Migraine provides some evolutionary/survival advantages to individuals and early societies
This section is excerpted from the upcoming 5th Edition of my migraine protocol
Note: This section is excerpted from the upcoming 5th Edition of my migraine protocol, which was most recently published in Inflammation Mastery 4th Edition (2016). I do not anticipate what I consider major changes in the protocol although obviously some new perspectives and interventions will be included. We are obviously at a time when we need a paradigm shift in the management of chronic pain conditions.
I have a positive view of migraine; I do not see it simply as a disease but rather as an evolutionary advantage that alerts to conditions of air quality, environmental danger, social stressors, and poor nutritional status
For migraine to affect ~15% of the human population, it has to meet at least 2 or perhaps 3 criteria: 1) migraine is not lethal early in life and does not majorly impact reproductive success and the ongoing transmission of causal genes (obvious), 2) migraine must have provided a worthwhile evolutionary/survival advantage to individuals and early societies (discussed below), and possibly 3) migraine may be symptomatic of our overpolluted environment and overprocessed food supply, at least to some extent (see detailed discussion in section on food/diet).
The evolutionary/survival advantages provided by migraine/headache include at least the following:
1. Migraine/headache is a behavior-modifying pain response that alerts to low oxygen, high altitude, increased carbon monoxide; alleviation/avoidance of migraine can be achieved in environments of improved oxygen availability: An early alert to low oxygen conditions would/does clearly provide a survival advantage. Migraine[1], high-altitude headache (HAH), and acute mountain sickness (AMS) are exacerbated at high altitudes, which provide less oxygen at less barometric pressure for the oxygen-hungry brain; “High-altitude headache is one of many neurological symptoms associated with the ascent to high altitudes. Cellular hypoxia due to decreased barometric pressure seems to be the common final pathway for headache as altitude increases.”[2] Including among normal/healthy people with no history of migraine, exposure to low oxygen concentrations mimicking high altitude leads to headache that simulates migraine and high-altitude headache.[3] Britze et al[4] wrote in 2017 that “Epidemiological studies suggest that living in high-altitude areas increases the risk of migraine and especially migraine with aura. Human provocation models show that hypoxia [low oxygen] provokes migraine with and without aura... Possible pathophysiological mechanisms include hypoxia-induced release of nitric oxide and calcitonin gene-related peptide, cortical spreading depression and leakage of the blood-brain barrier.” Exposure to carbon monoxide (CO) can cause a headache that can be mistaken for migraine[5]; very interestingly, the onset of headache may be delayed for several hours (range 3-12; average 7) following CO exposure.[6]
2. Migraine/headache is a behavior-modifying pain response that alerts to fire, risk of burn injury, air pollution: Some evidence suggests that exposure to smoke debris (particulate matter from wildfires) increases headache[7]; increased sensitivity—including with an adverse/pain response—to forest fires would obviously provide a person and their community/group with a survival advantage. Garg et al[8] wrote in 2022 that “There is accumulating evidence on the association between air pollution and headache disorders, especially migraine. Many classical and non-classical air pollutants have been associated with headache, including particulate matter, nitrogen dioxide, sulfur dioxide, ozone, carbon monoxide, as well as polycyclic aromatic hydrocarbons and volatile organic compounds. … The exact mechanisms underlying headache pathophysiology vis-à-vis air pollution are not precisely defined but include triggering of neuroinflammation and activation of the transient receptor potential ankyrin 1 (TRPA1)-associated pathways.” Higher temperatures and higher humidity can also exacerbate migraine, especially when combined with increased air pollution.
3. Migraine is a behavior-modifying pain response that alerts to poor nutritional status: As I have reviewed in the section on Food/Diet that follows, numerous studies have consistently demonstrated that poor nutritional status contributes to migraine and other headaches, especially high/excess intake of sodium and low intake of vitamin B6, vitamin D3, magnesium, and potassium. As such, increased migraine pain commonly serves as an alert and warning of poor nutritional intake/status—including or especially in overweight/obese patients—whether from environmental scarcity or—as is more common these days—poor dietary selection/availability, eg, paucity of healthy natural foods yet an overabundance of obesogenic nutrient-poor ultraprocessed food-like products.
4. Migraine is a behavior-modifying pain response that alerts to stress, overwork, and sensory overload: Stress, overwork, and sensory overload are well-established provocateurs of migraine in many patients, and as such provides a behavior-modifying signal to encourage rest and other forms of stress/stimulation management, most famous and popular of which is retreating to a dark quiet room. People who lack feedback mechanisms are at risk of overwork, burnout and eventual exhaustion.
5. Migraine is a behavior-modifying pain response that alerts to infection and inflammation and is thus a component of personally-protective and socially-protective “illness behavior”: Most types of infection and systemic inflammation raise levels of the proinflammatory cytokine tumor necrosis factor alpha (TNFa) which promotes migraine/headache by increasing release of the excitatory neurotransmitter glutamate (GLU) while also inhibiting its reuptake/clearance. Additionally, such infection/inflammation generally leads to activation of the tryptophan-catabolizing kynurenine pathway, which likewise contributes to fatigue, social withdrawal, “depression” and other characteristics of sickness/illness behavior; for a video explanation of this pathway, see
and also my videos on the gut-brain axis available at
Sickness/illness behavior is personally/socially protective as the sick person isolates from the group, thereby reducing patient-to-group transmission of contagious illness and also reducing group-to-patient transmission while the patient is unwell and more vulnerable..
6. Migraine is a vasodilatory reflex and behavior-modifying pain response that protects against nontraumatic/metabolic brain injury: The neuropeptide CGRP (detailed later) is a key mediator of migraine pain (alerting to behavior modification) and is also common considered the most potent vasodilator produced in the human body, thereby increasing oxygen and fuel supply to the energy-hungry brain. In essence from a CGRP perspective, pain is price paid for vasodilation and increased blood flow to the brain.
7. Migraine might serve as a reproductive impediment only within harmful/stressful/unstable environments: Since the risk of greater frequency/severity of migraine increases with adverse social/environmental conditions—pollution, malnutrition, stress/overwork—the possibility exists that it serves a beneficial purpose by delaying conception until healthier conditions are encountered, especially for mother and baby. Per Jones and Ndubisi[9], “Many women get migraines around ovulation, which is the most fertile time of the month. Not feeling well may prevent them from having sexual intercourse during this fertility window.” Delaying pregnancy until migraine-provoking conditions such as pollution, malnutrition, stress/overwork have been resolved/avoided would have survival and health benefits for mother and baby; as such, migraine serves as a behavior-modifying signal of unfavorable pregnancy/childbirth/childrearing conditions.
Note: This section is excerpted from the upcoming 5th Edition of my migraine protocol, which was most recently published in Inflammation Mastery 4th Edition (2016). I do not anticipate what I consider major changes in the protocol although obviously some new perspectives and interventions will be included. We are obviously at a time when we need a paradigm shift in the management of chronic pain conditions.
Citations are provided below for subscribers to inflammationmastery.substack.com and/or healthythinking.substack.com
Keep reading with a 7-day free trial
Subscribe to INFLAMMATION MASTERY clinical protocols InflammationMastery.com to keep reading this post and get 7 days of free access to the full post archives.