In his debate with Allan Young, David Kingdon ^{Reference Kingdon and Young1} has provided his perspective suggesting the dismissal of biological advancements and the promotion of psychosocial research instead. This is our humble attempt to challenge some of the points raised by him.

To discard the biological advances for being unable to pinpoint the ‘exact aetiology’ or ‘cure’ is unjust. It has remained elusive in the whole of medicine (90% of hypertension is idiopathic sans any ‘cure’; so is epilepsy). We never forget to take our antihypertensive pills – why make an exception for psychiatric illnesses?

As for the statement made by Kingdon, ‘research into psychosocial mechanisms, which has been much more productive’, ^{Reference Kingdon and Young1} we refer to a recent meta-analyses by Luborsky. ^{Reference Luborsky, Rosenthal, Diguer, Andrusyna, Berman, Levitt, Seligman and Krause2} These revealed that the effect size attributed to specific therapy techniques is only 0.2 and found common factors such as therapist–client alliance to be more important. ^{Reference Messer and Wampold3} This casts doubts over the clinical relevance of 400 different types of psychotherapies. Absence of large-scale well-controlled trials on efficacy of psychotherapy v. pharmacotherapy in major mental illnesses further leaves us wondering. In addition, the abandonment of once prevalent theories about ‘latent homosexuality’, ‘refrigerator mothers’ and ‘schizophrenogenic families’ only begs us to be doubly cautious before accepting empirical evidence as absolute.

Those who don't learn from mistakes made in the past are condemned to repeat them. We quote this in the context of the past 100 years of dementia research. Alzheimer's initial findings were dismissed as non-specific and most tributes on his death in 1915 did not even mention his, now significant, discovery. Psychological theories of dementia (‘elderly neglect/loneliness’) were in vogue until the 1960s. Ironically, we often dismiss the biological theories despite the preliminary evidence and go on to ‘believe’ the psychological theories without challenging the very basis of that belief.

Finally, in response to the issue of enhanced stigma associated with illness models, the study by Cunningham Owens et al ^{Reference Cunningham Owens, Carroll, Fattah, Clyde, Coffey and Johnstone4} showing enhanced suicidality cannot be overgeneralised and it would be erroneous to undermine the well-recognised benefits and enhanced treatment adherence after psychoeducation. Patients have a ‘right to know’ about their mental illness. We can draw a parallel with HIV or cancer. Have we ever considered shifting away from their biological causation because of stigma or enhanced suicidal risk? How to educate and update the general public with the available information in the most appropriate way is the research question: concealing the evidence is unfortunately not an answer.

In contrast to the 1950s, thanks to the contribution from biological research, current clinical practice rests on a consensus that bipolar affective disorder, schizophrenia, obsessive–compulsive disorder and attention-deficit hyperactivity disorder are primary biological diseases with strong genetic components and psychosocial factors that contribute to the disease process. We agree with Young ^{Reference Kingdon and Young1} when he brings up the bio-psychosocial model. Understanding all the complexities of biology is a ‘process’ and cannot be covered over a short period of biological research.

We can be optimistic at best and sceptical at worst about the clinical relevance of biological contribtions but cynicism and dismissal would be a big mistake.