for clinically significant discontinuation syndrome. The article is motivated to show that antidepressant withdrawal may be less common that is thought to be the case (see New Scientist article). The difficulty in obtaining estimates of incidence is made worse by the lack of methodologically rigorous, randomised placebo-controlled trials in real world settings, certainly over the longer-term rather than just after one week. In fact, initially on stopping antidepressants, people can be hopeful that they no longer need antidepressants. 

The data including in the meta-analysis was from 11 trials with short duration of use of antidepressant: 6 for 8 weeks; 4 for 12 weeks; and one for 26 weeks. People can stay on antidepressants for considerable periods of time and the risk of withdrawal symptoms increases with duration of use (see eg. Horowitz et al, 2025). This data obtained after one week discontinuation may well not be generalisable to the bulk of long-term users, particularly if followed up for more than a week.

The Telegraph reports that the research team have suggested guidelines need to be re-written to reassure people that they are unlikely to experience severe side effects when coming off antidepressants, which is clearly unjustified (see eg. article by Mark Horowitz & Joanna Moncrieff on The Conversation). Such advice is contrary to current guidance that people should be informed of the risk of withdrawal symptoms on first starting antidepressants (see eg. previous post). Doctors should be encouraged to follow this guidance, rather than the proposal by Kalfas et al. At least the researchers have subsequently admitted that most studies they reviewed had only followed up patients for two weeks and that antidepressant treatments they studied were shorter than those commonly prescribed in the real world, although this isn’t as explicit in the paper as it should be.