In short
Migraine is a neurological condition characterised by recurring severe headaches, typically unilateral, pulsating, lasting 4–72 hours, often accompanied by nausea, vomiting, and extreme sensitivity to light and sound. At CLCC, care for migraine follows a five-step structured assessment: Assess, Identify, Reduce, Restore, Continue, addressing the systemic contributors alongside standard medical treatment, rather than symptom management alone.
What Is Migraine
Migraine frequency is determined by threshold, and threshold is determined by nutritional, hormonal, and metabolic environment.
Migraine is a neurological condition characterised by recurring severe headaches, typically unilateral, pulsating, lasting 4–72 hours, often accompanied by nausea, vomiting, and extreme sensitivity to light and sound. In some patients, attacks are preceded by an aura, visual, sensory, or speech disturbances that reflect cortical spreading depression, the wave of neuronal and glial depolarisation that characterises the migraine brain during an attack.
The critical concept in migraine management is the migraine threshold. Every individual has a threshold below which attacks do not occur and above which they do. The threshold is not fixed, it is determined by the cumulative level of contributing factors active at any given time. This is why the same trigger (a glass of wine, a late night, bright light) produces a migraine on some days and not others: the threshold is lower on the days when other contributors are simultaneously elevated.
Magnesium deficiency lowers the threshold by reducing NMDA receptor regulation. Riboflavin (B2) deficiency impairs mitochondrial energy production in neurons that is specifically deficient in migraine brains. CoQ10 deficiency compounds this mitochondrial dysfunction. Hormonal fluctuations, particularly oestrogen withdrawal, are among the most powerful threshold-lowering events, explaining the strong female predominance and the predictable association with menstruation. Gut dysbiosis elevates systemic inflammatory markers that amplify neuroinflammation. Sleep disruption and sustained stress load each independently lower the threshold.
CLCC addresses the threshold, comprehensively. By identifying and correcting the specific contributors most active in each patient, the threshold is raised so that the same triggers that previously produced attacks no longer reach it.
Symptoms
What migraine typically feels like.
Severe throbbing or pulsating headache, typically one-sided
Prodrome symptoms 24–48 hours before attack: mood changes, food cravings, neck stiffness, yawning
Aura, visual disturbances (zigzag lines, blind spots), sensory changes, or speech difficulty before the headache phase
Nausea and vomiting during the attack
Extreme sensitivity to light (photophobia) and sound (phonophobia)
Postdrome, 'migraine hangover' of fatigue, cognitive fog, and residual head sensitivity for 24–48 hours after the attack
Menstrual migraine, attacks reliably clustering around menstruation
Attacks triggered by specific foods: red wine, aged cheese, chocolate, MSG, artificial sweeteners
Attacks triggered by environmental factors: bright light, strong smells, barometric pressure changes
Progressive increase in attack frequency over months or years
Potential Contributing Factors
Migraine rarely has a single cause.
Understanding which factors are most active in your case is the purpose of the CLCC assessment. Each of the following can sustain the condition independently.
Magnesium deficiency
Magnesium is the most extensively researched nutritional factor in migraine. It regulates NMDA glutamate receptors and voltage-gated calcium channels, both implicated in cortical spreading depression. Magnesium deficiency is found in significantly higher rates in migraine patients than in controls and directly lowers the migraine threshold.
Riboflavin (B2) and CoQ10 deficiency
The migraine brain has documented mitochondrial dysfunction, reduced energy production in neurons during and between attacks. Riboflavin (B2) and CoQ10 are essential mitochondrial cofactors whose supplementation at therapeutic doses helps reduce migraine frequency in clinical trials.
Hormonal fluctuations
Oestrogen withdrawal, at menstruation, during perimenopause, or with oral contraceptive pill withdrawal phases, is one of the most powerful migraine triggers. This trigger involves oestrogen's modulation of serotonin pathways and CGRP, the primary neuropeptide responsible for migraine pain.
Gut health and inflammation
Gut dysbiosis elevates systemic inflammatory markers and reduces serotonin production, 95% of the body's serotonin is produced in the gut. Gut health directly affects migraine threshold through serotonin modulation and neuroinflammation. Gut restoration helps reduce migraine frequency in patients with concurrent digestive symptoms.
Sleep disruption
Both insufficient and excessive sleep are among the most reliable migraine triggers. Sleep is the primary period of magnesium restoration and neurological recovery. Disrupted sleep lowers the migraine threshold independently of all other contributors.
Dietary triggers and blood sugar instability
Specific dietary compounds trigger migraine in susceptible individuals, tyramine, phenylethylamine, histamine, MSG. Blood sugar instability produces hypothalamic activation that independently lowers the migraine threshold. Meal skipping is among the most commonly reported triggers.
Impact on Daily Life
How migraine changes daily life.
→Attack days lost from work, study, or family life, typically 1–3 days per attack, multiplied by attack frequency
→Interictal anxiety, the persistent fear of the next attack, restricting spontaneity and travel
→Medication overuse headache, a common consequence of frequent analgesic or triptan use that transforms episodic into chronic migraine
→Sleep disruption both as trigger and consequence, creating a compounding cycle
→Social restriction, inability to commit to events, travel, or responsibilities due to unpredictable attack timing
→Career impact, particularly in roles requiring sustained concentration, screen use, or client-facing work
→Accumulating medication burden, preventive medications with significant side effects added progressively as attack frequency increases
The CLCC Method: Five Steps Applied
Each step separate. Each specific to your profile.
Full migraine profile assessment, nutritional, hormonal, gut, and metabolic
Magnesium, riboflavin, CoQ10, vitamin D levels assessed. Hormonal profile, oestrogen, progesterone cycle pattern, thyroid. Gut health indicators. Blood sugar regulation. Detailed trigger diary analysis. Sleep quality and stress load evaluated. Attack frequency, pattern, and duration documented at baseline.
Map the specific threshold-lowering contributors active in your migraine pattern
Which of nutritional deficiency, hormonal fluctuation, gut inflammation, sleep disruption, blood sugar instability, or dietary triggers is most active in your pattern. Menstrual migraineurs require different primary intervention emphasis than those with primarily nutritional or gut-driven threshold lowering.
Targeted nutritional correction alongside dietary and lifestyle threshold management
Therapeutic magnesium glycinate at evidence-based doses. Riboflavin B2 supplementation. CoQ10 where mitochondrial pattern is indicated. Hormonal support where oestrogen fluctuation is dominant. Gut restoration where gut-inflammation pattern is present. Dietary trigger elimination. Blood sugar stabilisation through meal timing correction.
Track attack frequency, severity, and duration at defined monthly intervals
Migraine diary reviewed at structured intervals, frequency, severity (pain scale), duration, and trigger pattern tracked. Nutritional marker levels rechecked. Protocol refined as threshold contributors are progressively corrected.
Sustain raised threshold through long-term nutritional and lifestyle maintenance
Migraine threshold returns to lower levels when nutritional deficiencies reaccumulate or lifestyle contributors reload. The Continue phase monitors nutritional markers, hormonal status where relevant, and attack frequency, maintaining the systemic environment that keeps the threshold above the attack level.
Frequently Asked Questions
Questions patients ask about migraine care.
Can nutritional supplementation reduce my migraine frequency?+
Clinical evidence for magnesium, riboflavin (B2), and CoQ10 in migraine prevention is among the most robust in nutritional medicine. High-dose magnesium glycinate helps reduce migraine frequency in deficient patients. Riboflavin at 400mg/day produces significant attack frequency reduction in controlled trials. These are not anecdotal approaches, they are first-line recommendations in international migraine guidelines. Therapeutic doses, not standard supplement doses, are required.
How is CLCC's approach different from preventive migraine medication?+
Preventive medications, beta-blockers, topical antidepressants, anticonvulsants, CGRP antagonists, reduce attack frequency by suppressing specific neurological mechanisms. They do not address the nutritional deficiencies, hormonal contributors, or gut health factors that are lowering the threshold. CLCC addresses these upstream contributors, which can produce comparable frequency reduction without the side effect burden of preventive medication, and which work additively with medication when both are used.
Can migraine be cured?+
There is no permanent cure for migraine, the genetic predisposition to a lower threshold remains. What structured care is designed to achieve is a sustained increase in the threshold, so that the same triggers that previously produced frequent attacks no longer reach the trigger point. Many patients achieve sustained periods of complete remission. The probability of remission depends on how comprehensively the threshold-lowering contributors are addressed and maintained.
Is migraine more common in women, and does that change the care plan?+
Migraine is approximately three times more common in women, primarily driven by oestrogen's powerful influence on the migraine threshold. For female patients, hormonal assessment is a primary component of the CLCC evaluation. Menstrual migraine, oral contraceptive-related migraine, and perimenopausal migraine each have distinct hormonal patterns requiring specific care plan adaptations.