A dietary supplement, sarcosine, may help with schizophrenia as part of a holistic approach complementing antipsychotic medication, according to a UCL researcher.
In an editorial published in the British Journal of Psychiatry, Professor David Curtis (UCL Genetics, Evolution & Environment and QMUL Centre for Psychiatry) suggests the readily available product could easily be incorporated into treatment plans, while calling for clinical trials to clarify the benefit and inform guidelines.
“Sarcosine represents a very logical treatment and the small number of clinical trials so far do seem to show that it can be helpful. It certainly seems to be safe and some patients report feeling better on it,” he said.
“Sarcosine may be a helpful treatment for schizophrenia but we should be carrying out further studies in order to find out for sure.”
Sarcosine naturally occurs in foods such as egg yolks, turkey and legumes, and can be bought as a dietary supplement, sometimes promoted as a ‘brain health supplement’, with various claims being made that are not all backed up by adequate evidence.
Professor Curtis writes that there is now good evidence from multiple lines of study that some patients with schizophrenia may have defects in the functioning of receptors for glutamate, a common neurotransmitter in the brain, and that sarcosine can help glutamate receptors to work better.
Researchers have been accumulating evidence that if these glutamate receptors did not function properly then people could develop psychosis and other symptoms of schizophrenia.
Professor Curtis and colleagues have recently added to the evidence, showing that genetic variants which damage this receptor increase the risk of schizophrenia.
The only risk identified so far seems to be that some people taking sarcosine to treat schizophrenia who are also on antidepressants may experience hypomania (disinhibition and euphoria), which Professor Curtis says highlights the importance of consulting with health professionals before taking sarcosine.
“Some studies have used it on its own as a treatment but I think the obvious thing to try first would be for patients to take it alongside their regular antipsychotic medication, in order to produce further improvement,” said Professor Curtis.
Professor Curtis and colleagues have recently added to the evidence, showing that genetic variants which damage this receptor increase the risk of schizophrenia.
He says that health professionals need to be aware of sarcosine so that they know how to respond if a patient asks them about it, given that it’s increasingly being used as an alternative therapy.
“I would encourage psychiatrists to review the evidence, and while they may reach different conclusions, it seems reasonable to conclude that suggesting sarcosine to a patient with schizophrenia would be defensible and evidence-based.
“Because it is freely available and fairly cheap, there is nothing to stop somebody with schizophrenia from buying it and trying it themselves, which underscores the need for health professionals to get our heads around it. I would certainly warn them not to stop their regular medication and to continue following the advice of their psychiatrist,” he said.
Glutamatergic system, the main stimulating system of the brain, plays an important role in the pathogenesis of schizophrenia.
Hippocampus, a structure crucial for memory and cognitive functions and rich in glutamatergic neurons, is a natural object of interest in studies on psychoses. Sarcosine, a glycine transporter (GlyT-1) inhibitor influences the function of NMDA receptor and glutamate-dependent transmission.
The aim of the study was to assess the effects of sarcosine on metabolism parameters in the left hippocampus in patients with schizophrenia.
Assessments were performed using proton nuclear magnetic resonance ((1)H NMR) spectroscopy (1.5T).
Fifty patients diagnosed with schizophrenia (DSM-IV-TR), with dominant negative symptoms, in stable clinical condition and stable antipsychotics doses were treated either with sarcosine (n=25) or placebo (n=25).
Spectroscopic parameters were evaluated within groups and between two groups before and after 6-month intervention. All patients were also assessed with the Positive and Negative Syndrome Scale (PANSS). In the sarcosine group, after 6-month treatment, we found significant decrease in hippocampal Glx/Cr (Glx-complex of glutamate, glutamine and GABA, Cr-creatine) and Glx/Cho (Cho-choline), while N-acetylaspartate (NAA), myo-inositol (mI), Cr and Cho parameters remained stable along the study and also did not differ significantly between both groups.
This is the first study showing that a pharmacological intervention in schizophrenia, particularly augmentation of the antypsychotic treatment with sarcosine, may reverse the pathological increase in glutamatergic transmission in the hippocampus. The results confirm involvement of glutamatergic system in the pathogenesis of schizophrenia and demonstrate beneficial effects of GlyT-1 inhibitor on the metabolism in the hippocampus and symptoms of schizophrenia.
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Original Research: Closed access
“A possible role for sarcosine in the management of schizophrenia”. David Curtisa.
The British Journal of Psychiatry doi:10.1192/bjp.2019.194
