When a young man was brought to my clinic after his first episode of psychosis, his parents wanted to know when he could return to college.
This is not an atypical first interaction. However, in many instances, after a few consultations later and especially once the immediate crisis had settled, the questions would take a different turn.
“Is this in our blood?” a parent would ask. And should their child undergo a genetic test?
I could often tell that they were thinking about whether they had ‘caused’ the illness, whether their child’s future was foregone, and whether the diagnosis would affect marriage prospects and the ability to have healthy children.
Broadly, families rarely ask about psychiatric genetics out of scientific curiosity. They ask because they are looking for an explanation and, indeed, relief from blame.
Sources of risk
This is where colloquialisms like “genes for schizophrenia” or “genes for depression” do a lot of harm. Psychiatric genetics has made remarkable progress in recent years and, as doctors and medical researchers, we know that genes do not determine a person’s destiny. But there is also another equally important message: vulnerability is distributed and complicated but also inseparable from the life in which it is expressed.
The engine of much of this progress is the genome-wide association study (GWAS). Instead of choosing a few candidate genes to study, researchers use GWAS to compare millions of common genetic variants across very large groups of people with and without a condition. The point is to find out whether some variants appear more often in one particular group.
In common psychiatric disorders, no single gene variant has an effect comparable to the effects of single genes in monogenic diseases like Tay-Sachs disease or Duchenne muscular dystrophy. In other words, risk is polygenic: it emerges from the combined influence of thousands of variants, along with rare genetic changes, development, environment, and chance.
Signals in genomes
In 2022, a landmark schizophrenia study involving tens of thousands of people identified associations at 287 genomic regions and pointed to genes active in neurons and synapses. A similarly large bipolar disorder study in 2021 identified 64 associated regions. Both these GWAS studies showed where researchers could look for biological mechanisms underlying these conditions — and possible treatment options.
That said, a genomic region is not the same as a gene, and association is not causation. Many ‘signals’ lie in stretches of DNA that regulate when and where genes are switched ‘on’ rather than directly encoding a protein. Several genes may sit near the same signal. The relevant effect may occur during a narrow period of brain development. A GWAS is more like a satellite map that highlights areas of interest; to drill down beyond that, scientists have to use other tools.
GWAS studies have also exposed a mismatch between traditional diagnostics and biology. For example, in a December 2025 study in Nature, researchers reported that some inherited risk is shared across schizophrenia and bipolar disorder. This does not mean diagnoses become meaningless. A diagnosis is still useful to guide treatment and communicate the prognosis to the patients and their families. At the same time, the finding suggests that nature has not organised mental illness according to the chapter headings of the Diagnostic and Statistical Manual of Mental Disorders (DSM).
Reasons to be cautious
Some groups have still tried to compress all these small effects into a combined polygenic risk score — a single number they intend to use to estimate a person’s inherited susceptibility. While such scores can be useful in specific areas of research, they cannot say whether a person will become ill, at what age, how severe the condition will be or which medicine will work. A person with a higher polygenic risk score may also remain well while a person with a lower score may develop illness. This is because the score captures only a part of genetic liability, and it does not ‘contain’ childhood adversity, sleep disruption, substance use, medical illness, social support, access to timely care, and so on.
The International Society of Psychiatric Genetics has cautioned that current polygenic risk scores for schizophrenia, bipolar disorder, and depression are not sufficiently accurate for routine clinical prediction.
Indian psychiatrists have one more reason to be cautious. Genomic databases have historically drawn disproportionately from people of European ancestry. Scores developed from those datasets are often less accurate in other populations because the frequencies and correlations of genetic variants differ by ancestry. Even “Indian ancestry” is too blunt a label. The GenomeIndia project, which generated whole-genome data from 10,000 healthy, unrelated Indians across 83 population groups, documented an extraordinary genetic diversity. India cannot simply import a score developed elsewhere, test it in a small urban sample, and assume it applies to all its peoples.
All this is to say that psychiatric genomics has its value when exercised properly: by involving diverse populations in research and clinicians and communities when deciding how data will be used, and protecting privacy and refusing to allow the enthusiasm of commerce to outrun science.
Protecting probabilities
What, then, can genetics usefully change in your consultation room today? It can reduce blame. A mother did not cause schizophrenia by being “too strict”. A father did not ‘transmit’ bipolar disorder through a moral failing. Biology matters and families often find that acknowledgement to be a relief.
Genetic vulnerability should not be converted into fatalism. The risks I encounter are often visible even without genetic sequencing: several nights without sleep before a manic episode, escalating cannabis use in a vulnerable young person, treatment stopped because of stigma, months lost because specialist care is too far away.
I told one of the families that mental illnesses can cluster in families but also that there is no genetic test yet that can declare their son to be ‘safe’ or ‘doomed’. He should not be treated as a patient-in-waiting. The more useful approach is to track the early warning signs, avoid intoxicants, sleep well, seek help promptly if sustained changes appear, and focus on recovery.
Psychiatric genetics will probably become clinically more useful as datasets become larger and more representative, and as scientists better combine genetic findings with developmental, clinical, and environmental information. It may even help divide broad syndromes into biologically meaningful subgroups or identify new drug targets. However, predicting what will happen in future will also remain probabilistic; that will not change. And just as well, we must work to keep probabilities from being misunderstood, stigmatised or commercialised.
If you take one message away from this article: psychiatric genetics will not identify people before they fall ill but it can replace superstition and blame with a more accurate account of vulnerability. Genes load the dice but you can still strategise your way through the game.
Dr. Alok Kulkarni is a senior consultant psychiatrist at the Manas Institute of Mental Health and Neurosciences, Hubballi, Karnataka.
Published – August 13, 2026 09:00 am IST
