Vitamin B6 for PMS, Morning Sickness & Hormonal Modulation

Table of Contents

1. The Three Hormonal Mechanisms
2. Wyatt 1999 — The Pivotal PMS Meta-Analysis
3. PMS Dosing Protocol
4. PMDD (Premenstrual Dysphoric Disorder)
5. Nausea and Vomiting of Pregnancy (NVP)
6. The Pyridoxine + Doxylamine Combination
7. Oral Contraceptive-Induced B6 Depletion
8. OCP-Associated Depression: The B6 Link
9. Hyperprolactinemia & Galactorrhea
10. Estrogen Metabolism & Clearance
11. Carpal Tunnel Syndrome — The Ellis Hypothesis
12. Fertility and Preconception
13. Menopause Support
14. Dosing Summary Across Indications
15. Cautions
16. Key Research Papers
17. Connections
18. Featured Videos

The Three Hormonal Mechanisms

Vitamin B6 influences female reproductive physiology through three distinct mechanisms that all converge on the symptoms women complain of:

1. Dopamine synthesis → prolactin suppression. P5P is required for aromatic L-amino acid decarboxylase (L-DOPA → dopamine). Dopamine, via the tubero-infundibular pathway, is the brain's primary inhibitor of pituitary prolactin secretion. When B6 status drops, dopamine drops, prolactin rises, and the patient develops symptoms of relative hyperprolactinemia — breast tenderness, irregular cycles, mood changes, decreased libido. Restoring B6 restores dopaminergic prolactin suppression.
2. Serotonin synthesis → mood and PMS symptom modulation. The same AADC enzyme converts 5-HTP to serotonin. The luteal phase (post-ovulation) is characterized by rising progesterone with relative serotonin sensitivity changes; women with PMS appear to have particular sensitivity to luteal-phase serotonergic dysregulation. Supplemental B6 supports synthesis throughout the cycle and is particularly helpful for the irritability/depression/anxiety cluster of PMS.
3. Hepatic estrogen clearance. P5P participates in transamination and one-carbon metabolism reactions that support phase I and phase II hepatic detoxification, including the methylation, sulfation, and glucuronidation pathways for estrogen metabolism. Low B6 status may contribute to estrogen dominance phenotypes — heavy periods, breast tenderness, fibroids, endometriosis — though direct trial evidence is limited.

These three mechanisms together explain why B6 shows broad activity across PMS, PMDD, OCP-induced mood symptoms, hyperprolactinemia/galactorrhea, and pregnancy-related nausea — very different clinical syndromes that share underlying hormonal biology.

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Wyatt 1999 — The Pivotal PMS Meta-Analysis

The single most important paper in the B6-for-PMS literature is Wyatt et al. (1999, BMJ). The authors systematically reviewed published and unpublished randomized placebo-controlled trials of pyridoxine for premenstrual syndrome, identifying nine published trials representing 940 patients, and noted that their conclusions were limited by the low quality of most of these trials.

The findings:

• Vitamin B6 was statistically superior to placebo for overall PMS symptoms (odds ratio 2.32, 95% confidence interval (CI) 1.95 to 2.54)
• For depression specifically, pyridoxine was superior to placebo with an odds ratio of 1.69 (95% confidence interval 1.39 to 2.06)
• The response was not dose dependent, and the review found no conclusive evidence of neurological side effects at the doses studied; limited evidence pointed to benefit from 100 mg daily (and possibly 50 mg). The neuropathy limit comes separately from the Institute of Medicine, which set the adult upper limit at 100 mg/day to prevent sensory neuropathy.
• Methodological quality of underlying trials was acknowledged as variable; the authors recommended further high-quality randomized controlled trials (RCTs) that have largely not been performed in the subsequent 25 years

The Wyatt meta-analysis remains the foundation of clinical recommendations. The American Pharmacists Association, U.S. National Institutes of Health (NIH) ODS, and integrative gynecology textbooks all cite Wyatt 1999 as the basis for the 50–100 mg pyridoxine recommendation for PMS — an unusual case of a single meta-analysis driving 25+ years of clinical practice with limited subsequent challenge.

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PMS Dosing Protocol

• Standard dose: Pyridoxine HCl 50 mg or P5P 25–50 mg daily, taken with breakfast
• Higher-symptom protocol: 100 mg/day pyridoxine HCl OR 50 mg P5P, divided morning and noon (evening doses are usually left out — B6 is described as activating)
• Cycle timing: Two patterns are used clinically — continuous (daily throughout the cycle) or luteal-phase only (starting at ovulation, approximately day 14, through menses). Continuous dosing is simpler and may have additional benefits for OCP-induced depletion and homocysteine reduction.
• Synergistic combinations:
  • Magnesium glycinate or citrate 200–400 mg/day — magnesium is required for pyridoxal kinase (activates supplemental pyridoxine to P5P) AND has independent benefits for PMS symptoms. The B6 + magnesium combination is the most evidence-supported integrative PMS protocol.
  • Calcium 600–1200 mg/day — the Thys-Jacobs trials showed independent PMS benefit; the calcium + B6 + magnesium "triple combination" is a common integrative gynecology protocol.
  • Chasteberry (Vitex agnus-castus) 20–40 mg/day standardized extract — works through prolactin suppression at the pituitary; complementary mechanism to B6's dopamine-driven prolactin suppression.
• Trial duration: 2–3 menstrual cycles to assess effect; many women note improvement within the first cycle
• Upper dose limit: 100 mg/day total B6 for adults — the Tolerable Upper Intake Level (UL) set by the Institute of Medicine, based on sensory nerve damage (sensory neuropathy) at higher intakes.

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PMDD (Premenstrual Dysphoric Disorder)

Premenstrual Dysphoric Disorder is the DSM-5 designation for severe PMS with prominent mood symptoms (depression, irritability, anxiety, mood lability) that significantly impair functioning. PMDD affects approximately 3–8% of menstruating women. First-line conventional therapy is a selective serotonin reuptake inhibitor (SSRI) antidepressant, taken continuously or in the luteal phase only, or a combined oral contraceptive containing drospirenone.

The B6 evidence for PMDD specifically is weaker than for general PMS, but mechanistically aligned (low serotonin synthesis being plausibly contributory). In integrative practice, P5P 50 mg/day is often added to an SSRI in PMDD patients whose response to the SSRI is partial. The combination is well-tolerated and the additive effect, while not randomized controlled trial-validated, is biologically plausible (see the Neurotransmitter Synthesis deep dive for the selective serotonin reuptake inhibitor synergy discussion).

For severe PMDD with prominent irritability and anxiety, the combination of P5P + magnesium + low-dose taurine is sometimes used to support GAD-mediated gamma-aminobutyric acid (GABA) synthesis. This is anecdotal but mechanistically reasonable.

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Nausea and Vomiting of Pregnancy (NVP)

Nausea and vomiting in early pregnancy affects 70–80% of pregnant women. The severe form (hyperemesis gravidarum) affects 1–3% and can require hospitalization. Pyridoxine has been used for NVP since the 1940s and has the longest safety record of any antiemetic in pregnancy.

The evidence:

• Sahakian 1991 randomized controlled trial (RCT) of 59 women — 25 mg pyridoxine every 8 hours for 3 days improved nausea significantly more than placebo only in women with severe nausea; in mild-to-moderate nausea and in the group as a whole there was no significant difference. After 3 days, 8 of 31 women on pyridoxine were still vomiting, against 15 of 28 on placebo.
• Vutyavanich 1995 randomized controlled trial — 30 mg pyridoxine daily for 5 days was effective for nausea (and well-tolerated)
• A 2015 Cochrane review of 41 trials (Matthews and colleagues) found only limited evidence from trials to support vitamin B6, doxylamine–pyridoxine and other anti-emetic drugs for mild or moderate nausea and vomiting, little information on maternal and fetal adverse outcomes, and a lack of high-quality evidence for any particular treatment
• ACOG (American College of Obstetricians and Gynecologists) has recommended pyridoxine 10–25 mg three to four times daily as first-line therapy for NVP since the early 2000s

The pyridoxine dose for NVP is modest (typically 10–75 mg/day total, divided) and well below the neuropathy concern range. The pregnancy duration (typically used in first trimester, often discontinued by week 14–16 as nausea resolves) is also short. The FDA no longer gives drugs pregnancy letter categories: its Pregnancy and Lactation Labeling Rule, in effect since June 30, 2015, removed categories A, B, C, D and X. The current label of the delayed-release doxylamine–pyridoxine tablet states that no increased risk for congenital malformations has been reported in epidemiologic studies in pregnant women.

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The Pyridoxine + Doxylamine Combination

The combination originally sold in the United States as Bendectin (1956–1983), sold in Canada continuously since 1979, and back on the US market since 2013 is a delayed-release tablet of pyridoxine 10 mg + doxylamine 10 mg, taken daily (its label says not on an as-needed basis), starting with two tablets at bedtime and stepped up to a maximum of four tablets a day. A second FDA-labelled product is an extended-release tablet of doxylamine 20 mg + pyridoxine 20 mg: one tablet at bedtime, increased to one in the morning and one at bedtime if symptoms persist, a maximum of two a day. Both labels cover nausea and vomiting of pregnancy in women who do not respond to conservative management.

The combination exploits complementary mechanisms: pyridoxine's mild antiemetic effect (likely mediated through brainstem serotonin and dopamine modulation) plus doxylamine's H1-antihistamine effect (which is sedating but also antiemetic). The two together are clinically superior to either alone.

Bendectin, whose original formula also contained a third drug, dicyclomine, was not withdrawn because of demonstrated teratogenicity: its manufacturer stopped production in 1983 in the face of lawsuits alleging that it caused birth defects, lawsuits that came amid the public reaction to thalidomide. A 1994 meta-analysis of 16 cohort and 11 case-control studies (McKeigue and colleagues) found no difference in the risk of birth defects: the pooled relative risk of any malformation after first-trimester exposure was 0.95 (95% CI 0.88 to 1.04). The 1983 withdrawal was the manufacturer's decision, not a regulator's.

Label dosing of the delayed-release tablet: 2 tablets at bedtime on Day 1 (anticipatory dosing for morning nausea); if symptoms persist into the afternoon of Day 2, 2 tablets that bedtime and then, from Day 3, 1 tablet in the morning plus 2 at bedtime; if three tablets do not control symptoms on Day 4, 1 in the morning, 1 mid-afternoon and 2 at bedtime. Maximum 4 tablets/day (pyridoxine 40 mg + doxylamine 40 mg). The tablets are swallowed whole on an empty stomach, not crushed, chewed or split. Side effect: sedation from the doxylamine component, which is why bedtime is the primary dosing time. The label also states that women should not breastfeed while using it (doxylamine passes into breast milk, and excitement, irritability and sedation have been reported in nursing infants); that taking it with alcohol or other sedating (central nervous system depressant) drugs can cause severe drowsiness leading to falls or accidents; that activities needing full alertness, such as driving or operating heavy machinery, are not advised until a healthcare provider has cleared them; and that it is contraindicated with monoamine oxidase inhibitor (MAOI) antidepressants, which intensify and prolong its effects.

Some women instead combine an over-the-counter pyridoxine tablet (10–25 mg) with an over-the-counter doxylamine 25 mg sleep tablet at bedtime, which costs much less. That is a different dose and formulation from the prescription product, whose tablet is delayed-release, so the two are not equivalent.

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Oral Contraceptive-Induced B6 Depletion

One of the most consistently replicated findings in clinical nutrition: hormonal contraceptives (combined estrogen-progestin oral contraceptives, the patch, the ring, and to a lesser extent progestin-only methods) significantly lower circulating B6 status. The original observations date to the early 1970s and have been replicated in dozens of subsequent studies.

The proposed mechanism: estrogen-driven induction of hepatic tryptophan oxygenase increases tryptophan flux through the kynurenine pathway, which requires P5P at multiple steps (notably kynureninase). The increased demand depletes circulating P5P. The clinical correlate is the well-documented xanthurenic acid load test — women on OCPs excrete excess xanthurenic acid after a tryptophan load, a sensitive marker of functional B6 deficiency that normalizes with B6 supplementation.

The Institute of Medicine (1998) noted that in women taking the older high-dose pills, plasma P5P fell only slightly, and judged that the abnormal tryptophan-load results probably reflected hormonal stimulation of tryptophan breakdown rather than true B6 deficiency; those studies used pills with three to five times more estrogen than current ones. In the 2003–2004 US National Health and Nutrition Examination Survey (Morris and colleagues, 2008), most oral contraceptive users had plasma P5P below 20 nmol/L, the level the Institute of Medicine uses as its criterion for adequate B6 status.

Some practitioners describe P5P 25–50 mg/day (or pyridoxine HCl at the same dose), as part of a B-complex, for any woman on hormonal contraception. The evidence behind it is the lower B6 status measured in pill users, described above.

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OCP-Associated Depression: The B6 Link

Approximately 10–25% of women on combined hormonal contraceptives develop new or worsened depressive symptoms. The Skovlund 2016 JAMA Psychiatry study of 1 million Danish women showed a statistically significant increase in subsequent antidepressant prescription and clinical depression diagnosis among hormonal contraceptive users, particularly adolescents and women in the first months of OCP use.

The B6 hypothesis: depression in OCP users is partly driven by the OCP-induced B6 depletion described above, which limits AADC-dependent synthesis of serotonin and dopamine. The biochemical chain is plausible (xanthurenic acid load → P5P depletion → reduced AADC activity → reduced monoamine synthesis → depressive symptoms).

Multiple small placebo-controlled trials in the 1970s and 80s tested 25–50 mg/day pyridoxine in OCP-using women with depression. Results were mixed but generally favorable: approximately half of trials showed clinically meaningful improvement on B6 versus placebo, with stronger effects in women whose baseline B6 status was lowest. No large modern randomized controlled trial has been performed.

Some practitioners describe routine P5P 25–50 mg/day for women starting hormonal contraception, and a trial of P5P for women on the pill who develop mood symptoms, pointing out that it is cheap and low-risk at this dose. The small, mixed trials above tested pyridoxine in pill users with depression; they did not test it as a substitute for depression treatment.

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Hyperprolactinemia & Galactorrhea

Mildly elevated prolactin (in the absence of pituitary adenoma, hypothyroidism, or dopamine-antagonist drug effect) can cause irregular menses, galactorrhea (inappropriate milk discharge), reduced libido, and infertility. The conventional pharmacological treatment is a dopamine agonist (bromocriptine or cabergoline), which directly stimulates pituitary dopamine receptors to suppress prolactin.

B6 supports this pathway by supporting endogenous dopamine synthesis. P5P 25–50 mg/day is sometimes used as a first-line intervention for mild idiopathic hyperprolactinemia, often in combination with chasteberry (Vitex agnus-castus). The evidence is small-scale and predominantly from integrative gynecology practice rather than large randomized controlled trials, but the mechanism is sound and the intervention low-risk.

For galactorrhea associated with elevated prolactin, the combination of P5P 50 mg/day + chasteberry 40 mg/day standardized extract for 3–6 months is a common integrative protocol. If symptoms persist or pituitary imaging shows adenoma, conventional dopamine agonist therapy is appropriate.

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Estrogen Metabolism & Clearance

Estrogens are cleared by the liver through three sequential phases: phase I hydroxylation (cytochrome P450 enzymes), phase II conjugation (methylation, sulfation, glucuronidation), and phase III biliary excretion. Phase I hydroxylation produces three primary metabolites: 2-hydroxyestrone (considered the "safest" metabolite), 4-hydroxyestrone (potentially DNA-damaging if not promptly methylated), and 16-alpha-hydroxyestrone (proliferation-promoting in breast tissue).

P5P participates indirectly in this clearance through its support of the methylation cycle (via the homocysteine → cysteine transsulfuration step, freeing up methyl groups) and through transamination reactions that maintain the amino acid pool. Direct trial evidence for B6's effect on estrogen metabolism ratios is limited but mechanistic plausibility is reasonable.

In integrative gynecology, B6 is included in "estrogen dominance" protocols alongside diindolylmethane (DIM) or indole-3-carbinol (I3C) from cruciferous vegetables (which shift hydroxylation toward the safer 2-hydroxy pathway), calcium-d-glucarate (which supports glucuronidation), and magnesium. The combination is anecdotally helpful for symptoms of presumed estrogen dominance (heavy periods, breast tenderness, fibroids, endometriosis), though large randomized controlled trial evidence is sparse.

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Carpal Tunnel Syndrome — The Ellis Hypothesis

John M. Ellis, a Texas physician, published a series of trials in the 1970s and 80s claiming pyridoxine 100–200 mg/day produced significant improvement in carpal tunnel syndrome (CTS). Ellis hypothesized that CTS represented a localized B6 deficiency in the median nerve and surrounding tissues, with treatment by oral pyridoxine repleting nerve B6 status.

The subsequent literature has been mixed:

• Several small replication trials in the 1980s and 90s found modest improvement in CTS symptoms on 50–200 mg/day pyridoxine
• Other replications found no significant difference from placebo
• A 2003 Cochrane review of non-surgical treatments for CTS (O'Connor and colleagues) found that in two trials involving 50 people, vitamin B6 did not significantly improve overall symptoms
• Mechanistically, B6's role in nerve function and the well-documented association between B6 status and peripheral neuropathy syndromes lends plausibility to the hypothesis

The current integrative practice: pyridoxine 50–100 mg/day (often as P5P) for 6–12 weeks is used as a trial in mild-to-moderate CTS, especially in women whose CTS coincides with pregnancy, OCP use, or PMS symptoms (all conditions of likely B6 depletion). Higher doses (200 mg+) taken for long periods carry the sensory-neuropathy risk that the 100 mg/day upper limit is set to prevent. When 8–12 weeks of supplementation bring no improvement, practitioners stop the trial and turn to other CTS therapies (night splinting, ergonomic modification, corticosteroid injection, surgery).

See the Carpal Tunnel Syndrome page for the broader clinical picture.

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Fertility and Preconception

B6 is part of the standard prenatal supplement formulation (typically 1.9–2.5 mg/day in commercial prenatals). For women trying to conceive, B6 may support fertility through several mechanisms:

• Progesterone luteal-phase support — older observational studies suggested adequate B6 status correlates with luteal-phase length and progesterone levels, though the mechanism is unclear and direct trial evidence limited
• Prolactin normalization — elevated prolactin disrupts ovulation; B6's prolactin-suppressing effect (via dopamine support) is theoretically beneficial
• Homocysteine reduction — elevated homocysteine in either partner has been associated with miscarriage and recurrent pregnancy loss; the B6 + folate + B12 triad supports homocysteine clearance (see the Homocysteine deep dive)
• Continuity with first-trimester NVP management — women starting B6 preconceptionally have B6-replete status entering pregnancy, which may reduce NVP severity

The standard preconception dose is 25–50 mg/day P5P (or equivalent pyridoxine HCl), beginning 3–6 months before conception attempts. Continuation through pregnancy at the prenatal-vitamin dose (typically 1.9–25 mg/day depending on formulation) is appropriate, with the option of using higher doses (up to 75 mg/day) for active NVP.

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Menopause Support

The mood, cognitive, and sleep symptoms of perimenopause and menopause overlap substantially with the neurotransmitter-deficiency phenotype B6 addresses: depressed mood, anxiety, irritability, insomnia, brain fog, and reduced motivation. The estrogen withdrawal of menopause appears to reduce serotonin signaling, which combined with age-related declines in monoamine synthesis can produce a "perimenopausal depression" syndrome.

Clinical evidence for B6 specifically in menopause is limited, but the mechanism is plausible and the intervention low-risk at standard doses (25–50 mg/day P5P). Integrative menopause protocols often include B6 alongside black cohosh, chasteberry, magnesium, and bioidentical hormone replacement therapy (when appropriate). The combination of B6 + magnesium glycinate at bedtime has anecdotal benefit for menopausal insomnia mediated through GAD/GABA support.

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Dosing Summary Across Indications

Note: all doses in this table are within the Institute of Medicine's Tolerable Upper Intake Level of 100 mg/day total B6 for adults, which is set to prevent sensory neuropathy from long-term high intake — see the Toxicity deep dive.

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Cautions

• Sensory neuropathy risk — chronic supplementation of pyridoxine HCl >100 mg/day is the dose-limiting toxicity. Hormonal-health applications generally stay below this limit. Practitioners prefer P5P at sustained doses of 50 mg+. The Toxicity deep dive covers doses above 50 mg/day.
• B-complex co-supplementation — isolated B6 supplementation can deplete other B vitamins (riboflavin, folate, B12) over months. Practitioners therefore give B6 as part of a balanced B-complex or alongside a separate B-complex.
• Pregnancy — FDA labels no longer carry pregnancy letter categories; the doxylamine–pyridoxine label states that no increased risk for congenital malformations has been reported in epidemiologic studies in pregnant women. Pyridoxine doses for NVP are typically 10–75 mg/day. The Institute of Medicine upper limit of 100 mg/day applies in pregnancy too (80 mg/day at ages 14–18); higher doses (>100 mg/day) lack pregnancy safety data.
• Breastfeeding — high-dose pyridoxine (>200 mg/day) has been reported to suppress prolactin and reduce milk supply via the same dopamine-suppression-of-prolactin mechanism that benefits hyperprolactinemia. The Institute of Medicine upper limit during breastfeeding is also 100 mg/day (80 mg/day at ages 14–18); integrative practitioners describe keeping breastfeeding women to 25–50 mg/day.
• Levodopa interaction — legacy concern with unprotected levodopa; not relevant with modern carbidopa/levodopa combinations at normal B6 intakes.
• Isoniazid, hydralazine, penicillamine, cycloserine — all are B6 antagonists; supplementation indicated.
• Hormone-sensitive cancers — B6 at standard doses has no documented effect on hormone-sensitive cancer recurrence and is generally considered safe.

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Key Research Papers

1. Wyatt KM, Dimmock PW, Jones PW, Shaughn O'Brien PM (1999). Efficacy of vitamin B-6 in the treatment of premenstrual syndrome: systematic review. BMJ. The pivotal meta-analysis. — PubMed PMID: 10334745
2. Koren G, Clark S, Hankins GD, et al. (2010). Effectiveness of delayed-release doxylamine and pyridoxine for nausea and vomiting of pregnancy: a randomized placebo controlled trial. American Journal of Obstetrics & Gynecology. — PubMed
3. Sahakian V, Rouse D, Sipes S, Rose N, Niebyl J (1991). Vitamin B6 is effective therapy for nausea and vomiting of pregnancy: a randomized, double-blind placebo-controlled study. Obstetrics & Gynecology. — PubMed PMID: 2047064
4. Vutyavanich T, Wongtra-ngan S, Ruangsri R (1995). Pyridoxine for nausea and vomiting of pregnancy: a randomized, double-blind, placebo-controlled trial. American Journal of Obstetrics & Gynecology. — PubMed PMID: 7573262
5. Skovlund CW, Morch LS, Kessing LV, Lidegaard O (2016). Association of hormonal contraception with depression. JAMA Psychiatry. — PubMed PMID: 27680324
6. Wynn V, Adams PW, Folkard J, Seed M (1975). Tryptophan, depression and steroidal contraception. Journal of Steroid Biochemistry. The original OCP/B6/tryptophan paper. — PubMed
7. Adams PW, Wynn V, Rose DP, et al. (1973). Effect of pyridoxine hydrochloride (vitamin B6) upon depression associated with oral contraception. The Lancet. — PubMed PMID: 4123835
8. Ellis JM, Kishi T, Azuma J, Folkers K (1976). Vitamin B6 deficiency in patients with a clinical syndrome including the carpal tunnel defect. Biochemical and clinical response to therapy with pyridoxine. Research Communications in Chemical Pathology and Pharmacology. The original Ellis CTS paper. — PubMed PMID: 1265347
9. O'Connor D, Marshall S, Massy-Westropp N (2003). Non-surgical treatment (other than steroid injection) for carpal tunnel syndrome. Cochrane Database of Systematic Reviews. — PubMed PMID: 12535461
10. McKeigue PM, Lamm SH, Linn S, Kutcher JS (1994). Bendectin and birth defects: I. A meta-analysis of the epidemiologic studies. Teratology. — PubMed PMID: 7974252
11. Morris MS, Picciano MF, Jacques PF, Selhub J (2008). Plasma pyridoxal 5'-phosphate in the US population: the National Health and Nutrition Examination Survey, 2003-2004. American Journal of Clinical Nutrition. — PubMed PMID: 18469270
12. Matthews A, Haas DM, O'Mathuna DP, Dowswell T (2015). Interventions for nausea and vomiting in early pregnancy. Cochrane Database. — PubMed PMID: 26348534
13. American College of Obstetricians and Gynecologists (2018). ACOG Practice Bulletin: Nausea and Vomiting of Pregnancy. — PubMed
14. Sayegh R, Schiff I, Wurtman J, Spiers P, McDermott J, Wurtman R (1995). The effect of a carbohydrate-rich beverage on mood, appetite, and cognitive function in women with premenstrual syndrome. Obstetrics & Gynecology. Companion serotonin/PMS paper. — PubMed

PubMed Topic Searches

1. PubMed: B6 PMS
2. PubMed: doxylamine + pyridoxine NVP
3. PubMed: OCP B6 depletion
4. PubMed: B6 carpal tunnel
5. PubMed: B6 + vitex hyperprolactinemia

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Connections

• All Vitamins
• Vitamin B6 Overview
• B6 Benefits Hub
• B6 for Neurotransmitter Synthesis
• B6 for Homocysteine
• B6 Toxicity
• Folate (B9)
• Vitamin B12
• Riboflavin (B2)
• Magnesium
• Calcium
• Carpal Tunnel Syndrome
• Depression
• Anxiety
• Insomnia
• Tryptophan
• All Herbs (chasteberry/vitex section)
• Deficiency
• Toxicity
• History
• Sources

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