Author: Petra Dujmic
Editor: Bhakti Vasani
Have you ever given sincere advice to a friend only to have them completely disregard it a few moments later? Yeah, me too! Your best insights went in through one ear and out through the other, making you think to yourself, “What am I, chopped liver?” But the thing is, you might actually be complimenting yourself by referencing chopped liver, because chopped liver might not be all that bad. In fact, it might not be bad at all. According to nutritionists, liver is actually one of the most nutritious natural sources of Vitamins A and B, nutrients essential to the maintenance of normal cognitive and homeostatic function. Liver is packed with proteins, iron, and choline, making it the perfect dish for an athlete. Most importantly, liver continuously tops the list of foods naturally fortified with niacin (a vitamin linked to the prevention of cognitive impairment), providing 91% of the RDA for men and more than 100% of the RDA for women per 3-ounce (85-gram) serving. So liver is undoubtedly healthy — but aren’t a lot of other foods also fortified with proteins and vitamins? What’s the big deal again? Well, it turns out liver, as a result of its unusually high niacin concentration, has a secret — a secret scientists are just beginning to discover!
Esme Fuller-Thompson is a neuroscientist at the University of Toronto researching the effects of vitamin supplementation on the prevention and treatment of cognitive disorders. His most recent hypothesis was inspired by studies looking at the prevalence of schizophrenia in developing countries, where more widespread vitamin fortification has yet to take hold. Collaborating with doctoral student Rukshan Mehta of the University of Toronto’s Factor-Inwentash Faculty of Social Work (FIFSW), Fuller-Thompson proposed an intriguing link between prenatal niacin deficiency and the higher rate of schizophrenia diagnoses in developing countries. A recent study in South India fueled his hypothesis by proffering two critical observations:
1.) Prenatal niacin deficiency was correlated with the presence of an activated variant of the NAPRT1 gene that impedes niacin uptake, and
2.) Expression of the NAPRT1 variant was associated with a lack of the typical dermatitis symptoms of pellagra patients.
Fuller-Thompson connected the two seemingly unrelated observations by suggesting the following: expectant mothers who experience niacin-deficiency during pregnancy are more likely to have children with the activated NAPRT1 variant. Should the offspring of the malnourished mothers experience niacin deficiency in postnatal life, they may be at risk for developing pellagra (a disease caused by niacin deficiency whose most common symptoms are dementia and dermatitis). The offspring afflicted with pellagra, however, typically do not present with dermatitis because of the expression of the NAPRT1 variant, despite the fact that they still experience psychotic episodes. The presentation of solely psychosis (and not dermatitis) may cause pellagra patients in developing countries to be misdiagnosed with schizophrenia. Thompson suggests such misdiagnoses may lead to the increased incidence of schizophrenia in developing countries.
But if increased schizophrenia incidence is due to underdiagnosis of pellagra, then what does that mean about the actual influence of vitamins on schizophrenia treatment? In other words, is there any evidence to suggest that niacin supplementation may facilitate schizophrenia treatment even in patients whose mothers were not niacin deficient during pregnancy? The answer to that question is a solid “maybe.” Research results have been relatively mixed regarding the effectiveness of any sort of vitamin supplementation on schizophrenia treatment. Appropriately, much of that variance has to do with the country in which the research study was conducted. One research team found that plasma folate and vitamin B12 levels were deficient in schizophrenia first-episode outpatients with psychosis in India, while another research team found no difference in plasma folate and B12 levels between Greek inpatients and controls. In attempts to flesh out a cause-and-effect relationship, Roffman et. al. randomly-assigned 140 schizophrenia patients to either 16 weeks with folate and B12 supplementation or a placebo. The results revealed that supplementation benefitted only those patients who expressed the low-functioning FOHL1 genotype, most likely because this subset of patients already had lower baseline folate levels to begin with. Still another team (Hill et. al.) reported a total lack of improvement with the vitamin supplementation altogether, so the answer really is indefinite.
What is definite, however, is the need to combat the alarming prevalence of micronutrient malnourishment in developing countries. According to the WHO, approximately 250,000 to 500,000 vitamin A-deficient children become blind annually, and about half of those children die within 12 months of losing their sight. In the 21st century (and at the dawn of a new decade!) such statistics are unacceptable! Thankfully, WHO along with its partners (including the Micronutrient Initiative) launched the Vitamin A Global Initiative in 1998, a medical intervention that seeks to provide “inexpensive vitamin A supplements twice a year to children in more than 70 countries.” To date, the programs implemented by the Vitamin A Global Initiative (in conjunction with sick-child visits and national poliomyelitis immunization days), have saved an estimated 1.25 million lives in 40 countries! Despite the noble success of the Vitamin A Global Initiative, there is still work to be done in the strive to end global micronutrient malnourishment. Research data, like those gathered by University of Toronto students in South India, are instrumental in garnering publicity and funding for organizations like the Micronutrient Initiative, and making niacin deficiency, in particular, an issue of the past!
In the end, although research results to date are promising, more research is needed to provide any conclusive results about the effects of vitamin supplementation on schizophrenia treatment. Researchers are currently working on measuring schizophrenia incidence in countries that are working to adopt folic acid fortification in grain products, as well as elucidating potential negative effects of incautious vitamin supplementation (which has been linked to cancer risk in certain meta-analyses). In the meantime, make sure you’re maintaining a nutritious, niacin-rich diet. Exercise more. Relax. Sleep. Buy some liver, maybe, and give it a try. Trust me, no matter what society might say, it’s not as bad as you may think!
Neuroscience News. “Could Some People with Schizophrenia in Poorer Nations Simply Have a Vitamin Deficiency?” Neuroscience News, 12 Dec. 2019,
“Micronutrient Deficiencies.” World Health Organization, World Health Organization, 9 Dec. 2013, www.who.int/nutrition/topics/vad/en/.
Brown, Hannah E, and Joshua L Roffman. “Vitamin Supplementation in the Treatment of Schizophrenia.” CNS Drugs, U.S. National Library of Medicine, July 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4083629/#!po=28.8462.
Julson, Erica. “16 Foods That Are High in Niacin (Vitamin B3).” Healthline, Healthline Media, 5 Oct. 2018, www.healthline.com/nutrition/foods-high-in-niacin.
Ritchie, Hannah, and Max Roser. “Micronutrient Deficiency.” Our World in Data, 11 Aug. 2017, ourworldindata.org/micronutrient-deficiency.