After tracking 140 people with schizophrenia for 16 weeks, researchers from Massachusetts General Hospital in Charlestown found that those with the so-called high-functioning FOLH1 gene variant responded more to folic acid and B12 supplements, compared to those with the low-functioning FOLH1 variant. According to study lead author Dr Joshua Roffman, this gene is key in metabolising the B vitamin folate: ‘That’s a gene that actually controls the digestion of folate (or folic acid) into the bloodstream.’
Your body uses folate, one of the B vitamins, to manufacture the neurotransmitters responsible for sending signals throughout the brain and body. Folate is found in leafy vegetables, citrus fruits, beans and fortified grain products, and Roffman explained that deficiencies in the vitamin have been tied to the development of schizophrenia since the 1960s. For instance, researchers have observed spikes in cases of the mental disorder after famines in China and the Netherlands.
The study looked at the effects of folate supplements in a large population of people with the condition, and is the first to do so. Examining patients from several medical centres in Massachusetts, New York and Michigan, the researchers, who published their findings in JAMA Psychiatry, targeted the so-called negative symptoms in schizophrenia patients, such as apathy, withdrawal and an inability to display emotion. According to wellness experts these symptoms, though less severe than the more well-known symptoms of schizophrenia (including hallucinations, delusions and paranoia) still lead to significant impairment because they are unaffected by traditional antipsychotic drugs.
Patients either received placebo pills or 2 milligrams of folic acid and 400 micrograms of vitamin B12, which increases folic acid’s effect, per day for 16 weeks. On the whole, the participants who took the supplements found an improvement in their symptoms at the end of the study, but when the researchers looked at each person’s FOLH1 gene type they identified who benefited the most. Those with the high-functioning version of the FOLH1 gene saw their negative symptom score drop by about 5 points, compared to no significant change in the placebo group members with high-functioning FOLH1 genes.