Migraines: Genes, Root Causes, and Personalized Solutions

Migraines impact over a billion people globally, and women are three times as likely than males to suffer from them.[ref] That’s a lot of people who have experienced the pain, mental fogginess, sensitivity to light, and overwhelming desire to crawl into a dark hole and hide from the world.

This article explores current research on why migraines happen and how genetics influences your risk of migraines. Understanding your genetic susceptibility can help you target solutions to try. The article ends with Lifehacks, a section on research-backed solutions combined with genetic connections. My hope is that you can use this information to find relief from the misery of migraines.

What is a migraine and why does it happen?

Migraine symptoms generally include:

  • headache (usually lasting 4 to 72 hours)
  • sensitivity to light, sounds, and smells
  • nausea or vomiting
  • sensory disturbances, aura (sometimes)

Somehow that list of symptoms doesn’t really do migraines justice.

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.

The different types of migraines:

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

Some people get premonitory or 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 affect around 2% of the population. When you have more than 8 migraine days each month, your migraines are considered chronic.[ref]

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

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.

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 over-responding to stimulus.[ref]

Long story short, research provides a lot of competing theories but no simple answers…

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)

How serotonin plays a role in migraines:

Part of what happens in your brain during a migraine suggests vasodilation, which is the widening of blood vessels in your brain. Vasodilation causes decreased blood pressure. The vasodilation reaction results from an initial period of vasoconstriction; however, this may not be something that occurs in the rest of the body. The blood vessels inside the cranium don’t always act in the same manner as the rest of the body.[ref]

These vascular (blood vessel) causes may be due, at least in part, to serotonin signaling.

Serotonin (a.k.a. 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. Keep in mind that serotonin is the signal, and it needs a receptor to cause an effect.  There are different serotonin receptors found throughout the brain and intestinal tract causing diverse effects of serotonin.[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]

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]

Using PET scans on people who had been migraine-free for at least 48 hours, researchers have begun studying the 5-HT1B (serotonin) receptor in the brain. These scans showed migraine patients with lower 5-HT1B binding than those without migraines.

The results of the study suggest two possibilities: [ref]

  • One, that lower serotonin receptors may either be causal (low serotonin causing migraines);
  • or, two, that serotonin receptors decrease over time because of repeated exposure to migraines.

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 are shown to increase 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 then breaks down (which happens pretty quickly), serotonin levels drop, causing vasodilation and headache pain.[ref]

Related article: Serotonin: How your genes affect this neurotransmitter

How does CGRP affect migraines?

Another key player in vasodilation during a migraine is the vasodilator 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 to the eyes and the jaw.

Time for a picture:

Trigeminal nerve illustration. (Public domain)

Notice how the trigeminal nerve goes to the root of the teeth.  My teeth often hurt during a migraine…

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]

CGRP, mast cells, and neuroinflammation in migraines:

The release of CGRP seems to activate receptors on several different cell types, including mast cells.

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.

So what exactly are mast cells, and could they cause migraines?

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, and inflammatory cytokines when activated by a pathogen, allergic reaction, or other signaling molecules (such as CGRP).[ref]

Some researchers theorize that mast cells and neuroinflammation are at the root of migraine pathology.

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

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

Can an electrolyte imbalance cause migraines?

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

Sodium, potassium, calcium, and chloride ions are integral parts of how neurons fire. Neurons send signals to other neurons by transmitting electrical impulses carried by positive and negative ions.

Electrical impulses travel the length of the neuron through sodium and potassium-gated ion channels opening and closing. (Image By Laurentaylorj – Own work, CC BY-SA 3.0)

A recent study found that sodium (Na) levels were higher in the cerebrospinal fluid (CSF) of people with migraines compared with a control group. It backs up previous work that also showed an increase in CSF sodium levels during a migraine. The other ion levels – calcium, potassium, and magnesium – did not change, nor did the sodium levels in the plasma.[ref][ref]

There have been large studies trying to determine if sodium intake affects migraine risk. One study found that for women with low BMI and men at any BMI, a low sodium intake slightly increased the risk of headaches and migraines.[ref]

Another study found that people who have migraines have, on average, lower magnesium levels than a healthy control group.[ref]

What causes the aura in migraines?

A migraine aura is the altered sensory perception, such as visual alterations like sparkles and the waviness of images.

The Mayo Clinic explains that “A visual aura is like an electrical or chemical wave that moves across the visual cortex of your brain. The visual cortex is the part of your brain that processes visual signals. As the wave spreads, you might have visual hallucinations.”  Sensory auras may also cause tingling and problems with speaking.

The aura is thought to result from cortical spreading depression (CSD). CSD is a massive depolarization of neurons that occurs in the brain. A wave of hyperexcitability of the neurons is followed by a wave of inhibition. This depolarization causes the release of potassium, hydrogen, nitric oxide, and glutamate ions as well as arachidonic acid.[ref]

Here is a visual:

Cortical spreading depression. Creative Commons Image.

This cortical spreading depression causes the pain receptors in the meninges to start firing after a bit of a delay. The firing of the pain receptors continues for a long while. Animal studies show that inducing CSD by various means caused the pain receptors to start firing about 14 minutes later.[ref]

Bringing the various research studies together:

Sometimes when reading a bunch of research studies on a topic, I feel like the analogy of the blind men describing different parts of an elephant.

To recap, here’s what research shows on migraines:

  • We have the involvement of the serotonin system that can cause changes in blood vessel dilation.
  • The trigeminal neurovascular system releases CGRP, which is a vasodilator that also acts on mast cells.
  • Activation of mast cells causes sterile neuroinflammation. Mast cells release histamine, tryptase, and other inflammatory cytokines.
  • The inflammation acts on the meninges, the lining of the cranium, causing pain.
  • If the migraine is preceded by an aura, the cortical spreading depression may be what is triggering the nociceptors (pain receptors) in the meninges to fire.

Migraine triggers:

People often identify various triggers for their migraines. Traveling, foods, stress, hormones, odors, sleep deprivation, and flashing/bright lights often top the list.

One problem with identifying migraine triggers is that the premonitory or prodromal symptoms  (up to a day or two ahead of the migraine) may overlap with what people identify as triggers.

  • Food cravings are one prodromal symptom, and various food triggers are often blamed. Thus, it is hard to separate the food craving due to prodromal symptoms from the unusual food that may seem like a trigger.
  • Altered sleep patterns are another thing identified as a trigger which could be a prodromal symptom. Instead of altered sleep causing a migraine, the prodromal migraine is causing altered sleep.
  • Bright light sensitivity could also fall into this conundrum.

While sometimes difficult to pin down, it does seem that there are specific triggers for some people. These include certain foods, scents, hormonal changes, and weather changes.

Which foods trigger migraines?

A lot of people have identified specific foods as being likely to cause migraines for them. Some of these include gluten, wine, cheese, and chocolate.

Genetics may come into play here:

Studies show, though, that ‘overall dietary patterns’ don’t relate to migraine risk. Dietary patterns refer to the big picture of your diet – vegetarian, carnivore, keto, fruitarian, etc. One study did show that women with migraines eat a slightly higher amount of fat and a slightly lower amount of protein on average.[ref][ref]

Why do scents trigger migraines?

Some people are sensitive to odors and find that certain smells (floral, perfumes, strong cleaning chemicals, paint, gasoline, plastics) can trigger migraines.[ref]

It isn’t just all in your head (pun intended). A small study looked at cerebral blood flow in people with migraines vs. a control group. The migraineurs had altered blood flow in certain areas of the brain when stimulated with odors.[ref]

What causes menstrual migraines?

One really common migraine trigger for many women is the change in estrogen levels around the time of their period or during ovulation. Migraines often go away for these women during pregnancy and after menopause.

Why would a change in estrogen levels trigger migraines? One reason is that mast cells have estrogen and progesterone receptors. The fluctuation of estrogen can cause mast cell degeneration and subsequent migraine pain.


Your Genes and Migraines:

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You may have noticed that migraines tend to run in the family. Estimates show migraines to be about 50% due to heredity factors (such as genetic variants), which combine with environmental factors (hormones, histamine intolerance) to cause migraines.[ref][ref]

In genetics studies, quite a few different gene variants show an association with either an increased or decreased risk of migraines.

How can you use this info? Identifying the genetic variants you carry that influence migraine susceptibility may help you figure out why YOU get migraines and, hopefully, which migraine ‘lifehacks’ will be most effective for you. Keep in mind that your 23andMe or AncestryDNA only covers part of your genes, so this section doesn’t cover every variant linked to migraines.

For members, there’s a genetics recap at the end of this article that summarizes these variants along with supplement options.

Pain Receptors Genes Associated with Migraines:

TRPM8 gene: encodes the cold and menthol receptors. When skin temperatures decrease by 15 degrees C, it hurts due to the activation of this pain receptor.[ref]

Check your genetic data for rs10166942 (23andMe v4, v5; AncestryDNA):

  • C/C: decreased risk of migraines[ref][ref]
  • C/T: slightly decreased risk of migraines
  • T/T: higher risk of migraines, less sensitive to cold[ref]

Members: Your genotype for rs10166942 is .

CGRP Pathway Genes Associated with Migraines:

CGRP and brain-derived neurotrophic factor (BDNF) coexpress on the trigeminal nerve terminals.[ref]

BDNF Gene: codes for brain-derived neurotrophic factor

Check your genetic data for rs6265 (23andMe v4, v5; AncestryDNA):

  • T/T:  increased risk of migraines[ref]
  • C/T: slightly increased risk of migraines
  • C/C: typical risk of migraines

Members: Your genotype for rs6265 is .

MMP16 gene: Large genome-wide association studies found a genetic variant on chromosome 8 near the MMP16 gene that is consistently associated with a reduced risk of migraines (without aura). The MMP16 gene codes for an enzyme involved in the breakdown of the extracellular matrix and tissue remodeling.

Check your genetic data for rs10504861 (23andMe v4, v5; AncestryDNA):

  • C/C: typical migraine risk
  • C/T: reduced risk of migraine
  • T/T: reduced risk of migraine[ref][ref]

Members: Your genotype for rs10504861 is .

 

Methylation Pathway Genes Associated with Migraines:

Methylation is important in converting serotonin into melatonin.

NNMT gene: The nicotinamide-N-methyltransferase (NNMT) gene codes for an enzyme that transfers a methyl group from SAMe to nicotinamide. There are links between the variants of this gene and increases in homocysteine levels.

Check your genetic data for rs694539 (23andMe v4, v5; AncestryDNA):

  • TT: a 4-fold increase in the risk of migraines in women[ref]
  • CT: typical migraine risk
  • CC: decreased migraine risk

Members: Your genotype for rs694539 is .

MTHFR gene: Several studies have linked the MTHFR C677T variant to an increased risk of migraines, but not all of the studies agree. This one may be a mild increase in risk or perhaps for just certain population groups.[ref]

Check your genetic data for rs1801133 (23andMe v4, v5; AncestryDNA):

  • G/G: typical risk of migraine
  • A/G: slightly increased risk of migraines
  • A/A: slightly increased risk of migraine[ref][ref][ref]

Members: Your genotype for rs1801133 is .

Serotonin Pathway Genes Associated with Migraines:

C7orf10 gene: codes for an enzyme involved in the production of glutarate from tryptophan (precursor for serotonin) and lysine.

Check your genetic data for rs4379368 (23andMe v4, v5; AncestryDNA):

  • C/C: typical risk of migraines
  • C/T: decreased risk of migraines
  • T/T: decreased risk of migraines (Caucasian ancestry)[ref] (opposite found in a Chinese population)[ref]

Members: Your genotype for rs4379368 is .

SLC6A4 gene: codes for a serotonin transporter.

Check your genetic data for rs2066713 (23andMe v4,v5; AncestryDNA):

  • G/G: typical risk of migraines
  • A/G: decreased risk of migraines
  • A/A: decreased risk of migraines[ref]

Members: Your genotype for rs2066713 is .

Note: a lot of other genetic variants in the serotonin transport and receptor genes have been studied and found not to be involved in migraine risk. 

Histamine / Mast Cell Activation Pathway Genes Associated with Migraines:

AOC1 gene: codes for diamine oxidase, which breaks down histamine in the gut.

Check your genetic data for rs1049793 (23andme v4; AncestryDNA):

  • C/C: typical
  • C/G: increased risk of migraines
  • G/G: increased risk of migraines[ref] (reduced DAO enzyme, which breaks down histamine from foods)

Members: Your genotype for rs1049793 is .

Check your genetic data for rs10156191 (23andMe v4; AncestryDNA):

  • C/C: typical
  • C/T: increased risk of migraines, especially in women
  • T/T: increased risk of migraines, especially in women[ref] (reduced DAO enzyme, which breaks down histamine from foods)

Members: Your genotype for rs10156191 is .

Inflammatory Pathway Genes Associated with Migraines:

TNF gene: tumor necrosis factor-alpha is one of the body’s main pro-inflammatory cytokines.

Check your genetic data for rs3093664 (23andMe v5; AncestryDNA):

  • G/G: increased risk of menstrual migraines[ref] (increased inflammatory response)
  • A/G: increased risk of menstrual migraines
  • A/A: typical

Members: Your genotype for rs3093664 is .

Check your genetic data for rs1800750 (23andMe v4, v5; AncestryDNA):

  • G/G: typical risk of migraines
  • A/G: increased risk of migraines
  • A/A: increased risk of migraines[ref] (increased inflammatory response)

Members: Your genotype for rs1800750 is .

Check your genetic data for rs1800629 (23andMe v4, v5; AncestryDNA):

  • A/A: increased risk of migraines[ref] (increased inflammatory response)
  • A/G: increased risk of migraines
  • G/G: typical

Members: Your genotype for rs1800629 is .

IL1A gene: codes for interleukin-1A, which is part of the body’s inflammatory response

Check your genetic data for rs17561 (23andMe v4; AncestryDNA):

  • C/C: typical
  • A/C: increased risk of migraines
  • A/A: increased risk of migraines[ref] (increased inflammatory response)

Members: Your genotype for rs17561 is .

Ion and neurotransmitter pathways associated with migraines:

KCNK18 gene: encodes a potassium receptor that regulates the excitability of neurons in pain, including the trigeminal nerve

Check your genetic data for rs869025175 (23andMe v5):

  • I/D: rare mutation, strongly linked to migraines due to potassium receptor loss of function mutation[ref]
  • I/I: Typical

Members: Your genotype for rs869025175 is .

MTDH gene:MTDH is known to downregulate EAAT2 (excitatory amino acid transporter 2), a major glutamate transporter, and could thus affect glutamate regulation at a synaptic level”[ref]

Check your genetic data for rs1835740 (23andMe v4, v5; AncestryDNA):

  • C/C: typical
  • C/T: increased risk of migraines
  • T/T: increased risk of migraines[ref][ref]

Members: Your genotype for rs1835740 is .

Cholesterol Pathway Genes Associated with Migraines:

LRP1 gene:  codes for an LDL cholesterol receptor. Migraine intensity and frequency link (in a small study) to cholesterol levels.[ref]

Check your genetic data for rs11172113 (23andMe v4, v5; AncestryDNA):

  • C/C: slightly decreased risk for migraines[ref]
  • C/T: slightly decreased risk for migraines
  • T/T: typical risk for migraines

Members: Your genotype for rs11172113 is .


Lifehacks: Preventing Migraines

Below are some research-based options for either reducing the frequency or taking away the pain of migraines.  Non-members can read about sleep, exercise, and medication lifehacks. Members get more, including details on natural supplements and diet changes that interact with their genetic variants.

Good sleep hygiene for migraine prevention:

Circadian Rhythm and Migraines:

  • A study of over 2000 people with migraines found that early morning onset was quite frequent (40%). The study also found that people with chronic migraines were more tired after circadian disruption (staying up late) and less able to cope with being active during times when they weren’t normally active.[ref]
  • The early morning onset could be due to increased histamine levels in the early morning hours (causing mast cell degranulation) or due to increased TNF-alpha at night.[ref][ref]
  • Blocking blue light at night, which causes an increase in melatonin, and sticking to a routine sleep schedule may help with migraine pain.

Meditation for Migraines: A study of mindfulness meditation did not find that it statistically reduced migraines, although there was a trend towards fewer migraines/ month.[ref]

Why does exercise help migraines?

Exercise and Migraines: While exercise is a known trigger for some people for migraines, it also raises BDNF levels. A study of exercise and migraines suggests that regular activity may help decrease the frequency of migraines in the long run.[ref]

Yoga: A clinical trial of yoga found that it did reduce the frequency and intensity of migraines.[ref]

Which medications work to treat migraines?

Talk with your doctor if you have questions about specific medications. This information on medication research is educational and not treatment advice. 

Migraine drug classifications include triptans, ergotamines, CGRP monoclonal antibodies, and botox.

One thing to note about clinical trials on preventative medications is that most consider ‘effectiveness’ to be a 50% reduction in migraine frequency. If you normally have six days of migraines per month, a medication is considered effective if it reduces migraines to 3 days/month.

Thus, the goal of these medications seems to be a reduction in frequency rather than actually eliminating or curing migraines.

Ergotamines:

Ergotamines were originally derived from ergot, a fungus that infects rye and other grains.

Ergot is famous for outbreaks in the Middle Ages causing what was known as St. Anthony’s fire. Ingesting grains infected with the fungus caused extreme vasoconstriction, causing a severe burning sensation in the limbs. Ergots also affect neurotransmission and cause hallucinations.

Ergotamines are available in prescription form for migraine attacks. They bind to serotonin receptors, causing vasoconstriction as well as other effects.[ref] Migergot is one brand name that combines ergot with caffeine. There are possible serious side effects (black box warning).

Triptans:

Triptans are often the first line of prescription medication offered to people with migraines, and they are used as a prophylactic to prevent migraines.

Triptans target specific serotonin receptors in the brain (5HT1B, 5HT1D). These receptors are located in the trigeminal nerve endings, so it is thought that activating them prevents the release of CGPG and substance P.[ref]

How well do triptans work? It depends… For some people, they seem to work a little better than aspirin or Advil.

A meta-analysis of 133 randomized controlled trials looked at the efficacy of triptan medications for migraines. The conclusion was “most triptans are associated with equal or better outcomes compared with NSAIDs, ASA (aspirin), and acetaminophen”.  Looking at the data, triptans relieved pain in two hours for between 42 and 76% of patients. NSAIDs, aspirin (ASA), and acetaminophen (Tylenol) relieved pain in two hours for 46 – 52% of patients.[ref]

What the meta-analysis showing that triptans and aspirin/NSAIDs are about equivalent doesn’t tell us is whether those ~50% of people that triptans work for are the same people that aspirin/NSAIDs work for…

In other words, if aspirin/NSAIDs don’t work for you, would triptans be a better option? Or are 50% of people just out of luck when it comes to effective migraine medications?

Another study compared naproxen sodium (Aleve) with a combo of naproxen sodium along with a triptan (Treximet, prescription med). The results showed that only naproxen sodium (Aleve) was statistically significant in reducing migraines, and Treximet was not. 43% of subjects who just took Aleve for migraine had a 50% reduction in migraine frequency (compared to 17% with the expensive prescription med).[ref] The current cost of Treximet is well over $200 for nine tablets[source], while Aleve is about $4 at Target.

CGRP receptor inhibitors in clinical trials:

Several small-molecule GCRP inhibitors have been tested and are in current clinical trials for migraine usage. They are generally termed ‘gepants’.

A new monoclonal antibody targeting CGRP, fremanezumab, was tested in a group of over 700 study participants. The injection of fremanezumab once a month reduced migraine frequency from 9 per month to 5 per month. It was compared with a placebo which reduced migraine frequency from 9 per month to 6.5 per month.[ref]

Botox:

OnabotulinumtoxinA, called Botox, is a neurotoxin injected into the face and approved to prevent chronic migraines (and wrinkles).

The PREEMPT study on the initial phase III clinical trial showed a statistical decrease in migraine-free days, going from 8.4 migraine days to 6.6 days per month on average.[ref]

One study compared botox injections to amitriptyline, a tricyclic antidepressant used for migraines. The results showed that both were about equally effective, with around 70% of trial participants having a reduction in the number of days of migraines each month.[ref]


Blueprint for Members:

This members-only section includes additional lifehacks including supplement research and topical migraine relief details. Additionally, you will see your genetic data matched to specific recommendations.  Consider joining today to see the rest of this article.

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Related Articles and Genes:

MTHFR and Migraines
The MTHFR C677T variant increases the risk of migraines. Learn how to check your genetic data and how to mitigate the risk.

PMS, Genetics, and Solutions
A lot of women know the moodiness and brain fog that comes with premenstrual syndrome (PMS). Studies estimate that PMS is up to 95% heritable – which means that it has a huge genetic component. Learn about the genes and find out which solutions may actually work for you. (Member’s article)

Serotonin Genes
Serotonin is a neurotransmitter that is important in depression, sleep, and many other aspects of health. Learn how your genetic variants in the serotonin receptor genes impact their function.

Histamine Intolerance
High histamine levels can cause a variety of symptoms including migraines, hives, sinus drainage, and stomach problems.

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An, Xing-Kai, et al. “Association of MTHFR C677T Polymorphism with Susceptibility to Migraine in the Chinese Population.” Neuroscience Letters, vol. 549, Aug. 2013, pp. 78–81. PubMed, https://doi.org/10.1016/j.neulet.2013.06.028.
Andreeva, Valentina A., et al. “Macronutrient Intake in Relation to Migraine and Non-Migraine Headaches.” Nutrients, vol. 10, no. 9, Sept. 2018, p. 1309. PubMed Central, https://doi.org/10.3390/nu10091309.
Anttila, Verneri, et al. “Genome-Wide Meta-Analysis Identifies New Susceptibility Loci for Migraine.” Nature Genetics, vol. 45, no. 8, Aug. 2013, pp. 912–17. PubMed Central, https://doi.org/10.1038/ng.2676.
—. “Genome-Wide Meta-Analysis Identifies New Susceptibility Loci for Migraine.” Nature Genetics, vol. 45, no. 8, Aug. 2013, pp. 912–17. PubMed Central, https://doi.org/10.1038/ng.2676.
Baena, Cristina Pellegrino, et al. “The Effectiveness of Aspirin for Migraine Prophylaxis: A Systematic Review.” Sao Paulo Medical Journal = Revista Paulista De Medicina, vol. 135, no. 1, Feb. 2017, pp. 42–49. PubMed, https://doi.org/10.1590/1516-3180.2016.0165050916.
Baj, Tirthraj, and Rohit Seth. “Role of Curcumin in Regulation of TNF-α Mediated Brain Inflammatory Responses.” Recent Patents on Inflammation & Allergy Drug Discovery, vol. 12, no. 1, 2018, pp. 69–77. PubMed, https://doi.org/10.2174/1872213X12666180703163824.
Bayerer, Bettina, et al. “Single Nucleotide Polymorphisms of the Serotonin Transporter Gene in Migraine–an Association Study.” Headache, vol. 50, no. 2, Feb. 2010, pp. 319–22. PubMed, https://doi.org/10.1111/j.1526-4610.2009.01553.x.
Benemei, Silvia, et al. “Triptans and CGRP Blockade – Impact on the Cranial Vasculature.” The Journal of Headache and Pain, vol. 18, no. 1, Oct. 2017, p. 103. PubMed Central, https://doi.org/10.1186/s10194-017-0811-5.
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About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.