*Acknowledgments to Claudio Lironcurti and Claudio Ricciardi
Introduction
Recent advances in genomic investigation techniques have favored the collaboration between psychiatrists and geneticists, aiming at identifying specific genetic profiles as putative causative factors of mental illness. This is resulting in an increased number of publications of data dealing with the role of genetic variants in determining the risk of psychiatric disorders – such asanorexia, ADHD, autism, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia and Tourette’s syndrome. In addition, these disorders have been grouped into three genetically related groups such as mood and psychotic disorders, early onset neurological disorders, and compulsive behavioral disorders. Genetic variants reported, mostly classified as polymorphisms, have been identified in genes withpleiotropic functions expressed in the central nervous system and involved in neuronal developmentprocesses. The hypothesis underlying these studies is that alterations in the expression of variants inthe second prenatal trimester could represent a risk factor – or even a causative factor – in the pathogenesis of psychiatric disorders. Accordingly, psychiatric genetics states that specific genetic profiles represent the main risk of predisposition (75%), while it attributes a much lesser role to environmental factors (25%, including traumatic human relationships). This suggests that focusing on the development of drugs able to inhibit the effect of variant genes would be a more appropriate therapy. However, the results of these studies do not seem to be sufficient to demonstrate the role of genetics in psychiatric disorders since, albeit on a large population sample, they are mainly based ongenotype-phenotype statistical correlation. Indeed, the published studies are unable to clarify how the effects produced by the presence of identified gene variants can alter the biological mechanisms underlying the functions of human nervous system. The consequence of this approach is developing therapies targeted against the symptoms, rather than the causes of disease, and this would severely limit the possibilities of psychiatric patients’ recovery.
We think that diagnosing mental illness based on the results of genetic tests is somehow unethical. We also consider unethical non-scientific media reporting that the genetic cause of psychiatric disorders has been fully proven. As well documented, attributing the cause of psychiatric disorders to genetics totally contrasts with the findings of Massimo Fagioli as described by the Human Birth Theory, where the main cause of mental illness is attributed to the alteration of inter-human relationship. Therefore, specific genetic profiles should be considered nothing else than “risk co-factors”, eventually contributing in part to the onset of illness, only when facing specific environmental hits.
Aims
In light of the foregoing, we intend to carry out a critical review of published data on genetic etiopathogenesis of psychiatric diseases. In addition, we intend to study the impact of the disclosure of the results of psychiatric genetics studies on public opinion. In fact, the strong ethical problem arising would concern the scientific communication by journalism and both public and political institutions, where a manipulative use of scientific data aims to a consensus from public opinion for ideological, cultural, political or economic purposes. This put the psychiatric research at a serious risk.
Conclusions
The purpose of this ongoing research is to verify whether studies in the field of psychiatric genetics have been biased by a distorted hypothesis influenced by organist preconceived ideas.
Bibliography
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