Vitality Chiropractic & Wellness alias Dr. Birth Control Migraine

Vitality Chiropractic & Wellness is not licensed or approved by Minnesota Board of Chiropractic Examiners to diagnose, treat, or cure Anxiety and depression are linked to lower serotonin levels found in the gut and brain, which causes migraines.

Anxiety and depression are linked to lower serotonin levels found in the gut and brain, which causes migraines

Supports

There is evidence that the serotonergic system is involved in both depression/anxiety and migraine, and that gut-derived serotonin contributes to overall serotonin signaling. Reviews of serotonin and mood disorders describe altered serotonin receptor function, transporter function, and signaling in anxiety and major depression, and note that antidepressants directly or indirectly increase serotonin system activity.^[21] These support a role for serotonin dysregulation (though not necessarily simple “low levels”) in depression and anxiety. Migraine pathophysiology literature consistently implicates serotonin; classic work proposed that low serotonin leads to vasodilation and migraine, and modern reviews describe serotonin receptors and metabolites as involved in migraine attacks.^[22][25] Gut–brain axis reviews indicate that gut microbiota regulate enteric serotonin and that gut-derived serotonin and tryptophan metabolism can influence brain function and mood, supporting a mechanistic link between gut serotonin, mood disorders, and possibly migraine via shared pathways.^[17][19][24] Thus, high-quality narrative and systematic reviews support that serotonin signaling abnormalities contribute to depression, anxiety, and migraine, and that the gut–brain axis and enteric serotonin are relevant to mood and pain modulation, partially supporting a broad “serotonin link” between these conditions. The perinatal depression meta-analysis and related reviews show decreased BDNF rather than directly measuring serotonin, but they support that neurobiological factors (including monoaminergic systems) are involved in depression pathophysiology.

Contradicts

High-quality evidence contradicts the simple statement that anxiety and depression are caused by lower serotonin levels, and that these low levels straightforwardly cause migraines. A major systematic umbrella review of the serotonin theory of depression found no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity; studies of serotonin and its metabolites in blood and CSF, receptor binding, transporter levels, and tryptophan depletion did not consistently show lower serotonin in depressed individuals.^[7][16][11] This directly contradicts the influencer’s claim that depression is due to low serotonin in the brain. Commentary on this umbrella review notes that the traditional “low serotonin” theory of depression has effectively been debunked and that depression is multifactorial, involving stress, environment, genes, and complex brain changes rather than a single neurotransmitter deficit.^[8][9][11] Migraine reviews acknowledge serotonin involvement but do not support a simple model in which low serotonin from anxiety/depression causes migraine; serotonin can be low or high at different phases of migraine, and the pathophysiology involves multiple systems (CGRP, trigeminovascular pathways) rather than a single causal chain from mood to low serotonin to migraine.^[22][25] Gut–brain axis and mood disorder reviews emphasize complex bidirectional interactions and note that enteric serotonin is heavily regulated by diet, microbiota, and immune factors; they do not show that low gut serotonin is a consistent finding in anxiety/depression or a direct cause of migraine.^[17][19][24] Overall, current high-quality evidence disputes a linear causal pathway of “low serotonin in gut and brain → anxiety/depression → migraines” and instead supports multifactorial, heterogeneous mechanisms with serotonin as one of many contributors.

Mainstream view

The mainstream medical and scientific view is that serotonin is one important neurotransmitter involved in depression, anxiety, and migraine, but these conditions are not simply caused by globally low serotonin levels in the gut and brain. For depression and anxiety, contemporary reviews and umbrella analyses conclude that evidence does not support the classic “low serotonin” hypothesis as a sufficient or primary cause; instead, these disorders are understood as multifactorial, involving genetic vulnerability, stress, inflammatory signals, neuroplasticity changes (e.g., BDNF), multiple neurotransmitter systems (serotonin, norepinephrine, dopamine, GABA, glutamate), and psychological and social factors.^{[7][8][9][16][21]} For migraine, mainstream neurology recognizes migraine as a brain network disorder with involvement of trigeminovascular pathways, CGRP, serotonin, and other modulators. Serotonin is implicated (and some antimigraine drugs target serotonin receptors), but migraine is not viewed as simply the downstream result of mood-related low serotonin; rather, depression/anxiety and migraine share overlapping biological pathways (including serotonin) and often co-occur, without a single, proven serotonin-deficit causal chain.^[22][25] Regarding the gut, the dominant

▶ 3:31In their own wordsWatch at 3:31Archived copy

“anxiety and depression are linked to lower levels of serotonin which is found in your gut and in your brain so if you have lower levels of serotonin there are supplements you can take that are precursors to serotonin”

Rule: Minn. Stat. § 148.01

Vitality Chiropractic & Wellness is not licensed or approved by Minnesota Board of Chiropractic Examiners to diagnose, treat, or cure Migraines are caused by vasodilation in your brain where arteries swell up, causing the pounding throbbing feeling.

Migraines are caused by vasodilation in your brain where arteries swell up, causing the pounding throbbing feeling

Supports

Older vascular theories of migraine proposed that vasodilation of intracranial and meningeal arteries contributes to the characteristic throbbing, pulsating headache, and this idea is still referenced historically in modern reviews of migraine pathophysiology.^[22] These theories are consistent with the observation that some migraine treatments (such as triptans and ergot derivatives) are cranial vasoconstrictors, which was taken as indirect support that dilated vessels contribute to migraine pain. Modern neurovascular models acknowledge that activation of the trigeminovascular system can lead to release of vasoactive neuropeptides (especially CGRP) that induce vasodilation and neurogenic inflammation in meningeal vessels, which may be temporally associated with headache and throbbing sensations.^[11][22][23] Several reviews emphasize that vascular changes, including alterations in vessel diameter and cerebral blood flow, are part of the migraine phenomenon, even if not the sole cause of the headache.^[15][18] In this sense, there is partial support that vasodilation occurs during migraine and may contribute to the pulsatile quality of pain, but this is embedded in a broader neurovascular framework rather than a simple “arteries swell up and cause migraine” mechanism.

Contradicts

Contemporary high-quality reviews explicitly state that the traditional view of migraine as primarily caused by cerebral and meningeal arterial vasodilation is no longer supported as a sufficient or necessary explanation for migraine pain.^{[1][3][4][22]} Neuroimaging and vascular studies have shown that headache can occur without significant dilation of extracranial arteries, and that changes in cerebral blood flow (including periods of decreased flow) do not neatly correlate with the onset or intensity of headache.^[7][12][15] Modern pathophysiological models emphasize that migraine is fundamentally a disorder of sensory processing and dysfunctional neuronal networks in brainstem and diencephalic regions, with vascular changes considered secondary phenomena rather than the primary cause.^[5][6][22] Reviews of the trigeminovascular system highlight that neurogenic inflammation, nociceptor sensitization, and CGRP-mediated signaling are central drivers of pain, and vessel dilation alone does not fully explain the throbbing quality or other migraine symptoms.^[11][14][23] Overall, current evidence contradicts the simplified claim that migraines are caused by vasodilation where arteries swell up and directly cause the pounding feeling; instead, vasodilation is one component within a complex neurovascular process.

Mainstream view

The mainstream medical and scientific position is that migraine is a complex neurovascular and brain disorder primarily driven by abnormal neuronal excitability, sensory processing dysfunction, and activation of the trigeminovascular system, with vascular changes (including vasodilation) playing a secondary and contributory but not purely causal role.^{[5][6][11][18][22][23]} Cortical spreading depression, brainstem and diencephalic network dysfunction, and trigeminal nociceptor sensitization are considered core mechanisms, while meningeal and intracranial vessel changes, including vasodilation and altered cerebral blood flow, are integrated into this broader framework rather than viewed as the sole origin of headache.^{[7][12][15][18][22]} The throbbing, pulsatile nature of migraine pain is thought to arise from the interaction between vascular pulsations and sensitized trigeminal afferents, not simply from arteries mechanically “swelling up”; thus, vasodilation is recognized but not regarded as the primary or sufficient cause of migraine attacks in current guidelines and expert reviews.^{[1][3][4][11][22]}

▶ 1:10In their own wordsWatch at 1:10Archived copy

“classic migraines can be caused by or migraines in general i should say are caused by vasodilation in your brain so the arteries in your brain they swell up and so the swelling causes kind of that pounding throbbing type of feeling”

Rule: Minn. Stat. § 148.01

Vitality Chiropractic & Wellness is not licensed or approved by Minnesota Board of Chiropractic Examiners to diagnose, treat, or cure Adjusting or switching hormonal birth control dosing/form can prevent migraines linked to the menstrual cycle.

Adjusting or switching hormonal birth control dosing/form can prevent migraines linked to the menstrual cycle

Supports

There is substantial evidence that stabilizing or modifying hormonal exposure with contraceptives can reduce menstrual-related or hormone-withdrawal migraines, particularly in migraine without aura. Reviews on estrogens and menstrual migraine note that combined hormonal contraception (CHC) can modify migraine patterns, and that reducing estrogen withdrawal (for example by continuous or extended-cycle regimens) is a plausible preventive strategy for perimenstrual attacks.^[2] Clinical literature and practice-based recommendations report that continuous combined oral contraceptive (COC) use, without a hormone-free interval, can reduce menstrual migraine frequency and severity by avoiding the sharp estrogen decline that triggers attacks.^[10][18][20] A randomized pilot trial of an extended COC regimen in women with menstrual-related migraine found that extended combined oral contraceptive use reduced daily headache scores and menstrual-related migraine severity compared with the pre-study (standard-cycle) baseline, supporting the idea that changing regimen can lessen attacks linked to cycle-related hormone changes.^[11] Major clinical recommendations and expert consensus statements on menstrual migraine management (e.g., American Migraine Foundation and other guideline-style resources) explicitly state that dosing birth control pills continuously or using extended-cycle regimens to eliminate or minimize the pill-free interval can be effective in reducing menstrual migraines.^{[15][17][18][20]} Hormone-focused reviews also note that systemic hormonal contraceptives that maintain relatively stable, low estradiol levels may reduce the number of menstrual migraines, especially in women whose attacks cluster around menses.^[10]

Contradicts

Evidence is not uniformly strong or conclusive, and results regarding COCs and menstrual migraine are described as inconsistent, with some women experiencing improvement and others no change or even worsening of migraines.^[10] High-quality RCT data specific to continuous or modified hormonal contraceptive regimens for menstrual migraine are still limited; at least one major trial (WHAT! trial) is ongoing and thus provides rationale but not outcome data yet, highlighting that the preventive effect of continuous COCs is not definitively established.^[14][19] Observational and safety-focused systematic reviews indicate that combined hormonal contraceptives, particularly in women with migraine with aura, are associated with a two- to fourfold increased risk of ischemic stroke, so using or intensifying estrogen-containing contraception to manage migraines may be contraindicated or require extreme caution in this subgroup.^{[5][6][20][22]} Some clinical reviews on hormonal options for women with headache underscore that CHCs may worsen headaches in some patients and that response is highly individual, so adjusting or switching hormonal birth control does not reliably prevent menstrual migraines for all users.^[4][8][20]

Mainstream view

The mainstream medical view is that menstrual and perimenstrual migraines are strongly influenced by estrogen fluctuations and withdrawal, and that carefully chosen hormonal strategies can be used as one option among several to reduce these attacks. In women with migraine without aura and appropriate vascular risk profiles, continuous or extended-cycle combined hormonal contraceptive regimens that minimize or eliminate the hormone-free interval are considered reasonable strategies to reduce menstrual-related migraines by stabilizing estrogen levels.^{[2][10][11][15][17][18][20]} However, for women with migraine with aura or significant cardiovascular risk factors, mainstream guidelines advise against or strictly limit estrogen-containing combined hormonal contraceptives because of elevated stroke risk, and favor non-estrogen methods (e.g., progestogen-only contraception) or non-hormonal preventive approaches.^{[5][6][8][20][22]} Overall, expert guidance frames hormonal contraception adjustments (continuous dosing, extended cycles, or switching to more stable regimens) as evidence-informed but not universally effective interventions, to be individualized, monitored for both migraine response and vascular safety, and integrated with other acute and preventive migraine treatments.^{[2][7][10][15][17][18][20]} Deterministic PubMed cross-check found no matching indexed studies for these terms (absence of indexed evidence is not evidence against the claim).

▶ 3:02In their own wordsWatch at 3:02Archived copy

“if you notice for example you're getting them closer to your menstrual cycle we may want to take a look at your hormonal birth control if that's what you're on and take a look and see if maybe we need to adjust the dosing or try to maybe switch the form of birth control that you're on”

Rule: Minn. Stat. § 148.01

Vitality Chiropractic & Wellness is not licensed or approved by Minnesota Board of Chiropractic Examiners to diagnose, treat, or cure Taking serotonin precursors (supplements) can help ward off migraines by increasing serotonin levels.

Taking serotonin precursors (supplements) can help ward off migraines by increasing serotonin levels

Supports

There is some limited clinical trial evidence that the serotonin precursor 5‑hydroxytryptophan (5‑HTP) can reduce migraine frequency. An older double‑blind crossover trial in children found that L‑5‑HTP led to a significant reduction in migraine index and attack frequency over time, but placebo produced a similar reduction and no clear superiority of 5‑HTP over placebo was demonstrated.^[21] Popular secondary summaries describe an older adult trial where daily 5‑HTP for 6 months reportedly prevented or significantly decreased migraine attacks in about 70% of participants, comparable to methysergide, but this evidence is dated and not replicated in recent high‑quality studies. Evidence that manipulating central serotonin pharmacologically can affect migraine comes from trials of serotonin–norepinephrine reuptake inhibitors (SNRIs), which show fewer migraine days versus placebo and comparable efficacy to other prophylactic drugs, indicating that serotonergic mechanisms can be leveraged in prevention, albeit via reuptake inhibition rather than precursor supplementation.^[13][18] Major guidelines acknowledge that serotonin pathways are relevant to migraine pathophysiology and list some serotonergic agents (e.g., certain antidepressants, triptans for acute therapy) among options for treatment, again supporting the general idea that serotonin is involved in migraine biology, though not specifically endorsing serotonin precursors.^[15][20]

Contradicts

The pathophysiology literature shows that the old concept of migraine as a simple “low serotonin” state is oversimplified and not consistently supported. Some imaging work has found high interictal brain serotonin levels in migraineurs between attacks, challenging the notion that globally increasing serotonin would be universally beneficial for prevention. Contemporary reviews emphasize complex tryptophan metabolism with both serotonin and kynurenine pathway products influencing migraine, rather than a straightforward deficiency that could be corrected by precursors alone.^[3][5][10] The pediatric double‑blind trial of L‑5‑HTP versus placebo showed no difference between L‑5‑HTP and placebo in the first treatment period and a strong period effect, suggesting that benefits may reflect nonspecific factors rather than a true drug effect.^[21] Modern prophylaxis guidelines from major neurology and headache societies do not recommend tryptophan or 5‑HTP as standard migraine preventive therapy and instead prioritize beta‑blockers, antiepileptics, certain antidepressants, and CGRP‑targeting agents, implying that evidence for serotonin precursors is considered weak or insufficient for guideline inclusion.^[15][20][24] Furthermore, several effective prophylactic drugs are antiserotonin agents (e.g., methysergide, other serotonin antagonists), and triptans used acutely are receptor agonists without altering serotonin synthesis, indicating that clinical benefit is mediated via specific receptor modulation rather than simply raising serotonin levels.^[7][22][23]

Mainstream view

Mainstream medical and scientific opinion is that serotonin and broader tryptophan metabolism play an important role in migraine pathophysiology, and that drugs acting on serotonergic receptors or reuptake can be effective in both acute treatment and prophylaxis. However, the evidence base for using dietary or supplement serotonin precursors such as tryptophan or 5‑HTP specifically to ward off migraines is limited, dated, and not sufficiently robust to support routine clinical use. Current major guidelines for migraine prevention do not recommend serotonin precursors and instead endorse better‑studied medications and some nutraceuticals with stronger trial support. Clinicians may view precursor supplements as experimental or adjunctive at best, with uncertain benefit and potential risks, rather than a proven strategy to prevent migraines by simply increasing serotonin levels.^[15][20][24] Deterministic PubMed cross-check found no matching indexed studies for these terms (absence of indexed evidence is not evidence against the claim).

▶ 3:37In their own wordsWatch at 3:37Archived copy

“if you have lower levels of serotonin there are supplements you can take that are precursors to serotonin meaning they're going to help your body more efficiently and effectively produce serotonin which can definitely help ward off those nasty headaches”

Rule: Minn. Stat. § 148.01

Vitality Chiropractic & Wellness is not licensed or approved by Minnesota Board of Chiropractic Examiners to diagnose, treat, or cure Supplementing with folic acid and B12 is important to prevent migraines, especially if consuming alcohol/caffeine.

Supplementing with folic acid and B12 is important to prevent migraines, especially if consuming alcohol/caffeine

Supports

Several randomized, double-blind, placebo-controlled trials suggest that high-dose folate (vitamin B9) in combination with other B vitamins can reduce migraine frequency and disability, particularly in migraine with aura. ^[38][39] One RCT using 2 mg folic acid plus vitamin B6 and B12 for 6 months in women with migraine with aura reported significant reductions in plasma homocysteine and migraine-related disability versus placebo, indicating a potential preventive effect of this combined B‑vitamin regimen. ^[33][40] Observational and meta-analytic work also links elevated homocysteine and lower folate/B12 status with migraine, supporting a plausible biological pathway via homocysteine metabolism and endothelial/neuronal function. A more recent double-blind, randomized, placebo-controlled trial in adults with migraine with aura found that 5 mg folic acid plus pyridoxine (B6) reduced headache severity, attack frequency, and disability compared with placebo, whereas folic acid alone did not show clear benefit. Another randomized trial in women with episodic migraine found that supplementation with B9 (folate), B12, and other B vitamins reduced headache attack frequency, abortive drug use, and migraine disability compared with placebo. Cross‑sectional NHANES analyses from large U. S. populations report that both higher dietary folate intake and higher serum folate levels are associated with lower odds of migraine or severe headache, which is consistent with but not proof of a preventive effect. ^[34][35][37] These strands of evidence together suggest that, in some patients—especially those with migraine with aura, elevated homocysteine, or relevant MTHFR polymorphisms—folate/B‑vitamin supplementation can contribute to migraine prophylaxis as an adjuvant, though doses and combinations matter. ^[36]

Contradicts

Evidence does not support the stronger influencer claim that folic acid and B12 supplementation are broadly "important" or universally required to prevent migraines, nor that this is specifically necessary because of alcohol or caffeine intake. ^[38] Trials showing benefit generally use high-dose folate combined with other B vitamins (often including B6), not folic acid or B12 alone; when folic acid was given by itself, benefits on migraine characteristics were not significant compared with placebo. ^[4][39] Some RCT data indicate that a lower-dose regimen (1 mg folic acid with B6 and B12) was less effective or not clearly effective compared with a higher-dose regimen, suggesting dose‑response uncertainty and that modest supplementation may not meaningfully prevent migraines. There are no high‑quality randomized trials demonstrating that taking folic acid and B12 specifically counteracts migraine risk from alcohol or caffeine use; the relationship between these substances and migraine is mediated by multiple pathways (vascular, sleep, dehydration, central nervous system excitability), and the homocysteine/folate axis is only one hypothesized contributor. ^[40] Current major clinical guidelines for migraine prevention focus on pharmacologic prophylactics (beta‑blockers, antiepileptics, CGRP‑targeted therapies), lifestyle triggers, and a few nutraceuticals (e. ^[3] g. , riboflavin/B2, magnesium, coenzyme Q10); they do not recommend routine folic acid or B12 supplementation as a standard or essential preventive measure in the general migraine population, reflecting limited and heterogeneous evidence and the absence of large, confirmatory trials. ^[33] Cross-sectional associations between folate status and headache do not prove causality, may be confounded by overall diet quality, and do not identify optimal dosing or define who benefits most. ^[34][35][37] Overall, the evidence is insufficient to claim that everyone with migraine—especially those consuming alcohol or caffeine—should take folic acid and B12 as a key preventive strategy, and the alcohol/caffeine-specific justification is essentially unsupported. ^[36]

Mainstream view

The mainstream medical view is that folic acid and vitamin B12 are not established first-line or universally recommended migraine preventives, but they may be reasonable adjuvant options in selected patients, particularly those with migraine with aura, elevated homocysteine, or documented folate/B12 deficiency. ^{[33][34][35][36][38][39][40]} Standard migraine prophylaxis is based on medications with robust evidence (such as beta-blockers, topiramate, valproate, tricyclics, and newer CGRP pathway therapies) and, among supplements, riboflavin (B2), magnesium, and coenzyme Q10 have the strongest support; folate and B12 are considered experimental or adjunctive, with some promising but not definitive data. ^[1][37] Clinicians may consider measuring homocysteine and B‑vitamin status in refractory or aura‑dominant migraine and trialing appropriate supplementation, but routine folic acid/B12 supplementation for all migraine patients, or specifically to offset alcohol or caffeine consumption, is not part of guideline-driven ^[4]

▶ 3:58In their own wordsWatch at 3:58Archived copy

“nowadays we're in such a stressed environment that we deplete vitamin b very very quickly so supplementing your diet with a good folic acid b12 supplement is always important”

Rule: Minn. Stat. § 148.01