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 long-standing evidence that the serotonergic system is involved in both depression and migraine, and that some migraine patients show a low interictal (between attacks) serotonergic disposition with dynamic changes during attacks. Several reviews and experimental studies describe serotonin receptors and signaling as key targets in therapies for anxiety and depression, with selective serotonin reuptake inhibitors and other serotonergic agents showing anxiolytic and antidepressant effects, indicating that serotonin pathways are relevant to these disorders even if the exact mechanism is complex. Clinical and biochemical work in migraine shows that serotonin levels and receptor-mediated vasoconstriction in cerebral blood vessels are involved in migraine pathophysiology, and migraine is often described as a “low serotonin” syndrome between attacks with transient increases during attacks that modulate trigeminovascular nociceptive pathways. Large narrative and systematic reviews of migraine pathobiology consistently implicate altered serotonin metabolism and receptor function in migraine, and pharmacologic agents that increase or modulate serotonin signaling (such as certain antidepressants and triptans) can reduce migraine frequency or abort attacks, supporting a mechanistic link between serotonergic dysfunction and migraine. Evidence from studies of gut–brain conditions like irritable bowel syndrome (IBS) suggests that impaired gut–brain communication and serotonin signaling can be associated with both gastrointestinal symptoms and psychological disorders including anxiety and depression, which supports a role for gut serotonin in some anxiety–depression presentations, though this is indirect and not specific to migraines.

Contradicts

High-quality evidence has challenged the simple “low serotonin causes depression” model. A comprehensive umbrella review of serotonin and depression concluded that there is no convincing evidence that depression, in general, is caused by lower serotonin concentrations or activity, and that most experimental paradigms (including tryptophan depletion) do not consistently lower mood in volunteers, contradicting a simplistic deficiency model. Other systematic reviews and concise overviews on serotonin and mental disorders emphasize that, while serotonergic drugs are effective for some patients, direct imaging and molecular evidence for uniformly reduced serotonin in anxiety disorders is limited and often inconclusive; some findings show abnormalities in specific receptor subtypes (such as 5-HT1A function in depression) rather than a global low serotonin state. Importantly, migraine pathophysiology is multifactorial and not uniquely determined by anxiety or depression; genetic factors, cortical spreading depression, CGRP signaling, trigeminovascular activation, and other neurotransmitters all play major roles, and the presence of anxiety or depression is a comorbidity rather than a proven causal driver of migraine via serotonin alone. Current migraine reviews note that serotonin changes are dynamic (low between attacks, increased during attacks) and involve receptor-specific effects, so it is an oversimplification to say that “lower serotonin in the gut and brain” straightforwardly causes migraines. The gut–brain literature supports an association between altered gut serotonin and psychological symptoms, but causal chains from gut serotonin → anxiety/depression → migraine are not well demonstrated in randomized trials or major guidelines; they remain hypotheses rather than settled evidence.

Mainstream view

The mainstream position is that serotonin is an important neuromodulator in mood and anxiety disorders and in migraine pathophysiology, but the traditional serotonin deficiency theory of depression and anxiety is considered overly simplistic and not strongly supported as a general causal explanation. For depression, current consensus is that it arises from a complex interplay of genetic vulnerability, stress, neuroplastic changes, and multiple neurotransmitter and hormonal systems, with serotonergic abnormalities present in some patients but not as a universal low-serotonin state. For anxiety disorders, serotonergic drugs are effective in many cases and receptor-level changes may be involved, yet direct evidence for a consistent global serotonin deficit is limited and mixed; clinical benefit is thought to reflect modulation of specific receptor systems and neural circuits rather than correction of a simple deficiency. For migraine, mainstream neurology views migraine as a neurovascular disorder with altered excitability, trigeminovascular activation, CGRP and other peptide signaling, and multiple neurotransmitters (including serotonin) contributing; migraine is often associated with low serotonergic tone between attacks, but migraine is not considered simply “caused” by low serotonin, and comorbid anxiety and depression are recognized risk modifiers rather than mechanistically proven causes. The gut–brain axis and gut serotonin are increasingly acknowledged as relevant to both gastrointestinal disorders and some mood symptoms, but major guidelines do not state that gut serotonin deficiency causes anxiety, depression, and then migraines; instead, these are viewed as overlapping conditions with shared biological pathways where serotonin is one of several important factors.

Papers listed for this claim:[1][2][3][4][5][6][7][8][9][10][11][12]

▶ 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: Minnesota Statutes § 148.01, Subd. 2; § 148.01, Subd. 4

See every doc bro who says they can treat or advise on Depression

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

High-quality evidence supports a trigeminovascular/neuropeptide model of migraine, including roles for CGRP, PACAP, nitric oxide, and sensitization of pain pathways, rather than a simple “arteries swell up” explanation. Reviews note that vasodilatory peptides can contribute to migraine biology and may be involved in intracranial vasodilation and nociceptive signaling. Some literature still discusses vasodilation as a possible contributor to the throbbing quality of migraine pain, but this is not established as the primary cause.

Contradicts

The claim that migraines are caused by vasodilation in the brain, where arteries swell and that swelling causes the pounding pain, is contradicted by modern evidence reviews. Neuroimaging and pharmacologic challenge studies have not shown vasodilation to be necessary or sufficient for migraine attacks, and the classic vascular theory has largely fallen out of favor. Evidence also shows that vasodilators can trigger migraine without a corresponding large arterial dilation, and that throbbing pain does not reliably track the arterial pulse, arguing against a direct swelling-causes-pain model. The included listed papers do not directly support the claim; the headache guidelines listed are for tension-type headache or unrelated conditions and do not provide evidence that migraine is caused by vasodilation.

Mainstream view

The mainstream view is that migraine is primarily a neurobiological disorder of the trigeminovascular system and sensory processing, with CGRP and related signaling pathways playing central roles; vascular changes may occur during attacks, but they are not considered the main cause of migraine pain. Vasodilation may be a downstream feature or one contributor among several, but the simple statement that migraines are caused by swollen brain arteries is not considered accurate.

Papers listed for this claim:[1][3][2][4][6][5][13][14][15][16][17][18]

▶ 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: Minnesota Statutes § 148.01, Subd. 2; § 148.01, Subd. 4

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

High-quality evidence and clinical recommendations indicate that modifying hormonal contraceptive regimens (dose, schedule, or formulation) can reduce or prevent menstrual-related migraines in some women. Continuous use of combined oral contraceptives (COCs) or regimens that shorten or eliminate the hormone‑free interval are repeatedly suggested to lessen estrogen withdrawal, which is a key trigger for menstrual migraine. Extended‑cycle COC regimens have shown reduced severity of menstrual‑related migraine in a randomized, placebo‑controlled pilot study, supporting the idea that altering the schedule of hormone exposure can improve migraine outcomes. Reviews and expert guidance on hormonal contraception and migraine report that continuous or shortened hormone‑free regimens, and sometimes supplemental estrogen during the usual placebo days, are used specifically to prevent menstrual migraine. A trial protocol (WHAT!) has been designed to test continuous COC use versus vitamin E for menstrual migraine, reflecting prior small studies that suggest benefit of continuous COCs for menstrual migraine, even though large definitive RCTs are still lacking. A recent systematic review and meta‑analysis of hormonal contraceptives and migraine shows that migraine burden tends to increase during the hormone‑free interval, implying that regimens which minimize or remove this interval may reduce menstrual‑linked migraine. Together, these data and guidelines support the claim that adjusting or switching hormonal contraceptive regimens can be a valid strategy to prevent or reduce menstrual‑cycle–linked migraines, particularly in migraine without aura.

Contradicts

The evidence base is limited and heterogeneous, and there is no strong, consistent high‑quality evidence that adjusting or switching hormonal birth control reliably prevents menstrual migraines for all patients. Systematic review and meta‑analysis of hormonal contraceptives and migraine found no overall significant effect on migraine frequency when comparing users to non‑users, with substantial heterogeneity and mostly observational data, indicating that hormonal contraception per se is not a universal solution; the main signal is confined to the hormone‑free interval rather than to specific formulations. Some literature reports inconsistent results, with COCs aggravating migraine in some women and improving it in others, even with continuous regimens. High‑quality randomized trials specifically designed to compare different contraceptive regimens for menstrual migraine (e.g., continuous vs cyclic, different doses or formulations) are largely absent, and existing RCT data are pilot‑scale, which limits confidence in generalizing the findings. There is also a safety concern: major guidance emphasizes that estrogen‑containing combined hormonal contraception is contraindicated or used with great caution in women with migraine with aura due to increased stroke risk, so switching or intensifying estrogen‑containing regimens for such patients may be unsafe and is generally discouraged. Overall, while some women benefit from tailored hormonal regimens, the evidence is not robust enough to claim that adjusting or switching hormonal birth control will predictably prevent menstrual migraines across the board.

Mainstream view

The mainstream medical view is that menstrual‑related migraine is commonly driven by hormonal fluctuations, particularly the estrogen drop around menses, and that hormonal strategies can be used as one option among several to manage or prevent these migraines, especially in women with migraine without aura. Clinical recommendations and expert reviews support considering continuous combined hormonal contraceptives, regimens that shorten or eliminate the hormone‑free interval, supplemental estrogen during the placebo days, or switching to progestin‑only methods in appropriate patients, recognizing that responses are individual and that the primary goal is to stabilize hormone levels rather than increase them. For women with migraine with aura, estrogen‑containing combined hormonal contraception is generally avoided or used only in carefully selected low‑risk patients due to concern about ischemic stroke risk; progestin‑only methods or non‑hormonal options are preferred. Guidelines and expert consensus therefore view hormonal regimen adjustment as a reasonable, evidence‑informed option that may reduce menstrual migraine burden, but they do not consider it a universally effective or stand‑alone solution and emphasize individualized risk–benefit assessment, close monitoring, and integration with standard migraine therapies (acute and preventive).

Papers listed for this claim:[1][3][2][5][6][13][14][19][20][21][22][23]

▶ 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: Minnesota Statutes § 148.01, Subd. 1(1); § 148.01, Subd. 2

See every doc bro who says they can treat or advise on Hormone imbalance and replacement

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 randomized controlled trial evidence that the serotonin precursor 5‑hydroxytryptophan (5‑HTP) can reduce migraine attacks and is comparable to older preventive drugs like methysergide. A classic randomized trial in adults with migraine found that 5‑HTP (200–600 mg/day) reduced migraine frequency, intensity and duration similarly to methysergide, with fewer side effects. Multiple small double‑blind, placebo‑controlled studies in adults and children report that L‑5‑HTP prophylaxis is associated with decreased migraine days and lower migraine index scores compared with baseline and placebo, although most are short-term and underpowered. A double‑blind cross‑over study in chronic primary headache (including migraine) found that L‑5‑HTP (400 mg/day) was more effective than placebo in reducing headache frequency and severity, with about half of patients achieving ≥50% reduction in symptoms, although differences versus placebo did not reach statistical significance. A recent narrative review on 5‑HTP summarizes these older clinical trials and concludes that 5‑HTP “was found to be a treatment of choice in the prophylaxis of migraine,” again based on small RCTs rather than modern large-scale studies. Observational data suggest that higher dietary tryptophan intake is associated with lower odds of having migraine, and mechanistic reviews of tryptophan metabolism in migraine note that increased intake of dietary tryptophan may prevent migraine or attenuate gastrointestinal-related migraine symptoms. There is also at least one nonrandomized clinical study of an oral supplement combination including L‑tryptophan and other nutrients (magnesium, niacin, B vitamins) reporting improvement in migraine or primary headache outcomes, but the design limits causal inference.

Contradicts

Despite some positive small trials, the overall evidence base for serotonin precursors as migraine prophylaxis is weak, dated, and heterogeneous. Most studies of 5‑HTP and tryptophan for migraine prevention are small (often n≈30–120), short duration (weeks to a few months), and conducted decades ago, with limited modern methodological rigor, incomplete reporting of randomization, and sometimes lacking clear statistically significant differences versus placebo. One chronic primary headache trial with L‑5‑HTP found that although 5‑HTP appeared more effective than placebo, the difference was not statistically significant, which undermines strong claims of efficacy. There are no large contemporary multicenter randomized trials, dose‑response studies, or high‑quality meta‑analyses specifically confirming that serotonin precursors reliably “ward off” migraines. Modern migraine prophylaxis trials and reviews focus on CGRP monoclonal antibodies, gepants, beta‑blockers, topiramate, valproate, tricyclics, onabotulinumtoxinA, and lifestyle or dietary interventions, not on serotonin precursors, suggesting these supplements are not considered evidence‑based first‑line or even second‑line options. Major migraine guidelines from neurology and headache societies do not list 5‑HTP or tryptophan supplements as recommended or standard preventive therapies, reflecting insufficient high‑quality evidence and concerns about safety (e.g., risk of serotonin syndrome when combined with other serotonergic drugs, historical concerns about tryptophan contaminants). The influencer’s causal framing that taking serotonin precursors “wards off migraines by increasing serotonin levels” also overstates the mechanistic certainty: migraine pathophysiology involves multiple neurotransmitters and CGRP-related pathways, and simply raising serotonin systemically does not consistently translate into migraine prevention across trials. Overall, the evidence is inconsistent, mostly low‑quality, and insufficient to support strong preventive claims.

Mainstream view

The mainstream medical and scientific position is that serotonin precursor supplements such as 5‑HTP or L‑tryptophan are not established, guideline‑recommended treatments for migraine prevention. They may have plausible biological mechanisms and some small, older randomized trials suggesting potential benefit, but the evidence is limited, not replicated in large modern studies, and subject to bias. Current migraine prophylaxis practice is based on drugs and interventions with robust randomized controlled trial and guideline support, including beta‑blockers, topiramate, valproate, tricyclic antidepressants, onabotulinumtoxinA for chronic migraine, CGRP monoclonal antibodies and gepants, and selected nonpharmacologic approaches such as behavioral therapies, exercise, sleep hygiene, and certain dietary patterns. Serotonin precursors are generally considered experimental or complementary options at best, and clinicians usually caution about limited data, variable supplement quality, potential drug interactions (especially with other seroton

Papers listed for this claim:[24][25][26][27]

▶ 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: Minnesota Statutes § 148.01, Subd. 1(1); § 148.01, Subd. 2

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 controlled trials report benefits of combined B‑vitamin supplementation (including folic acid and B12) in people with migraine, especially migraine with aura. One double‑blind placebo‑controlled RCT in 52 patients with migraine with aura found that daily supplementation with 2 mg folic acid, 25 mg B6, and 400 µg B12 for 6 months reduced plasma homocysteine by about 39%, and significantly improved migraine disability, headache frequency, and pain severity compared with placebo. Another RCT in 300 women with migraine with aura using a lower dose (1 mg folic acid + B6 + B12) found less benefit and concluded that the higher-dose folate regimen was more effective, supporting a dose-dependent effect on migraine-related outcomes. A more recent double-blind placebo-controlled trial in 120 women with episodic migraine showed that 12 weeks of supplementation with B1, B6, B9 (folate), B12, or a B‑complex significantly reduced headache frequency, migraine disability scores, and use of abortive drugs versus placebo, suggesting that folate and B12 as part of B‑vitamin regimens may have prophylactic value. Systematic reviews and meta-analyses of homocysteine, folate, and B12 in migraine report that migraine patients tend to have elevated homocysteine and lower folate and B12 levels than controls, and propose that correcting these deficiencies might be useful as prophylactic or therapeutic interventions, although direct interventional evidence is still limited. A narrative review focused on MTHFR and migraine notes that preliminary studies support folate, B6, and B12 for prevention of migraine, especially in genetically susceptible patients with MTHFR variants, while also emphasizing the need for larger trials. Overall, there is moderate-quality RCT evidence that folate plus B‑vitamins (including B12) can reduce migraine-related disability and frequency in some populations and that this effect is plausibly mediated by homocysteine-lowering.

Contradicts

Major headache guidelines do not recommend routine folic acid or B12 supplementation as a standard or first-line migraine preventive, indicating that evidence is considered insufficient or preliminary. The EFNS guideline on tension-type headache does not recommend B‑vitamin supplementation as a core treatment, reflecting a broader pattern that B‑vitamins are not established guideline-backed preventives for primary headaches. Contemporary migraine practice guidelines and consensus documents (outside the list) similarly rate the evidence for B‑vitamin supplementation, including folate and B12, as low or inconclusive, and generally do not advise routine testing or supplementation in all migraine patients. Systematic reviews highlight significant heterogeneity, small sample sizes, and limited replication of RCTs; they emphasize that while homocysteine, folate, and B12 levels are associated with migraine, causality and the clinical impact of supplementation remain uncertain. The specific influencer claim that folic acid and B12 supplementation is “important” to prevent migraines, especially in the context of alcohol and caffeine intake, is not directly supported by high-quality trials: existing RCTs did not focus on alcohol or caffeine consumption as a modifier of treatment effect, nor do guidelines single out alcohol or caffeine users as needing folate/B12 supplementation for migraine prevention. Furthermore, some RCTs demonstrate that lower-dose folate plus B‑vitamins (e.g., 1 mg folic acid) may have little or no effect on migraine disability or frequency, suggesting that any benefit is regimen-specific and not a generalizable rule that “folic acid and B12 prevent migraines.” Overall, the evidence base is too narrow to justify describing folic acid and B12 supplementation as broadly “important” for migraine prevention, and the alcohol/caffeine-specific aspect of the claim is unsupported.

Mainstream view

The mainstream medical view is that folate and vitamin B12 supplementation are not established first-line or routine preventive treatments for migraine. Standard migraine prophylaxis relies on therapies with robust RCT and guideline support (such as beta-blockers, certain antiepileptics, antidepressants, CGRP-targeting therapies, and lifestyle measures), while B‑vitamins, including folate and B12, are considered adjunctive or experimental options in selected patients, especially those with documented hyperhomocysteinemia or folate/B12 deficiency or relevant genetic variants (e.g., MTHFR). Guidelines and expert reviews acknowledge that some

Papers listed for this claim:[1][3][2][4][5][6][13][14][28][29][30][31]

▶ 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: Minnesota Statutes § 148.01, Subd. 1(1); § 148.01, Subd. 2