Impact of Dietary Folate Intake on Depressive Symptoms in Young Women of Reproductive Age

Watanabe, Hiroko; Ishida, Sadayo; Konno, Yoshie; Matsumoto, Momoyo; Nomachi, Shinobu; Masaki, Kiyoko; Okayama, Hisayo; Nagai, Yasushi

doi:10.1111/j.1542-2011.2011.00073.x

Cited by 20 publications

(9 citation statements)

References 23 publications

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“…The association between folate status and depression, and the effect of folate administration in the treatment of depression have been addressed by several studies [72,128]. Supplementation of FA [24] or 5-methylfolate [36] may enhance the antidepressant action of certain medications.…”

Section: Protective Effects Of Folate Beyond Ntd Preventionmentioning

confidence: 99%

Is 5-methyltetrahydrofolate an alternative to folic acid for the prevention of neural tube defects?

Obeid

Holzgreve

Pietrzik

2013

Journal of Perinatal Medicine

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Women have higher requirements for folate during pregnancy. An optimal folate status must be achieved before conception and in the first trimester when the neural tube closes. Low maternal folate status is causally related to neural tube defects (NTDs). Many NTDs can be prevented by increasing maternal folate intake in the preconceptional period. Dietary folate is protective, but recommending increasing folate intake is ineffective on a population level particularly during periods of high demands. This is because the recommendations are often not followed or because the bioavailability of food folate is variable. Supplemental folate [folic acid (FA) or 5-methyltetrahydrofolate (5-methylTHF)] can effectively increase folate concentrations to the level that is considered to be protective. FA is a synthetic compound that has no biological functions unless it is reduced to dihydrofolate and tetrahydrofolate. Unmetabolized FA appears in the circulation at doses of > 200 μg. Individuals show wide variations in their ability to reduce FA. Carriers of certain polymorphisms in genes related to folate metabolism or absorption can better benefit from 5-methylTHF instead of FA. 5-MethylTHF [also known as (6S)-5-methylTHF] is the predominant natural form that is readily available for transport and metabolism. In contrast to FA, 5-methylTHF has no tolerable upper intake level and does not mask vitamin B 12 deficiency. Supplementation of the natural form, 5-methylTHF, is a better alternative to supplementation of FA, especially in countries not applying a fortification program. Supplemental 5-methylTHF can effectively improve folate biomarkers in young women in early pregnancy in order to prevent NTDs.

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Section: Protective Effects Of Folate Beyond Ntd Preventionmentioning

confidence: 99%

Is 5-methyltetrahydrofolate an alternative to folic acid for the prevention of neural tube defects?

Obeid

Holzgreve

Pietrzik

2013

Journal of Perinatal Medicine

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“…12 Here, we further found a suggestive inverse association between dietary vitamin B6 intake at baseline and depressive symptoms after 3 years. Of seven cross-sectional studies that have examined the association between vitamin B6 intake and depressive symptoms [9][10][11][12][13][14][15] , four have observed an inverse association. [10][11][12]15 Moreover, only two studies have examined the prospective association between vitamin B6 intake and depressive symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…However, a systematic review reported that vitamin B6 had no apparent treatment effect on depression. 8 Although seven crosssectional [9][10][11][12][13][14][15] and two prospective 16,17 studies have examined the association between dietary vitamin B6 intake and depressive symptoms, inconsistent findings were reported. Moreover, only two cross-sectional studies have found an inverse association between depression and plasma concentrations of pyridoxal 5 0 -phosphate (PLP), which is the major and active form of vitamin B6.…”

Section: Introductionmentioning

confidence: 99%

Serum pyridoxal concentrations and depressive symptoms among Japanese adults: results from a prospective study

et al. 2013

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“…Parkinson's disease 76,105 . Supplementation with B-vitamins and folate has enjoyed moderate clinical success in alleviating depressive symptoms 91,92,106 . Recently, S-adenosyl methionine has been touted as a potential treatment for depression, both alone and in conjunction with prescription serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) 94,107 .…”

Section: Introductionmentioning

confidence: 99%

“…. Further studies showed that high plasma homocysteine and low serum folate both increased the risk of depression and increased the duration of depressive episodes, an effect that is especially pronounced in pregnant and postpartum women [90][91][92] .…”

mentioning

confidence: 99%

Oral S-adenosyl methionine (SAM) mediates disruptions in methyl group metabolism due to retinoic acid therapy and alters neurotransmitter metabolism: implications for major depressive disorder

Smazal

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Disruptions in methyl group metabolism have been associated with a number of disease states, including birth defects, cardiovascular disease, and neurological disorders. Therefore, characterization of the factors that regulate folate and methyl group supply is essential for the development of disease treatments and prevention. Glycine N-methyltransferase (GNMT), an enzyme essential to methyl group balance, is markedly increased by retinoic acid treatment. Furthermore, retinoid therapy has been shown to impact neurotransmitter metabolism, thereby contributing to the development of major depressive disorder. Recently, it has been shown that depressed patients have low levels of folate, other B-vitamins, and S-adenosyl methionine (SAM), all compounds essential for maintaining effective methyl group metabolism. The following studies were conducted to further characterize the impact of oral retinoic acid administration, and to investigate the potential prevention of any detrimental effects by administering oral SAM. In the preliminary study (Chapter 2), as expected, GNMT activity was significantly increased in rats receiving all-trans retinoic acid (ATRA). Additionally, whole brain serotonin levels were decreased by 46% in rats receiving ATRA, an effect that was partially attenuated by oral SAM. The experiment was repeated with an improved dosing method, longer duration of treatment, and another form of retinoic acid, 13-cis retinoic acid (13CRA). Retinoic acid was shown to increase liver lipids and triglycerides, decrease hepatic SAM, and mildly elevate serotonin, in contrast to the first experiment. ATRA slightly decreased whole brain dopamine transporter (DAT) and 13CRA slightly decreased whole brain norepinephrine transporter (NET); these effects were not seen in rats that received supplemental SAM. Furthermore, SAM abrogated liver lipid content in rats receiving 13CRA, partially prevented increases in liver triglycerides, and restored hepatic SAM levels in both retinoic acid groups. Rats that received only SAM supplementation had extremely high dopamine, and increased ix norepinephrine. SAM supplementation may be an effective therapy for both the mitigation of retinoic acid-related side effects and the prevention or treatment of major depressive disorder.

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Impact of Dietary Folate Intake on Depressive Symptoms in Young Women of Reproductive Age

Cited by 20 publications

References 23 publications

Is 5-methyltetrahydrofolate an alternative to folic acid for the prevention of neural tube defects?

Is 5-methyltetrahydrofolate an alternative to folic acid for the prevention of neural tube defects?

Serum pyridoxal concentrations and depressive symptoms among Japanese adults: results from a prospective study

Oral S-adenosyl methionine (SAM) mediates disruptions in methyl group metabolism due to retinoic acid therapy and alters neurotransmitter metabolism: implications for major depressive disorder

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