This is both a medical and ethical question. Because the medications are not without side-effects, should we prescribe a drug in the absence of identifiable illness?

Usage of atypical antipsychotic during puberty alleviate schizophrenia like behavioral and anatomical deficits in rats after maternal immune activation which is a schizophrenia risk factor in humans (Piontkewitz, Assaf & Weiner, 2009). To gain evidence that same approach will also make in humans, a study should be designed with people with high risk of schizophrenia (schizophrenia in relative e.g.) and then they should be assigned blindly to treatment or placebo group and also their psychological conditions should be monitored from puberty till end of high risk period for schizophrenia (from 14 to 30 for males, up to +35 for females). As far as, I know there is not such a study and conduction such a study is not easy if multiple hospitals and labs not are agreed to conduct such a long study. Also necessary ethical approval should be taken as atypical antipsychotic use might have side effects on teenagers.

Edit:

This relevant article just came to my attention:

https://pubmed.ncbi.nlm.nih.gov/16648318/#:~:text=Efficacy%20measures%20included%20the%20conversion,psychosis%2C%20a%20nearly%20significant%20difference.

This is both a medical and ethical question. Because the medications are not without side-effects, should we prescribe a drug in the absence of identifiable illness?

Exactly there is an ethical side but in my opinion if someone with high risk of schizophrenia approve for this, there is no ethical problem.

Maybe you can focus also on the nurture or environmental components regarding the development of schizophrenia in genetically vulnerable individuals. Focus on breeding styles, trauma avoidance, cognitive and psychoeducational support, drug-use avoidance and similar approaches could help prevent schizophrenia development as well as antipsychotic drugs, without side effects and allowing a more naturalistic course. This article explores interventions in adolescence, you might find it helpful.

Gomes, F. V., Rincón-Cortés, M., & Grace, A. A. (2016). Adolescence as a period of vulnerability and intervention in schizophrenia: Insights from the MAM model. Neuroscience and biobehavioral reviews, 70, 260–270.

There is no vaccine for schizophrenia, among other reasons because schizophrenia is not a single disease or univocal.

Administering an antipsychotic medication preventively is ethically inadmissible and psychopharmacologically inappropriate.

My advice would be to wait for the appearance of a prodromal stage and once clearly objectified, and then act according to biopsychosocial criteria.

Open dialog method is not enough for schizophrenia. Excessive limbic dopamine activity plays a role in psychosis and antipsychotic drugs block postsynaptic D2 receptors in CNS.

Although a number of genes have been found defective in schizophrenia, these genes account only for a small number of cases. Thus, the consensuses on the genetic predisposition for schizophrenia have not reached yet. Drug treatment is decided primarily on the basis of positive, negative and general symptoms of psychosis.

Its a good question but maybe It is not possible today, according to the pathophisiology and with actual medicine, we are only abble yo treat symptoms, and no everybody with a genetical predispisition Will get the illnes

Patients off antipsychotics do about four times better on all metrics than those on medication after about 2-4 years.

Factors Involved in Outcome and Recovery in Schizophrenia Patients Not on Antipsychotic Medications: A 15-Year Multifollow-Up Study ~ Harrow 2007

Does treatment of schizophrenia with antipsychotic medications eliminate or reduce psychosis? A 20-year multi-follow-up study. ~ Harrow 2014

For all we know, we would just be making a lot of healthy people sick.

The old thought was that D2 receptors in limbic system of brain were the sole cause. Now pharmacologically we realize that there is 5HT-2a (serotonin) component to schizophrenia psychosis. So the goal of effective pharmacology is aimed at low anatagonism of D2 and high antagonism of 5HT2a to reduce extrapyrimidal SE that are seen in the “typical” antipsychotics. These drugs that are weak D2 antagonists and potent 5HT2a antagonists are known as “atypical” antipsychotics. Only reason I say all this, is because it highlights the fact that we still don’t understand physiologicaly what exactly is happening/causing this disease. Furthermore there is only DSM-5 diagnostic criteria (which are signs and symptoms) that Patient must fit to be able to make that Dx. Lastly there (at this point) is no real objective test we can use to measure ones level of disease, so I would have to agree with others statements that it would be morally wrong to start a tx for a patient that could result in more harm than good (because they don’t actually have this disease and they will still experience SE from regimen).

I would recommend one to investigate what counseling interventions could be used to help people who may seem to have a predisposition so we could study that population genetically and try to better identify genotypes associated with this disease to better understand the disease as a whole.

https://www.ncbi.nlm.nih.gov/m/pubmed/14642974/