Migraine Solutions Tailored to Your Genes: Triggers, Treatments, and Tools

Key takeaways:

• When looking at the root causes of migraines, three pathways seem to be involved: vascular, neural, and pain/nerve pathways.
• Researchers estimate that migraines are  ~50% due to hereditary factors (such as genetic variants), which combine with environmental factors (hormones, high histamine foods) to cause migraines
• Genetic variants in these different pathways may help you pinpoint your triggers of migraines.
• There are natural options backed by research that may help with preventing migraines – or at least decreasing the number of migraine days. Genetics may give you the starting point to figure out which prevention strategies are more likely to work for you.

Members will see their genotype report below, plus additional solutions in the Lifehacks section. Consider joining today. 

Background science: What happens in the brain with a migraine?

Migraines impact over a billion people globally, and women are three times as likely as men to suffer from them.[ref]

Migraine symptoms generally include:

• Headache, usually lasting 4 to 72 hours
• Sensitivity to light, sounds, and smells
• Nausea or vomiting
• Sensory disturbances, aura (sometimes)

For many, migraines are more than a headache — and, usually, the pain isn’t even the worst part. Instead, it’s the altered ability to think, irritability, nausea, slowed reflexes, and body temperature fluctuations. 

There are different types of migraines:

• migraines with aura (about 1/3 of migraineurs get auras)
• migraines without aura
• hemiplegic migraines (rare numbness/tingling on one side of the body)

Some people get prodromal symptoms, which may appear up to a day or two before the migraine. Irritability, fatigue, food cravings, stiff neck, sensitivity to sounds, and yawning are some of the warning signs. On a PET scan, these symptoms accompany an increased blood flow to the hypothalamus.[ref]

Chronic migraines:
Around 2% of the population is affected by chronic migraines, which are usually defined by having 8+ migraine days each month.[ref]

What is going on in your brain when you have a migraine?

Research shows that migraines are complex, with dysfunction occurring in multiple systems rather than a simple, single cause.

Serotonin? In the 1960s, researchers found that people with migraines had higher levels of a serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in their urine. This has prompted a lot of research over the past five decades into the relationship between the serotonergic system and migraines.

Neurovascular changes: More recently, researchers have also investigated how CGRP (calcitonin gene-related peptide), neuroinflammation, and altered ion levels impact migraines.[ref]

Brain electrical storm: Migraines are often described as an excitatory state in the brain – also known as a state of hypersynchrony. Other researchers describe migraines as the brain overresponding to stimuli.[ref]

Migraine research breaks down into three paths:

• vascular causes (intracranial constriction and vasodilation of blood vessels)
• neural events (hyperexcitability and cortical spreading depression)
• nociceptive causes (pain pathways, activation of the trigeminal nerve, neuropeptides)

Vasodilation and migraines:

Part of what happens in your brain during a migraine suggests vasodilation, which is the widening of blood vessels in your brain that decreases blood pressure. The vasodilation reaction follows an initial period of vasoconstriction. The changes in pressure and expansion in the blood vessels are thought to trigger pain receptors in the nerves surrounding the vessels.[ref]

These vascular changes may be due (at least in part) to serotonin signaling. Serotonin (5-hydroxytryptamine, 5-HTP) is a neurotransmitter that causes the signal to flow from one neuron to the next. It is found in abundance in both the digestive system and the brain. Brain morphology, the way the neurons in the brain are shaped and formed, is also affected by serotonin.

Serotonin is a signaling molecule, and it needs a receptor to bind to and cause an action. Different types of serotonin receptors are found throughout the brain and intestinal tract, causing diverse effects of serotonin.[ref]

One big link between migraines and serotonin is that triptans, the most commonly used migraine prescription medication, work by amplifying the serotonin signal. Triptans act on the serotonin receptors (5-HT1B) in the blood vessels of the brain, constricting them and inhibiting the release of neuropeptides.[ref]

Genetic studies show a link between migraine susceptibility and a type of genetic variant known as a variable number tandem repeat in a serotonin transporter gene.[ref]

Using PET scans on people who had been migraine-free for at least 48 hours, researchers can study the 5-HT1B (serotonin) receptor in the brain. These scans showed that migraine patients had lower 5-HT1B binding than those without migraines. The results of the study suggest two possibilities:[ref]

1. Low numbers of serotonin receptors may either be causal (low serotonin causing migraines)
   – or-
2. Serotonin receptors decrease over time because of repeated exposure to migraines.

In other words, it isn’t determined if low serotonin causes migraines or if migraines cause changes to the expression of serotonin receptors. (Check your serotonin variants in the genotype report below)

Melatonin and migraines:

Researchers also found low melatonin levels in people with chronic migraines when compared to a control population. It is notable, especially because serotonin is needed for the reaction in the pineal gland that produces melatonin.[ref]

tryptophan -> serotonin -> melatonin

One study explains that serotonin levels are low between migraine attacks, but levels increase rapidly at the beginning of a migraine. This initial surge of serotonin causes vasoconstriction and is thought to be part of the aura phase. When serotonin breaks down (which happens pretty quickly), serotonin levels drop, causing vasodilation and headache pain.[ref]

Related article: Serotonin: How your genes affect this neurotransmitter

CGRP in migraines: Neurons + vascular changes

Another key player in migraines is CGRP. CGRP stands for calcitonin gene-related peptide and is released from the trigeminovascular system. The trigeminovascular system includes both the trigeminal nerve neurons and the cerebral blood vessels.

The trigeminal nerve is the largest cranial nerve. It branches from the temple to over the eyebrows, and down to the teeth and jaw.  Here’s a graphic showing where the trigeminal nerve is located:

The sensory nerve fibers of the trigeminal nerve can activate the release of neuropeptides, including CGRP, substance P, and neurokinin A.

CGRP is a potent vasodilator, making it important for both migraines and normal blood pressure regulation in the body. It is also thought to influence the pain portion of migraines.[ref][ref]

There are a lot of new migraine drugs being developed that focus on CGRP. However, a CGRP isn’t solely responsible for migraines, and medications that target CGRP only work for a portion of patients.[ref] CGRP can also bind to the amylin 1 receptor in the brain. New research points to this being a possible pathway involved in the way that is involved in causing migraines.[ref]

(Check your CGRP variants in the genotype report below)

Neuroinflammation in migraines:

The release of CGRP activates receptors on several different cell types, including mast cells. Mast cells are part of the body’s immune system and are found in all of our body tissues. They stand ready to release a payload of histamine, serotonin, tryptase, and inflammatory cytokines when activated by a pathogen, allergic reaction, or other signaling molecules (such as CGRP).[ref]

The activated mast cells can degranulate, releasing histamine and pro-inflammatory compounds. This degranulation of mast cells causes a “prolonged state of excitation in meningeal nociceptors”. The meninges line the skull, and nociceptors are pain receptors.[ref][ref]

Here is an image of the meninges, which includes three layers surrounding the brain (dura mater, arachnoid, and pia mater).

The brain itself doesn’t have pain receptors, but there are pain receptors and blood vessels throughout the meninges.

Some researchers theorize that mast cells and neuroinflammation are at the root of migraine pathology. Here are two reasons pointing to mast cell degranulation as a root cause:

1. Histamine, released when mast cells degranulate, is elevated during migraine attacks.[ref]
2. Tryptase is also released during degranulation and is thought to sensitize pain receptors.[ref]

(Check your histamine variants in the migraine genotype report below)

Other researchers theorize that central sensitization is at the root of migraines. Central sensitization involves enhanced signaling through pain pathways and is caused by overexcited pain receptors and decreased inhibition. This term applies to various pain-related conditions such as peripheral neuropathy, IBS, and migraines.[ref]

Related article: Mast cells: MCAS, genetics, and solutions

Ion levels: Can an electrolyte imbalance cause migraines?

Another observation of researchers is that ion levels are often altered in migraineurs.

Related Articles and Topics:

MTHFR and Migraines

PMS, PMDD, Genetics, and Solutions

Histamine Intolerance: Genetic Report, Supplements, and Real Solutions

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