Lipid profile reveals why some marijuana users develop schizophrenia while others do not

Scientists have identified obvious metabolic fingerprints in the blood, which may ultimately explain why some marijuana users develop schizophrenia while others do not – despite similar levels of exposure to the drug.

This pioneering study published in a scientific report reveals how specific fatty acid patterns in blood samples serve as early warning signs for those with an increased risk of psychosis in marijuana use.

For millions of dollars in marijuana use worldwide, these findings may ultimately lead to personalized risk assessments that can help users make smarter decisions about spending.

“We found a large difference between these individual groups. By comparing the number of certain metabolites (fatty acids), we were able to completely differentiate the three patient populations,” stressed Leyre Urigüen, research coordinator at the University of Basque (UPV/EHU). “This suggests that there are altered or different metabolisms between these three groups.”

The researchers analyzed blood samples from four different groups: people with schizophrenia who do not use marijuana, people who use marijuana and have marijuana use disorders, patients with schizophrenia and marijuana use disorders (dual diagnosis), and a healthy population who neither suffers from mental illness nor medication.

Using advanced fatty states – a comprehensive study of fatty acids and related compounds – the team identified 119 different metabolites in blood samples, some of which showed significant differences between groups.

The most striking finding was a significant decrease in compounds called acylcarnitine (particularly l-octanoylcarnitine and l-decanoylcarnitine) in all patient groups compared with the control group. These molecules play a crucial role in energy metabolism, neuroprotection, and maintaining cell membrane stability in the brain.

Cannabis users without schizophrenia show significant reductions in compounds called N-acyl amino acids, especially N-thyroxinethreonine and N-thyroxine serine – molecules that help regulate brain signaling and provide neuroprotective effects. Interestingly, schizophrenia patients showed similar reductions, suggesting common disruption of these protective pathways.

Meanwhile, levels of 7-hydrothyroxine protease, a compound involved in cholesterol synthesis, are elevated in schizophrenia patients (including and those who do not use marijuana) – although this change may be associated with antipsychotics rather than antipsychotics, not the disease itself.

This study provides some initial concrete evidence that marijuana use and schizophrenia may produce potential metabolic disruptions that may explain its frequent simultaneous occurrence. Nearly one-third of people diagnosed with schizophrenia also meet the criteria for marijuana use disorder, with up to 42% of people with schizophrenia suffering from marijuana use disorder.

“We propose that some fatty acids can distinguish groups using marijuana from those with schizophrenia and those with dual diagnosis. These molecules may be biomarkers,” Urigen said.

The team used liquid chromatography and high-resolution mass spectrometry to detect subtle differences in these metabolic compounds. This complex analytical method was developed by the IBEA research team at UPV/EHU under the guidance of Professor Nestor Etxebarria, who works closely with the Neuropsychopharmacology Group of Urigüen.

For Dr. Urigüen, this discovery marks an important starting point: “I think being able to find blood biomarkers that can help predict the risk of mental illness, such as schizophrenia caused by marijuana use, this study has proven to be the beginning of this process. Now, this study must be compared to a larger population, which we have already done a larger study of us.

While the sample size of the study was relatively small – 24 people with cannabis disease, 18 schizophrenia, 12 with dual diagnosis and 50 controls, the researchers believe their methodology provides templates for large studies that can confirm these potential biomarkers.

These implications not only go beyond predicting risk. Understanding the shared metabolic pathways between marijuana use and schizophrenia may lead to new treatments that can directly target these disruptions and may prevent or alleviate the development of psychiatric disorders in vulnerable groups.

As marijuana legalization expands globally and climbs in usage rates, identifying people at an increased risk of adverse psychiatric effects has had a good impact on new urgency. This metabolic approach provides promising avenues to achieve this goal – it goes beyond genetic biochemical processes that may link cannabis use to the development of schizophrenia in susceptible populations.

As these researchers continue to refine their understanding of these metabolic characteristics, this day may be a simple blood test that can help cannabis users assess their personal risk of suffering from severe mental illness, which may change how we deal with cannabis use and prevent schizophrenia.