The effect of folic acid and B12 vitamin supplementation on mental well-being in pregnant women: A possible role in the prevention of postpartum depression

Mariola Herian¹, Ksenia Mazur², Weronika Curyło³, Alicja Winkowska⁴, Alina Grudina¹, Jan Szerocki⁴, Wiktoria Nowakowska⁵, Katarzyna Chwaleba¹, Katarzyna Milewska-Plis³, Monika Karalus⁶

¹University Hospital in Cracow, Kraków, Poland, ²Independent Public Clinical Hospital No.2 of the Pomeranian Medical University in Szczecin, Szczecin, Poland, ³Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland, ⁴Independent Public Health Care Center Of the Ministry of Internal Affairs and Administration in Cracow, Kraków, Poland, ⁵ORTOMED PLUS Dental Practice, Poznań, Poland, ⁶Independent Public Clinical Hospital named after Prof. W. Orłowski, Center of Postgraduate Medical Education, Warsaw, Poland

Corresponding author: Mariola Herian, MD, E-mail: mariola.herian@gmail.com

How to cite this article: Herian M, Mazur K, Curyło W, Winkowska A, Grudina A, Szerocki J, Nowakowska W, Chwaleba K, Milewska-Plis K, Karalus M. The effect of folic acid and B12 vitamin supplementation on mental well-being in pregnant women: A possible role in the prevention of postpartum depression. Our Dermatol Online. 2025;16(e):e27.

Submission: 11.08.2025; Acceptance: 20.08.2025

DOI: 10.7241/ourd.2025e.27

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ABSTRACT

Background: Postpartum depression (PPD) is a common and serious psychiatric disorder that affects 10–30% of mothers worldwide. Untreated PPD is associated with adverse consequences for both maternal well-being and child neurodevelopment. While the pathophysiology of PPD is multifactorial and not fully elucidated, nutritional factors – particularly B-vitamins – have emerged as modifiable risk contributors due to their roles in neurodevelopment, neurotransmitter synthesis.

Material and Methods: This narrative review aims to evaluate the current evidence on the relationship between B-vitamin status during pregnancy and maternal mental health, with a focus on their potential preventive effect against postpartum depression. A literature search was conducted in PubMed and Google Scholar for studies published between 1997 and May 2025. Eligible articles included clinical trials, observational studies, and meta-analyses published in English or Polish.

Results: Deficiencies in folate and vitamin B12 disrupt the folate cycle, leading to hyperhomocysteinemia, oxidative stress, and impaired monoamine neurotransmitter synthesis, which are implicated in the pathogenesis of depression. Several studies indicate that low levels of B6 (pyridoxine), B9 (folate), and B12 (cobalamin) are associated with increased risk and severity of depressive symptoms during and after pregnancy. Supplementation, particularly with pyridoxine and folate, has shown promising results in improving maternal mood and reducing depressive symptoms.

Conclusion: B-vitamin supplementation during pregnancy may represent a low-risk, cost-effective strategy to support maternal mental health and potentially reduce the incidence of postpartum depression. Further randomized controlled trials are warranted to confirm these findings.

Key words: Folate, B-vitamins, Postpartum depression, Maternal mental well-being, Pregnancy, Supplementation

INTRODUCTION

During pregnancy and the postpartum period, women undergo profound biological, psychological, and neuroendocrine changes. This time is also marked by significant physical transformations, shifts in social and demographic roles, and increased responsibilities related to infant care and development. According to published data, 85% of women experience some form of mood dysregulation during the perinatal phase, ranging from transient “baby blues” to clinically significant depressive episodes or bipolar disorder [1]. Postpartum depression (PPD) is a prevalent and serious mental health condition that typically emerges within the first few weeks to months following childbirth, although symptom onset may occur during pregnancy or even prior to conception. It shares the same diagnostic criteria and symptomatology as major depressive disorder, including loss of interest and pleasure, fluctuations in mood, disturbances in sleep and appetite, impaired concentration, psychomotor agitation or retardation, fatigue, feelings of worthlessness or excessive guilt, and recurrent thoughts of death or suicidal ideation. These symptoms must occur during the same two-week period, represent a change from previous mental state, and cause clinically significant distress or impairment in important areas of functioning. The diagnosis requires that the symptoms are not attributable to the physiological effects of a substance or another medical condition [2]. PPD etiology is complex and multifactorial, with a heterogeneous underlying pathophysiology, which is not fully understood. Untreated PPD has been associated not only with a deterioration in maternal well-being, but also with adverse and long-lasting effects on the child’s emotional regulation, cognitive functioning, and overall neurodevelopment. Globally PPD affects an estimated 10–30% of mothers [3]. The prevalence varies among countries, from 7-13% in high-income countries to over 20% in low-and middle-income countries [2]. A study conducted by Wisner KL et al. shows that 33% of women with PPD actually report symptom onset during pregnancy and 27% pre-pregnancy, underscoring the need for early screening and intervention strategies [4]. Despite the high prevalence, current evidence regarding effective preventive interventions for PPD remains limited. Nutritional status during pregnancy has emerged as a potential modifiable risk factor influencing maternal mental health. B-vitamins play essential roles in neurodevelopment, neurotransmitter synthesis, and one-carbon metabolism, processes that are critical for maintaining emotional stability and cognitive function. Deficiencies in these vitamins have been associated with increased homocysteine (Hcy) levels, altered methylation patterns, and impaired synthesis of serotonin and other monoamine neurotransmitters, which may contribute to the onset or exacerbation of depressive symptoms [5]. Given the high global burden of PPD and the limitations of current preventive strategies, there is increasing interest in exploring the potential role of nutritional interventions as a cost-effective, low-risk approach to support maternal mental health.

This review aims to examine current evidence on the potential role of B-vitamin complex supplementation in supporting maternal mental health during pregnancy, and its possible preventive effect on the development of PPD.

MATERIAL AND METHODS

This narrative review was conducted to explore the current state of knowledge regarding the role of B-vitamin complex supplementation in maternal mental health during pregnancy and the prevention of PPD. A comprehensive literature search was performed using the PubMed and Google Scholar databases. The literature included in this review was selected primarily from studies published within the last 15 years (2010–2025), with a few exceptions where earlier foundational works were deemed relevant. Appropriate studies were identified using the following keywords: folate, B vitamins, postpartum depression, maternal mental well-being, pregnancy, supplementation. Both clinical trials and observational studies, as well as systematic reviews and meta-analyses, were considered if they addressed the relationship between B-vitamin status and maternal psychological outcomes during pregnancy or the postpartum period. Articles were included if they were published in peer-reviewed journals and available in English or Polish. Non-human studies, case reports, and editorials were excluded. After screening titles and abstracts for relevance, full texts of selected articles were reviewed to identify those that provided substantial data on biochemical, neuropsychiatric, or clinical aspects of B-vitamins in relation to mood disorders during the perinatal period.

RESULTS

The role of folates and B group vitamins in the methylation cycle and neurotransmitter synthesis

The term folate comprises a group of chemically related compounds: naturally occurring folate is a water-soluble vitamin that primarily exists in the human body as tetrahydrofolate (THF), its biologically active form, and as 5-methyltetrahydrofolate (5-MTHF), the predominant circulating form in plasma. Folic acid (FA), by contrast, is a synthetic, fully oxidized form of folate that is commonly used in dietary supplements. It does not occur naturally in significant amounts in the bloodstream unless consumed through fortified foods or supplementation [5,6]. The bioactivation of folic acid requires enzymatic reduction by dihydrofolate reductase (DHFR), a hepatic enzyme with relatively low activity in humans. To become biologically active and participate in folate-dependent metabolic pathways, folic acid must first be reduced to dihydrofolate (DHF), and subsequently to tetrahydrofolate (THF), before being further converted to 5-MTHF, which is the only form of folate that crosses the blood-brain barrier. The demethylation of 5-MTHF is facilitated by the enzyme methionine synthase (MS), which catalyzes the transfer of the methyl group to Hcy, the sole physiological methyl group acceptor in this reaction. This process results in the remethylation of Hcy to methionine (Met) and the concurrent regeneration of THF, thereby sustaining the proper metabolic function of the folate cycle. Conversion of 5,10-methylenetetrahydrofolate back to 5-MTHF is catalyzed by the enzyme methylenetetrahydrofolate reductase (MTHFR), encoded by the MTHFR gene [7,8]. Vitamin B12 (cobalamin) serves as an essential cofactor for MS; therefore, a deficiency in vitamin B12 impairs this enzymatic activity, effectively disrupting the folate cycle (Figure 1). This can lead to elevated plasma Hcy levels, increased Met concentrations (hypermethioninemia), THF deficiency, megaloblastic anemia, and may also contribute to infertility. These metabolic pathways are particularly critical during the early stages of pregnancy, when adequate folate levels influence placental development and fetal neurodevelopment [6,9]. Methylation is a fundamental biochemical reaction that involves the covalent addition of methyl groups to various molecular targets. It plays a crucial role in two major global regulatory mechanisms—epigenetic modifications and genomic imprinting—primarily through the methylation of histones and DNA. Folate, in the form of 5-MTHF, serves as a methyl group donor in the remethylation of Hcy to Met, which is subsequently metabolized by methionine adenosyltransferase (MAT), along with the vitamin B12, to form S-adenosylmethionine (SAM). SAM functions as a universal methyl donor, methylating specific cytosine residues in DNA and contributing to the regulation of gene transcription. In the context of folate deficiency, intracellular SAM levels are reduced, leading to DNA hypomethylation, which may in turn potentially result in the aberrant expression of proto-oncogenes [10,11].

Figure 1: One-carbon folate methylation pathways. BHMT-betaine: homocysteine methyltransferase; CBS-cystathionine-synthetase; DMG-dimethylglycine; Gly-glycine; Hcy-homocysteine; MAT- methionine S-adenosyltransferase; MTHF- 5-methyltetrahydrofolate; MTHFR- 5-methyltetrahydrofolate reductase; SAH- S-adenosylhomocysteine; SAHH- S-adenosylhomocysteine hydrolase; SAM- S-adenosylmethionine; Ser- serine; THF- tetrahydrofolate

Folate cycle is directly linked to and supports the one-carbon cycle (1-CC), where one-carbon units are carried by THF and transferred into various substrates for biosynthesis and methylation reactions. Moreover, 1-CC is particularly critical to the transmethylation processes in the central nervous system and plays a key role in metabolizing monoamine neurotransmitters such as dopamine, norepinephrine and serotonin. Together, these two metabolic pathways are vital for maintaining cellular stability, developmental disorders and mental health [6,9].

Homocysteine, oxidative stress and cerebral perfusion disorder, its influence on depression

According to the literature, Hcy is an amino acid with a thiol group that is naturally produced through metabolic processes in the human body. Hcy levels are critical for physiological balance, with elevated concentrations contributing to a range of systemic dysfunctions encompassing excitotoxicity, genomic instability, oxidative stress and inflammatory response. Raised plasma Hcy concentrations have been identified as a risk factor for Parkinson’s disease, cardiovascular diseases and cognitive decline. Furthermore, it has been linked to various neurodegenerative and psychiatric conditions, for example schizophrenia, and anxiety disorders. Reduction of its level is regulated mainly through two metabolic pathways dependent on B-group vitamins, primarily B6 (pyridoxine hydrochloride), B9 (folic acid), and B12 (cobalamin), whereas a minor portion undergoes renal elimination. Consequently, disturbances in processes of its elimination will lead to increased Hcy concentrations, clinically referred to as hyperhomocysteinemia (HHcy). The etiology of HHcy is multifactorial. Routine lifestyle factors associated with the development of HHcy including: exaggerated alcohol intake, smoking, hyperlipidaemia induced by some lipid-lowering medications, arterial hypertension, high coffee intake, renal insufficiency, physical inactivity as well as deficiency of folic acid and vitamin B12. Of the factors mentioned above, the final ones serve as the central focus of this article [12,13].

The mechanism of HHcy-related neurotoxicity

As demonstrated in the study by Bhatia P elevated Hcy levels have been shown to stimulate the production of excitatory amino acid neurotransmitters, such as homocysteic acid (HCA) and cysteine sulfinic acid (CSA), which in turn activate N-methyl-D-aspartate (NMDA) glutamate receptors. This receptor activation induces a transient elevation in intracellular calcium (Ca²⁺) concentration within neurons, contributing to neuronal damage and overall brain injury. Stimulation of NMDA receptors is further associated with increased generation of reactive oxygen species (ROS), which inhibit Na⁺/K⁺-ATPase activity – enzyme that maintains membrane potential of neuron cells, pH homeostasis, and overall cellular energetics. This inhibition exacerbates neurotoxic processes [8]. Above findings are consistent with those reported by Bukharaeva E et al. who emphasize that excessive activation of NMDA receptors is commonly linked to oxidative stress, intracellular Ca²⁺ dysregulation, and increased production of ROS. Hcy contributes to neurotoxicity via a dual mechanism of action on NMDA receptors. These receptors possess distinct binding domains for both glutamate (an excitatory neurotransmitter) and glycine (an inhibitory co-agonist). Hcy functions as an agonist at the glutamate site while simultaneously acting as a partial antagonist at the glycine site, resulting in excessive receptor activation. This dysregulation enhances glutamatergic neurotransmission while impairing glutamate reuptake at synaptic terminals, leading to elevated glutamate concentrations in the synaptic cleft and subsequent excitotoxic neuronal death. Additionally, Hcy indirectly promotes Ca²⁺ influx, disturbing the excitatory/inhibitory neurotransmitter balance, particularly within the hippocampus. Moreover, HHcy disrupts extracellular levels of both excitatory (e.g. aspartate) and inhibitory (e.g. GABA) neurotransmitters, contributing to an increased risk of seizure activity and excitotoxic neuronal injury [8,14].

Association between plasma Hcy concentrations and the presence of depressive symptoms

The relationship between Hcy concentrations and the diagnosis of depression remains inconclusive, with current evidence failing to establish a consistent or definitive association.

In a study conducted by Chung KH et al., based on blood samples collected from a cohort of 650 school-aged children between 6 and 13 years old with anxiety and depression, Hcy levels were measured. The findings indicated a positive correlation between the presence of depressive and anxiety disorders and elevated Hcy concentrations in older boys [15]. In turn, T. Bottiglieri et al. conducted a study involving 46 patients with severe depression, examined their cerebrospinal fluid (CSF) to investigate potential associations between folate status, SAM, and monoamine neurotransmitter metabolism. The study found that nearly one-third of the depressed patients had folate deficiency indicated by red blood cell folate concentrations below 150 μg/L. Additionally, mean total plasma Hcy levels were significantly elevated in the depressed group compared to the healthy control group. The study further demonstrated that patients with elevated plasma Hcy had significantly reduced concentrations of CSF monoamine metabolites, suggesting impaired metabolism of serotonin, dopamine, and norepinephrine, all of which have been implicated in the pathophysiology of affective disorders [16]. Saraswathy KN et al. conducted a study involving 303 participants of both sexes not related up to first cousins aged 25 to 65 years, who were positively assessed for depression and generalized anxiety disorder (GAD). Standard protocols were employed to perform DNA extraction, biochemical analyses and genotyping of the MTHFR C677T polymorphism. HHcy was associated with a more than threefold and sixfold elevated risk of developing depression and GAD, respectively. The data suggest that elevated Hcy levels may be driven by vitamin B12 deficiency in individuals with these conditions. Although the T allele of the MTHFR C677T polymorphism appeared to be linked to a higher risk of depression and anxiety, this association did not reach statistical significance. Furthermore, no direct relationship was identified between the status of vitamin B12 or folate and the presence of depression or GAD. This suggests the potential role of micronutrient deficiencies in the pathogenesis of mood and anxiety disorders [17]. The correlation between abnormal levels of folate, vitamin B12, and Hcy and treatment efficacy was investigated in 213 patients (mean age 39.9±10.5 years, 56% women) diagnosed with major depressive disorder. Treatment with fluoxetine, a selective serotonin reuptake inhibitor (SSRI), revealed that patients with low folate levels demonstrated a greater tendency to exhibit melancholic depression. Furthermore, these patients showed a poorer therapeutic response to fluoxetine. In contrast, elevated Hcy and reduced vitamin B12 levels were not significantly associated with depressive phenotype or treatment outcome [18].

B-complex vitamins deficiency during pregnancy

During pregnancy, with the increased physiological demand of fetal development, mothers are more susceptible to nutritional deficiencies. Especially adequate folate intake is essential for proper placental development and for long-term maternal and fetal health (Table 1). Despite the common folate supplementation of pregnant women, their diet is often reduced in vitamin B12, which alters the optimal folate/B12 ratio and therefore initiates changes in the methylation pathways. Due to folate’s critical role in DNA synthesis and cell replication during pregnancy, its requirements increase from 400 to 600μg a day to ensure fetal and placental growth. Dietary sources of folate include dark green leafy vegetables, legumes, certain fruits, yeast, eggs and offal. Despite its presence in a broad range of products, folate is highly sensitive to environmental factors, and substantial losses may occur during agricultural processing, transportation, and cooking [5,19]. Meanwhile, according to the National Institutes of Health, the most bioavailable and nutritionally significant dietary sources of vitamin B12 are animal-derived products such as clams and beef liver. Fish, meat, poultry, eggs, milk, and other dairy products are also rich sources of this essential cobalamin. In addition, some fortified breakfast cereals and nutritional yeasts can serve as sources of vitamin B12, particularly for individuals following plant-based diets [20]. Folate deficiency in pregnancy is traditionally related to the increased risk of development of neural tube and abdominal wall defects and adverse pregnancy outcomes. As noted above folate deficiency leads to HHcy and that increases the risk of vascular abnormalities and contributes to developing preeclampsia. HHcy is also responsible for recurrent pregnancy loss, preterm deliv- ery, placental abruption, fetal growth restriction, and gestational diabetes [21].

Table 1: Recommended Daily Intake and Upper Limits for B vitamins During Pregnancy According to European Food Safety Authority (EFSA) [25–32].

Vitamin B12 deficiency has also been associated with developmental complications in infants including: defects of neural tube, cerebral atrophy, delays and abnormal electroencephalogram, neurodegenerative and psychiatric illness. It should also be noted that vitamin B12 deficiency may negatively affect the cardiovascular system and contribute to an increased risk of developing type 2 diabetes in the future [22]. Recent studies have shown that malnutrition and deficiencies in nutrients such as vitamin B12 and D, iron, folates and other antioxidants increase the PPD incidence [3,23]. Folate deficiency has been linked to an elevated risk of more severe depressive symptoms, longer episodes and an increased probability of depressive symptom relapse [21,24].

DISCUSSION

The etiology of PPD remains incompletely understood. However, it is widely accepted that its pathogenesis is multifactorial, involving a complex interplay of biological, genetic, hormonal, psychosocial, and environmental influences. In recent years, nutritional factors have also been recognized as potential contributors to the development of PPD. Key nutrients implicated include folate, vitamin B12, calcium, iron, selenium, zinc, and polyunsaturated fatty acids [3,33]. While numerous studies have investigated the association between various micronutrients and the risk of PPD, relatively few have specifically focused on the role of folate and other B vitamins in the onset and progression of this condition.

Yelverton CA et al. explored the relation between nutrition and mental well-being during early pregnancy, identifying specific nutrients that may have an impact on developing depression. This study noted significant associations between niacin (B3 vitamin), thiamine (B1 vitamin) and folate (B9 vitamin) intake and maternal well-being. Niacin is an essential component of nicotinamide adenine dinucleotide (NAD⁺) and nicotinamide adenine dinucleotide phosphate (NADP⁺), cofactors that are critical for cellular metabolism and proper functioning of both peripheral and central nervous system cells. This biochemical role may underlie the potential influence of B vitamins on mental health. Moreover, folate is frequently co-administered with antidepressants to enhance their therapeutic efficacy, indicating a possible role in mood regulation. Thiamine deficiency has been associated with neurological manifestations, including depressive symptoms. This study highlights the importance of optimizing maternal diet, which might potentially translate into maternal well-being [34]. Interesting conclusions were also reached by Khodadad M. et al. In a single-blind, placebo-controlled clinical trial, the researchers studied 81 Iranian women identified as being at high risk for PPD based on standardized assessment scales. From the 28^th week of pregnancy until delivery, 41 women in the intervention group received a daily dose of 80 mg of pyridoxine, while 40 women in the control group received a placebo. The analysis revealed a statistically significant reduction in mean depression scores among those receiving vitamin B6 supplementation. In contrast, a slight post-intervention increase in depression scores was observed in the control group. These findings suggest that pyridoxine supplementation may have clinical relevance in the prevention of PPD among high-risk populations [35]. In contrast, Yoshihiro Miyake et al. conducted a study involving 865 Japanese pregnant women. Dietary information was collected during pregnancy using a validated, self-administered diet history questionnaire. PPD was defined as an Edinburgh Postnatal Depression Scale (EPDS) score of at least 9, assessed between 2 and 9 months after delivery. The analysis was adjusted for a range of factors, including maternal characteristics, lifestyle and socioeconomic factors, and infant-related variables. Study has shown that among all study participants, postpartum depression occurred in 121 women (14%). Only riboflavin (B2 vitamin) intake in the third quartile, compared to the first, was independently associated with a lower risk of PPD. Conversely, no significant associations were found between the intake of folate, cobalamin or pyridoxine and the lower risk of developing PPD [36]. A similar conclusion was reached by Rouillon F et al. In an early prospective cohort study serum vitamin B9 status was recorded on the third day postpartum and measured PPD at 1, 2 and 3 months postpartum. The authors found no correlation between vitamin B9 status and PPD [37]. These findings indicate potential variability in the impact of specific B vitamins on postpartum mental health.

Jing Yan et al. examined the association between duration of folic acid supplementation during pregnancy and the risk of developing PPD. The prevalence of PPD was significantly higher among participants who reported taking folates for a duration of ≤ 6 months during pregnancy than those who reported supplementing them for a duration of >6 months during pregnancy [33].

CONCLUSIONS

This review emphasizes the critical role of folate and vitamin B12 supplementation during pregnancy as essential elements for improving maternal mental well-being and potentially reducing the risk of (PPD). Folate and vitamin B12 deficiencies have been closely linked with elevated homocysteine levels, impaired neurotransmitter synthesis, and subsequent neurotoxic effects that significantly contribute to depressive symptoms. Ensuring adequate levels of these vitamins supports the methylation cycle, optimizes neurotransmitter metabolism, and mitigates oxidative stress, thus playing a pivotal role in maternal mental health. Given the low-risk, cost-effective nature of nutritional supplementation, integrating routine screening for B-vitamin deficiencies and providing tailored supplementation recommendations should be considered a key component of prenatal care. Currently, there is insufficient evidence to safely prevent or treat PPD solely by dietary changes or supplementation. Before clinical professionals can create diet and supplement strategies to prevent and treat PPD, more study on the relationship between micronutrients and PPD is required. Although current evidence does not unequivocally support the role of folate supplementation in the prevention of PPD, its routine use during pregnancy remains essential. Periconceptional folate intake is a well-established intervention for the prevention of neural tube defects and is also associated with a reduced risk of other adverse pregnancy outcomes. Therefore, despite inconclusive data regarding its effect on maternal mental health, folate supplementation continues to be a fundamental component of prenatal care due to its proven benefits for fetal development and pregnancy maintenance. Further rigorous randomized controlled trials are necessary to solidify the evidence base for comprehensive B-vitamin supplementation protocols, ultimately aiming to optimize maternal and infant health outcomes.

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