Definition

What Is Migraine?

Migraine is a neurological disorder characterized by recurrent episodes of moderate-to-severe headache, typically unilateral, pulsating, aggravated by physical activity, and accompanied by nausea, vomiting, and sensitivity to light and sound. Episodes last 4–72 hours and can be completely disabling.

The pathophysiology involves cortical spreading depression (CSD), a wave of abnormal electrical activity across the brain cortex, followed by activation of the trigeminal pain pathway and release of CGRP (calcitonin gene-related peptide), the primary neuroinflammatory molecule responsible for migraine pain.

The gut-brain connection is central to migraine biology: 90% of serotonin is produced in the gut, and gut dysbiosis directly alters serotonin availability and neuroinflammatory signaling in the brain. Patients with migraine have significantly higher rates of SIBO, Candida, IBS, leaky gut, and altered gut microbiome composition compared to non-migraineurs.

⚠️ Medication Overuse Headache² (MOH), "rebound headache", affects up to 1 in 50 adults. Taking acute migraine medication more than 10–15 days/month causes chronic daily headache. Breaking this cycle requires supervised withdrawal and replacement with preventive strategies.

Migraine, neurological head pain and triggers

Types of Migraine

🌀 Migraine Without Aura (Common)

The most prevalent type (75% of cases). Recurrent unilateral, throbbing headache with nausea and light/sound sensitivity. No preceding neurological warning symptoms. Often worse with physical movement, bright light, or noise. Requires quiet, dark rest for recovery.

⚡ Migraine With Aura (Classic)

25% of migraineurs experience aura, transient neurological symptoms lasting 5–60 minutes before or during headache onset. Visual aura (scintillating scotoma, zig-zag lines, blurred vision) is most common. Motor, sensory, and speech auras also occur. Migraine with aura carries a small but real increased stroke risk⁷, particularly in women on estrogen-containing contraceptives who smoke.

📅 Chronic Migraine

Defined as ≥15 headache days/month for 3+ months, with ≥8 meeting migraine criteria. Often develops from episodic migraine through neuroplastic changes and medication overuse. More disabling and more likely driven by gut dysbiosis, hormonal dysregulation, nutritional deficiencies (magnesium, B2, CoQ10), and unaddressed triggers than episodic migraine.

Symptoms & Triggers⁶

Migraine Phases, Symptoms & Key Triggers

Understanding the four phases of a migraine attack, and identifying personal triggers, is the cornerstone of effective management.

🧠 The Four Phases of Migraine

🌤️

Prodrome (1–2 Days Before)

Early warning signs: food cravings (especially for carbohydrates), yawning, neck stiffness, mood changes (depression or euphoria), increased thirst and urination, fatigue, cognitive slowing. Recognizing prodrome allows early intervention before the headache phase begins.

⚡

Aura (20–60 Minutes)

Transient focal neurological symptoms, visual (scintillating scotoma, fortification spectra, visual loss), sensory (tingling or numbness spreading from fingertips to face), speech (dysphasia), or motor (weakness). Each symptom typically spreads gradually, distinguishing aura from TIA which strikes suddenly.

💢

Headache Phase (4–72 Hours)

Severe, throbbing, often unilateral headache (though bilateral in 40%). Accompanied by nausea/vomiting (80%), photophobia (90%), phonophobia (80%), and osmophobia (smell sensitivity). Worsened by physical activity, bending forward, coughing. Requires rest in a dark, quiet environment.

😴

Postdrome ("Migraine Hangover")

After the headache resolves, profound fatigue, cognitive impairment ("brain fog"), emotional lability, weakness, and difficulty concentrating lasting 24–48 hours. Often as disabling as the headache itself, yet rarely recognized or addressed in conventional treatment.

🚨 Common Migraine Triggers

🍷

Dietary Triggers (Most Common)

Red wine and alcohol (histamine, tyramine, sulfites), aged cheeses (tyramine), processed meats (nitrates, tyramine), MSG, artificial sweeteners (aspartame), chocolate (phenylethylamine), caffeine (both excess and withdrawal), skipped meals (hypoglycemia), and dehydration are the most consistently reported dietary triggers.

🌙

Sleep & Circadian Disruption

Both too little AND too much sleep trigger migraines. Irregular sleep schedules, shift work, jet lag, and lying in on weekends ("weekend migraine") all disrupt the circadian rhythm of melatonin and serotonin synthesis, directly lowering the migraine threshold.

🌸

Hormonal Fluctuations

Estrogen withdrawal (premenstrual drop) is the most powerful trigger in women, explaining the 3:1 female predominance and the clustering of migraines in the perimenstrual window. Perimenopause, oral contraceptives, and HRT can all exacerbate or trigger migraine in susceptible women.

💡

Environmental & Sensory Triggers

Bright or flickering lights (photosensitivity is intrinsic to migraine, not just a symptom), strong smells (perfumes, chemical fumes), weather changes (barometric pressure drops), loud noise, and screen time. Migraine brains have persistent interictal hypersensitivity to sensory input.

Root Cause

The Gut-Brain Connection in Migraine

The gut is the missing piece in most migraine treatment plans. The evidence for gut dysbiosis as a driver of migraine is compelling and growing.

🧬 Serotonin Deficit

95% of serotonin is produced in the gut by enterochromaffin cells, regulated by the gut microbiome. Migraine patients have lower serotonin levels interictally, with surges before attacks and crashes during them. Gut dysbiosis disrupts serotonin synthesis and metabolism, lowering the migraine threshold chronically. Healing the gut microbiome restores serotonin availability without drug dependency.

🔥 Gut Inflammation & Leaky Gut

Intestinal permeability allows bacterial lipopolysaccharides (LPS) and inflammatory cytokines (TNF-α, IL-1β, IL-6) to enter systemic circulation, cross the blood-brain barrier, and directly activate trigeminal neurons, the pain pathway of migraine. Studies show migraine patients have significantly higher intestinal permeability and circulating LPS than healthy controls.

🦠 Histamine Intolerance & SIBO

Many migraineurs have histamine intolerance, an inability to adequately break down dietary and endogenous histamine due to low diamine oxidase (DAO) enzyme activity, often caused by SIBO. Histamine directly dilates cerebral blood vessels and activates the trigeminal pathway. Treating SIBO and supporting DAO enzyme function can dramatically reduce histamine-triggered migraine attacks.

Diagnosis

Investigating Migraine & Its Root Causes

🏠 Tracking & Self-Assessment

📔 Headache Diary

The most important diagnostic tool for identifying personal triggers. Log: date, time, duration, severity (1–10), phase symptoms, foods/drinks consumed 24h before, sleep hours, menstrual cycle day, medications taken, stress level, weather, and activity. After 2–3 months, patterns reveal dominant triggers with precision impossible from memory alone.

🍽️ Elimination Diet (Low-Tyramine / Low-Histamine)

A structured 4–6 week elimination of the most common dietary triggers (aged cheeses, red wine, processed meats, MSG, chocolate, caffeine, artificial sweeteners, citrus) followed by systematic reintroduction, one food per 3 days, while tracking headache frequency. Identifies personal food triggers with high precision.

🔬 Clinical Tests

🧲 MRI Brain (Rule Out Structural Causes)

MRI is recommended for: new onset headache over age 50, progressively worsening headache, "thunderclap¹" headache (sudden onset of worst headache of life), headache with neurological signs, or headache awakening from sleep. Normal in migraine, but essential to rule out intracranial pathology before accepting a primary headache diagnosis.

🧬 Nutritional & Functional Lab Panel

RBC magnesium³ (better than serum, serum is normal even when cells are depleted), Vitamin D 25(OH)D, B2 (riboflavin⁴) status, CoQ10 plasma level, plasma homocysteine (elevated in MTHFR mutation, drives migraine), DAO enzyme activity (histamine intolerance marker), thyroid panel, cortisol rhythm (diurnal cortisol pattern by saliva).

🦠 SIBO Breath Test & Stool Analysis

Given the strong gut-migraine connection, SIBO testing (lactulose breath test) and comprehensive gut microbiome analysis (stool DNA test) are valuable, especially for migraineurs with concurrent digestive symptoms, histamine intolerance, or poor response to conventional treatments.

Treatment Comparison

Holistic vs. Conventional Treatment for Migraine

🌿 HOLISTIC

💊 CONVENTIONAL

🌿

Holistic / Functional Approach

Magnesium, Riboflavin (B2), CoQ10, Butterbur, trigger elimination, gut healing, sleep optimization

Migraine Reduction

Mg + B2 + CoQ10 combination reduces attack frequency by 50–70% in controlled trials

Key Supplements

Magnesium glycinate, Riboflavin, CoQ10, Butterbur (Petasites), Feverfew, Melatonin

Timeline

Supplement benefits build over 3 months; trigger elimination effects visible within 6–8 weeks

Advantage

Addresses nutritional deficiencies, neuroinflammation, and gut dysfunction, the actual drivers of migraine biology

Full Holistic Prevention Protocol

Magnesium glycinate (400–600mg/day), among the better-evidenced supplements for migraine prevention. The upper intake level for supplemental magnesium is 350 mg/day; above that the usual effect is loose stools rather than harm, but it is worth knowing.; corrects near-universal magnesium deficiency in migraineurs
Riboflavin (Vitamin B2, 400mg/day), improves mitochondrial energy efficiency in neurons; reduces attack frequency by 50% in 3 months in trials
CoQ10 (300mg/day, ubiquinol), reduces neuronal energy deficits; multiple trials show 47–55% reduction in migraine frequency
Butterbur (Petasites hybridus, 75mg 2x/day), reduces CGRP release and neurogenic inflammation; shown to reduce migraine frequency by 58% (Level A evidence from American Academy of Neurology)
Feverfew (100–150mg dried leaf extract/day), parthenolide inhibits serotonin release from platelets and prostaglandin synthesis; reduces severity and frequency
Melatonin (3–5mg before bed), regulates serotonin-melatonin axis and circadian rhythm; reduces migraine frequency comparably to amitriptyline without weight gain
Elimination diet and gut healing, remove dietary triggers, treat SIBO if present, support DAO enzyme for histamine intolerance
Consistent sleep schedule (same bedtime/wake time 7 days a week), the single most important lifestyle variable for migraine frequency
Hydration protocol (2.5L+/day), dehydration is the #1 most commonly reported acute migraine trigger

✅ Butterbur note: Only use PA-free certified Butterbur extracts (Petadolex brand or equivalent), pyrrolizidine alkaloids (PAs) in non-certified butterbur are hepatotoxic. PA-free extracts are safe and highly effective.

💊

Conventional / Medical Approach

Triptans⁵, CGRP inhibitors, beta-blockers, topiramate, amitriptyline, Botox injections

Acute Treatment

Triptans (sumatriptan, rizatriptan), most effective; CGRP antagonists (Ubrelvy, Nurtec), newer class, fewer side effects

Preventive Treatment

Beta-blockers (propranolol), Topiramate, Amitriptyline, CGRP monoclonal antibodies (Aimovig, Ajovy, Emgality)

Chronic Migraine

OnabotulinumtoxinA (Botox), 31 injections every 12 weeks; FDA-approved for chronic migraine prevention

Side Effects

Topiramate: cognitive impairment ("dopamax"), weight loss; Amitriptyline: weight gain, sedation, cardiac risk; Triptans: chest tightness, medication overuse headache risk

Conventional Treatment Stepladder

Acute: NSAIDs (naproxen, ibuprofen) + antiemetics for mild-moderate attacks
Acute: Triptans (sumatriptan, rizatriptan, eletriptan), serotonin 5-HT1B/1D agonists; contraindicated in cardiovascular disease
Acute: CGRP antagonists (ubrogepant/Ubrelvy, rimegepant/Nurtec), oral gepants; no cardiovascular contraindications; can be used preventively
Preventive: Propranolol (beta-blocker, 40–240mg/day), modest effect; causes fatigue and exercise intolerance
Preventive: Topiramate (anticonvulsant, 50–200mg/day), effective but causes word-finding difficulty, paresthesias, kidney stones in 5%
Preventive: CGRP monoclonal antibodies (erenumab/Aimovig, fremanezumab/Ajovy, galcanezumab/Emgality), monthly/quarterly injections; highly effective; very expensive
Chronic migraine: Botulinum toxin (Botox), 31 injection sites every 12 weeks; reduces monthly headache days by ~8–9

⚠️ Medication overuse: Using triptans or simple analgesics on >10 days/month leads to MOH (Medication Overuse Headache), a transformation to chronic daily headache driven by neuroplastic sensitization from frequent analgesic use. This worsens migraine dramatically and creates drug dependency.

Nutritional Strategy

Migraine Diet: Eliminate Triggers, Heal the Gut

Diet plays a dual role in migraine management, eliminating direct neurochemical triggers while healing the gut-brain axis that lowers the migraine threshold.

✅ Brain-Protective & Anti-Inflammatory:

🥬 Anti-Inflammatory Whole Foods

Dark leafy greens (magnesium), fatty fish (omega-3s for neuroinflammation), colorful vegetables (antioxidants), berries (flavonoids), ginger and turmeric (anti-inflammatory). Reducing systemic inflammation through diet lowers the frequency and severity of neuroinflammatory migraine attacks.

💧 Consistent Hydration

Dehydration is the single most commonly reported acute migraine trigger, even mild dehydration (1–2% body weight) can precipitate an attack. Drink 2.5–3L of water daily, more in heat or exercise. Electrolyte supplementation prevents dehydration-driven migraine more effectively than water alone.

🌾 Regular Meal Timing

Skipping meals and prolonged fasting trigger migraines through hypoglycemia and cortisol elevation. Eat at consistent times, include protein and fat at every meal to stabilize blood glucose, and never skip breakfast. The migraine brain is extremely sensitive to metabolic stress.

❌ Common Dietary Triggers:

🍷 Tyramine-Rich Foods

Aged cheeses (parmesan, cheddar, blue), red wine, beer, fermented foods, smoked/cured meats, soy sauce, miso, MSG. Tyramine triggers migraine by causing norepinephrine release from nerve terminals, producing vasodilation and neuroinflammation in susceptible individuals.

🥩 Histamine Sources

Histamine content is highest in: red wine, fermented foods (kimchi, sauerkraut), aged cheeses, processed meats, leftover fish, and spinach. In patients with low DAO enzyme activity (often caused by SIBO or gut damage), even small amounts of dietary histamine can precipitate a migraine attack within hours.

☕ Caffeine (Both Excess & Withdrawal)

The relationship with caffeine is paradoxical: acute caffeine can abort a migraine (hence its inclusion in Excedrin), but chronic use leads to withdrawal-triggered migraines when caffeine is missed. Limit to 1 cup of coffee/day maximum, always at the same time, consistency prevents the withdrawal trigger.

🍬 Artificial Sweeteners

Aspartame (converted to phenylalanine and methanol) and sucralose have been consistently reported as migraine triggers in clinical surveys and case series. Eliminate all artificial sweeteners during a diagnostic elimination period, they are present in diet sodas, sugar-free gum, protein powders, and "light" products.

Supplement Protocol

Evidence-Based Supplements for Migraine Prevention

The following supplements have Level A–B evidence from the American Academy of Neurology or multiple RCTs for migraine prevention. They address the core neurobiological mechanisms, mitochondrial dysfunction, magnesium depletion, neuroinflammation, and gut-brain axis dysregulation.

Supplement	Mechanism & Evidence	Suggested Dose	Timing	Notes
Magnesium Glycinate	Magnesium deficiency is present in 50% of migraineurs during attacks and 30% interictally. Magnesium regulates NMDA glutamate receptor activity (excitatory, excess glutamate lowers migraine threshold), prevents cortical spreading depression, and reduces CGRP release. IV magnesium aborts acute attacks in many patients. Oral supplementation reduces frequency by 41–45% in prevention trials. Level B evidence from AAN.	400–600mg elemental magnesium/day (as glycinate)	With dinner; or split morning and evening	RBC magnesium (not serum) accurately reflects total body status. Glycinate form: best absorbed, no laxative effect. Avoid citrate form if loose stools are present. The upper intake level for supplemental magnesium is 350 mg/day; above that the usual effect is loose stools rather than harm, but it is worth knowing.
Riboflavin (Vitamin B2)	Riboflavin is the rate-limiting cofactor for Complex I and II of the mitochondrial electron transport chain. Migraine patients have documented mitochondrial dysfunction, reduced phosphorylation potential in neural tissue. High-dose B2 (400mg/day) restores mitochondrial energy production, reducing attack frequency by 50% within 3 months. A 2004 RCT showed equivalence to propranolol (a first-line preventive drug) with zero side effects.	400mg/day	With breakfast (fat-soluble vitamins aid absorption)	High doses cause bright yellow/orange urine, normal and harmless. Takes 3 months to reach full benefit. Available OTC; extremely safe; no drug interactions.
CoQ10 (Ubiquinol)	CoQ10 is the electron carrier between mitochondrial Complex I–II and III, essential for neuronal ATP production. Plasma CoQ10 deficiency is present in 33% of chronic migraine patients. A 2005 RCT (Sandor et al.) showed 300mg/day reduced migraine frequency by 48% over 3 months. The combination of Mg + B2 + CoQ10 produces greater-than-additive effects on migraine prevention.	300mg/day (ubiquinol form)	With a fat-containing meal, essential for absorption	Ubiquinol is the pre-reduced, active form, 3–4x more bioavailable than ubiquinone, especially important for age-related CoQ10 decline. Combine with B2 and Mg for synergistic mitochondrial support.
Butterbur (Petasites hybridus)	PA-free butterbur extract contains petasin and isopetasin, sesquiterpene compounds that inhibit leukotriene synthesis and block CGRP release from trigeminal neurons. A 2004 RCT (Diener et al.) in Neurology showed 75mg 2x/day reduced migraine frequency by 58% over 4 months, the strongest effect size of any herbal supplement. The American Academy of Neurology awarded it Level A evidence for migraine prevention.	75mg 2x/day (PA-free certified extract)	With meals	MUST be PA-free (pyrrolizidine alkaloid-free), look for "Petadolex" brand or certifications. PAs in non-certified butterbur cause serious liver damage. PA-free extracts are completely safe and highly effective.
Feverfew (Tanacetum parthenium)	Parthenolide, the active compound, inhibits platelet serotonin release, blocks prostaglandin synthesis, and reduces NF-κB-mediated neuroinflammation in trigeminal neurons. A Cochrane review of 6 trials found feverfew modestly but consistently reduces migraine frequency and severity. Most effective for prevention when taken continuously, not for acute treatment.	50–150mg/day (standardized to 0.2–0.6% parthenolide)	With food	Do NOT stop abruptly after prolonged use, can cause "post-feverfew syndrome" (rebound headaches, nervousness, insomnia). Taper gradually. Avoid in pregnancy.
Melatonin	Migraine is associated with disrupted melatonin secretion, migraineurs have lower nocturnal melatonin peaks and altered circadian rhythms. Melatonin has direct antinociceptive (pain-reducing) properties, reduces serotonin synthesis in the pineal gland (regulating serotonin-melatonin axis), and restores sleep architecture. A 2016 randomized trial found melatonin effective for migraine prevention, without weight gain or sedation, though comparative data against prescription therapy is limited.	3–5mg at bedtime	30–60 minutes before sleep, in dim light	Take in dim or red light, bright light exposure immediately before bed blocks endogenous melatonin production, negating the supplement benefit. Use consistently at the same time each night for circadian entrainment. Melatonin is commonly sold at doses well above what is needed, and more is not better. Start at the lowest available dose. Discuss it with your prescriber if you take sedatives, anticoagulants, or immunosuppressants.
5-HTP (5-Hydroxytryptophan)	The direct precursor to serotonin, bypassing the rate-limiting tryptophan hydroxylase step. Raises serotonin levels in both the gut and brain, addressing the serotoninergic deficit underlying migraine pathophysiology. Studies show 400–600mg/day reduces attack frequency comparably to methysergide (a prescription prophylactic). Also improves sleep quality and mood, both of which influence migraine threshold.	100–200mg/day (starting low)	Before bed (serotonin → melatonin pathway supports sleep)	Do NOT combine with SSRIs, SNRIs, triptans, or MAOIs, risk of serotonin syndrome. Must be used alone or under physician supervision if on serotonergic medications.
Alpha-Lipoic Acid (ALA)	A lipophilic and hydrophilic antioxidant that crosses the blood-brain barrier and directly reduces neuroinflammation and oxidative stress in trigeminal pathways. A 2019 RCT found 600mg/day ALA reduced migraine frequency by 49% over 3 months. Particularly effective when combined with the Mg + B2 + CoQ10 mitochondrial protocol for synergistic neuroprotective effects.	600mg/day (R-ALA preferred)	30 minutes before a meal	R-ALA form is significantly more bioavailable. Stabilized sodium R-ALA (Na-RALA) prevents thermal degradation. Synergistic with CoQ10 for mitochondrial antioxidant defense.

References & Evidence Notes

Each numbered entry below is either a source you can follow or a note setting out what the evidence does and does not support. Both are numbered together so the markers in the text line up.

Last reviewed 27 August 2026. Supplement entries are cross-checked against the NIH National Center for Complementary and Integrative Health and the Linus Pauling Institute Micronutrient Information Center.⁸ Two safety points before the nutrition. A sudden, severe headache that peaks within seconds to a minute, the worst of your life, is not a migraine until proven otherwise, and needs emergency assessment for subarachnoid haemorrhage. So does a headache with fever and neck stiffness, new neurological signs, a headache starting after 50, or one that wakes you from sleep or worsens progressively. Second, and much commoner: the treatment can become the cause. Taking acute migraine medication on more than about 10 to 15 days a month, depending on the drug, produces medication overuse headache, and the way out is withdrawal with support rather than more medication. Migraine with aura also carries a small increased stroke risk, which matters if you smoke or use estrogen-containing contraception.

On red flags. Thunderclap onset, headache with fever and neck stiffness, new focal neurological deficit, headache after head injury, new headache over the age of 50, headache worsening with posture or Valsalva, headache in pregnancy or postpartum, and new headache in someone immunosuppressed or with cancer all warrant urgent assessment rather than migraine treatment. ↩
On medication overuse headache. Regular use of acute treatments beyond roughly 10 days a month for triptans, ergots, opioids and combination analgesics, or 15 days for simple analgesics, can transform episodic migraine into a chronic daily headache. Those are the thresholds used to define acute medication overuse in recent migraine trials, PubMed 38924724. It is common, frequently unrecognised, and improves with withdrawal of the offending agent, generally alongside preventive treatment. Recognising it changes the whole management plan. ↩
On magnesium: magnesium is among the better-evidenced supplements for migraine prevention, with Level B evidence in American Academy of Neurology guidance, typically at 400 to 600 mg of elemental magnesium daily. That is above the 350 mg upper intake level for supplemental magnesium, and the practical consequence of exceeding it is usually loose stools rather than harm; glycinate is better tolerated than citrate or oxide. Better-evidenced is relative, though. A meta-analysis of randomized trials found oral magnesium reduced attack frequency and intensity, PubMed 26752497, while a later systematic review concluded the evidence is insufficient to say whether it works at all, PubMed 30764890. The trials are small, and the honest summary is that this is a reasonable thing to try rather than a reliable one. ↩
On riboflavin and coenzyme Q10: riboflavin at 400 mg daily has supportive randomized evidence. A pooled analysis of trials at 400 mg daily for three months found significant effects on migraine days, duration, frequency and pain score, PubMed 33779525. Coenzyme Q10 at around 300 mg daily is less settled. One meta-analysis found it reduced attack duration and frequency, PubMed 33402403, and another found no significant reduction in frequency and judged the evidence insufficient, PubMed 30764890. Effects, where they appear, take two to three months rather than working immediately. Both are low-risk. Riboflavin turns urine bright yellow, which is harmless and expected. ↩
On preventive medication and newer options: beta blockers, candesartan, amitriptyline, topiramate and sodium valproate are established preventives, with valproate avoided in women of childbearing potential, since in a population cohort of prenatal anti-seizure drug exposure it was among the drugs associated with neurodevelopmental disorders in the child while several alternatives were not, PubMed 41813017. CGRP monoclonal antibodies and gepants are newer, well-tolerated and effective for people who have failed older preventives. If migraine is disabling and supplements have not helped, this is worth pursuing rather than persisting. ↩
On triggers, honestly: the evidence for specific dietary triggers is weaker than the folklore suggests, and premonitory-phase food cravings are frequently mistaken for triggers, meaning the attack had already started. Skipped meals, dehydration, disrupted sleep and alcohol have better support than chocolate or cheese. A headache diary distinguishes real personal triggers from coincidence better than an elimination diet does. ↩
On aura and vascular risk: migraine with aura is associated with a modest increase in ischaemic stroke risk, amplified by smoking and by combined hormonal contraception: a BMJ meta-analysis found the raised risk concentrated in migraine with aura, absent without it, and further increased by smoking and oral contraceptive use, PubMed 19861375. Guidance generally advises against estrogen-containing contraceptives in women with migraine with aura, which is a conversation worth having explicitly. ↩
National Center for Complementary and Integrative Health (NIH), nccih.nih.gov, and the Linus Pauling Institute Micronutrient Information Center, lpi.oregonstate.edu/mic.