Hacking your migraines: solutions personalized for you

Migraines plague more than a billion people worldwide and affect women three times more often than men.[ref] That is a lot of people who know the pain, mental fogginess, sensitivity to light, and overwhelming desire to crawl into a dark hole and hide from the world.

What is a migraine and why does it happen?

Migraine symptoms generally include:

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

Somehow that list of symptoms doesn’t really do a migraine 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.

There are a couple of 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 – these symptoms can occur up to a day or two prior to the migraine. Premonitory symptoms can include irritability, fatigue, food cravings, stiff neck, sensitivity to sounds, and yawning. On a PET scan, these symptoms accompany an increased blood flow to the hypothalamus.[ref]

Chronic migraines affect around 2% of the population. This condition differentiates from regular migraines when a person has at least migraines 8 days per month and headaches at least 15 days per month.[ref]

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

In the 1960s, researchers found that people with migraines have higher levels of a serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in their urine. This 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]

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

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]

The research breaks down into three paths:

  • vascular causes (intracranial constriction and vasodilation)
  • 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 – or the increase in the size of the blood vessels in your brain. This causes decreased blood pressure. The vasodilation reaction results from an initial period of vasoconstriction; however, the blood vessels inside the cranium don’t always act in the same manner as the rest of the body.[ref]

These vascular causes 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. 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 the serotonin gene.[ref]

One big link between migraines and serotonin is that triptans, the most commonly used migraine prescription medication, works 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 having lower 5-HT1B binding than people without migraines. One caveat the study suggests the lower serotonin receptors may either contribute to the cause of migraines or decrease over time as a result of repeated exposure to migraines.[ref]

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

One review that considers the role of serotonin in migraines found that the data supports the idea 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), the 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.

These sensory nerve fibers of the trigeminal nerve can activate the release of neuropeptides 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 the migraine.[ref][ref]

Mast cells and neuroinflammation in migraines:

The release of CGRP seems to activate receptors on a number of different cell types including mast cells. These mast cells 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.

Let’s return to what mast cells are and how they can cause problems in 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, which is released when mast cells degranulate, is found in elevated amounts during migraine attacks.[ref] Tryptase is also released in 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 is applied 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 are integral parts of how neurons fire. Neurons send signals to other neurons by transmitting electrical impulses that are carried by positive and negative ions.

How the electrical impulse travels 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 are higher in the cerebral spinal fluid (CSF) of people with migraines compared with a control group. This backs up previous work that also showed an increase in CSF sodium levels during the course of 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 intake of sodium 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 that migraine sufferers experience. These include 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 be a result of 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. This firing of the pain receptors continues for a long while. Animal studies show that inducing CSD by various different means caused the pain receptors to start firing about 14 minutes later.[ref]

Tying this all together:

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. This causes sterile neuroinflammation. Mast cells release histamine, tryptase, and other inflammatory cytokines. This is acting 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.

What triggers migraines?

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. Altered sleep patterns are another thing identified as a trigger but could be a prodromal symptom. Bright light sensitivity could also fall into this conundrum.

Which foods trigger migraines?

That said, 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. (Read more about tyramines increasing blood pressure and genes related to histamine intolerance.) Other top triggers for migraines include MSG and beer.[ref][ref]

Studies show, though, that overall dietary patterns don’t relate to migraine risk. One study did show that women with migraines eat a slightly higher amount of fat and a very 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]

This 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 a migraine? Mast cells have estrogen and progesterone receptors, and the fluctuation of estrogen can cause mast cell degeneration and subsequent migraine pain.

Which medications work for migraines?

Migraine drug classifications include triptans, ergotamines, CGRP monoclonal antibodies, and botox.  One thing to note about these trials on preventative medications is that most are investigating an endpoint that represents a 50% reduction in migraine frequency. If you normally have 6 days of migraines per month, a medication is considered effective if it reduces migraines to 3 days/month. So, the goal of these medications seems to be a reduction in frequency rather than actually eliminating 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 the 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. They 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. Triptans are used as prophylactics to prevent migraine attacks.[ref]

How well do triptans work? They seem to work better for some people than others…

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, 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 the people just kind of screwed when it comes to effective medications?

Another study comparing naproxen sodium (Aleve, OTC headache medicine) with a combo naproxen sodium along with a triptan (Treximet, prescription med) found that only naproxen sodium (Aleve) was statistically significant in the reduction of migraines and Treximet was not. The current cost of Treximet is well over $200 for 9 tablets[source]. 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]

CGRP receptor inhibitors:

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. This was compared with placebo which reduced migraine frequency from 9 per month to 6.5 per month.[ref]

Botox:

OnabotulinumtoxinA, often called Botox, is a neurotoxin injected into the face and approved for the prevention of chronic migraines.

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]

Members perk: Genetic Lifehacks members can easily see their genetic data for all of the genetic variants listed below on the Disease Prevention Topic Summary.

What can genetics tell you about the root cause of your migraines?

There are several ways to approach a medical problem:

  • The most common is to look at the symptoms and manage them with a pill. (migraine – pain medicine)
  • Another option is to figure out what leads up to the medical problem. (migraine – triggers such as red wine, hormone changes)
  • Researchers look at the changed and altered metabolites in the blood. (hard to get live samples from the brain / central nervous system)
  • Geneticists look at genetic variants found in people with medical conditions. This shows which genetic variants link to an increased risk of disease — and shed some light on the underlying cause.

In studies, quite a few different gene variants show an association with either an increased or decreased risk of migraines. You will find below a few of those variants commonly included in 23 and Me or AncestryDNA testing. This isn’t the whole picture, but it does cover quite a few of the variants involved in migraine risk.

Estimates show migraines to be about 50% due to heredity factors that combine with environmental factors to cause migraines.[ref][ref]

How do you use this info? Identifying the genetic variants you carry that influence migraine susceptibility may help you figure out how you get migraines and, hopefully, which migraine ‘lifehacks’ will be most effective for you.

Pain Receptors Genes Associated with Migraines:

Member’s – log in to see your data. Not a member? Join now.
TRPM8 gene: codes for 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: Several genome-wide association studies looking at large population groups found a genetic variant in chromosome 8 near the MMP16 gene 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:

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: possibly increased risk of migraines
  • A/A: possibly 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 which breaks down histamine)

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 which breaks down histamine)

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 proinflammatory 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-1 a 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 .

Cholesterol Pathway Genes Associated with Migraines:

LRP1 gene:  codes for an LDL cholesterol receptor. Migraine intensity and frequency have links (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:

Below are some research-based options for either reducing the frequency or taking away the pain of migraines.

Supplements for migraine relief:

Tryptophan to increase serotonin, melatonin:

Serotonin derives from the amino acid tryptophan. A study using a tryptophan-depletion diet showed that it worsened headaches and nausea in migraine sufferers.[ref]

Tryptophan is generally abundant in diets that contain enough protein. However, if you don’t eat a lot of protein, you may want to track the amount of tryptophan you eat and increase your intake of tryptophan-containing foods such as salmon, eggs, poultry, cheese, and spinach.[ref]

Alternatively, tryptophan is available as a powdered supplement. For it to cross the blood-brain barrier, tryptophan must be eaten with carbs and without other branch chain amino acids.

Melatonin supplements:

A couple of clinical trials have evaluated the efficacy of melatonin for preventing migraines.  One study compared 3 mg melatonin to placebo and to amitriptyline (25 mg). Melatonin showed to be significantly better than placebo, but about the same as amitriptyline. Another clinical trial compared melatonin to placebo and to sodium valproate (prescription migraine med). Melatonin again seems to be superior to placebo and similar to sodium valproate in reducing migraines. In addition, it also seems to have fewer side effects than sodium valproate.[ref][ref]

Tryptophan also is the precursor amino acid for melatonin, so supplementing with tryptophan (with carbs, without other branch chain amino acids) has been shown in studies to increase melatonin levels.

Blocking blue light (from TV, laptop, phone, bright overhead lights) at night also naturally increases your melatonin levels.

Riboflavin:

A placebo-controlled study investigated riboflavin for migraine prevention. The trial used 400 mg of riboflavin daily for 3 months. About 60% of the participants had reduced migraine frequency using riboflavin (compared to 15% placebo effect).[ref]

Riboflavin is also effective for lowering homocysteine and is important in the methylation cycle. So this may be a good ‘hack’ to try if you have either of the methylation cycle pathway variants listed above.

Aspirin:

A study that looked back over medical records for a decade found that people taking aspirin regularly as a way to prevent migraines had fewer migraines.[ref] A meta-analysis of 8 different migraine prevention studies showed that aspirin statistically reduced migraine frequency at a dose of 325mg/day (a single regular strength aspirin).[ref] Of course, you would need to weigh the slight risk of increased bleeding with daily aspirin and talk with your doctor if you have questions on this.

Magnesium to prevent migraines:

The studies showing that people with migraines have lower magnesium levels combine well with a trial of magnesium for the prevention of migraines.  With this in mind, if you think you are low in magnesium, it may be a good supplement to try.[ref][ref]

Foods high in magnesium include legumes, nuts, chocolate, and avocados.  When it comes to supplemental magnesium, most of the migraine studies used magnesium oxide. You may find other forms of magnesium, such as magnesium glycinate are better absorbed.

Decreasing TNF-Alpha:

If your genetic risk factors for migraines include the TNF-alpha variants, you may want to try decreasing TNF-alpha through some natural supplements.

Black seed oil – Nigella sativa – has been shown to reduce TNF-alpha. In an animal study, it reduced mast cell degranulation in the meninges.[ref][ref] You can get black seed oil at your local health food store or online.

Curcumin has been shown to reduce inflammatory cytokines in the brain, including TNF-alpha. A clinical trial found that the combo of curcumin and CoQ10 was effective for reducing the number of migraines.[ref][ref] You can get curcumin in your diet by using turmeric. Or it is available as a supplement online or at your local store- best absorbed with piperine included.

Does the ketogenic diet prevent migraines?

A ketogenic diet works for certain types of epilepsy, so it makes sense that it may help with migraines as well. And it might help, a little, maybe, for some people…or perhaps just cleaning up your diet, in general, would help.

A study of 96 overweight women with frequent migraines investigated whether a keto diet would help. Half of the women went on a keto diet for 6 months, and the other half went on a standard lower calorie diet. Both groups met with a nutritionist to plan out their diets. The women on the keto diet went from a baseline migraine frequency of 2.9 migraines per month to 2.2 migraines per month at month 6.  The women on the standard diet went from 3.2 migraines/month to 2.4 migraines per month.[ref] You should go read the title and abstract of the study – there is a definite bias towards keto, and the results are made to sound like the keto diet worked great. But when you read through the results in the behind-a-paywall study, the standard diet group had just as much improvement over the course of the six months as the keto diet group. Perhaps a better conclusion is that meeting with a dietician helps to decrease migraine frequency a little bit.

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]

Topical migraine relief:

Heat, Cold, and Peppermint:

The TRPM8 cold/menthol receptor is active in the meningeal inflammation of a migraine. Studies show that cooling the head (ice pack) or peppermint oil (menthol) on the forehead is effective for migraine relief for some people.[ref]

Trigger Point Therapy:

Myofascial trigger points are associated with the pain of migraines. These trigger points are often found in the areas around the trigeminal nerve.  Here is a good resource on the topic: Temporalis Trigger Points. Or if you like books: Trigger Point Therapy for Headaches and Migraines.


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.

References:

admin_tpselfhelp. “Temporalis Trigger Points and Referred Pain Patterns.” Triggerpointselfhelp.Com, 3 Mar. 2019, https://triggerpointselfhelp.com/temporalis-trigger-points-and-referred-pain-patterns/.
Amin, Faisal Mohammad, et al. “The Association between Migraine and Physical Exercise.” The Journal of Headache and Pain, vol. 19, no. 1, Sept. 2018, p. 83. PubMed Central, https://doi.org/10.1186/s10194-018-0902-y.
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.
—. “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.
—. “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.
—. “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.
BORAN, H. Evren, and Hayrunnisa BOLAY. “Pathophysiology of Migraine.” Nöro Psikiyatri Arşivi, vol. 50, no. Suppl 1, Aug. 2013, pp. S1–7. PubMed Central, https://doi.org/10.4274/Npa.y7251.
Buldyrev, Ilya, et al. “Calcitonin Gene-Related Peptide Enhances Release of Native Brain-Derived Neurotrophic Factor from Trigeminal Ganglion Neurons.” Journal of Neurochemistry, vol. 99, no. 5, Dec. 2006, pp. 1338–50. PubMed, https://doi.org/10.1111/j.1471-4159.2006.04161.x.
Cady, Roger, et al. “SumaRT/Nap vs Naproxen Sodium in Treatment and Disease Modification of Migraine: A Pilot Study.” Headache, vol. 54, no. 1, Jan. 2014, pp. 67–79. PubMed, https://doi.org/10.1111/head.12211.
Cameron, Chris, et al. “Triptans in the Acute Treatment of Migraine: A Systematic Review and Network Meta-Analysis.” Headache, vol. 55 Suppl 4, Aug. 2015, pp. 221–35. PubMed, https://doi.org/10.1111/head.12601.
Chasman, Daniel I., et al. “Genome-Wide Association Study Reveals Three Susceptibility Loci for Common Migraine in the General Population.” Nature Genetics, vol. 43, no. 7, July 2011, pp. 695–98. www.nature.com, https://doi.org/10.1038/ng.856.
—. “Genome-Wide Association Study Reveals Three Susceptibility Loci for Common Migraine in the General Population.” Nature Genetics, vol. 43, no. 7, July 2011, pp. 695–98. www.nature.com, https://doi.org/10.1038/ng.856.
Chehl, Navdeep, et al. “Anti-Inflammatory Effects of the Nigella Sativa Seed Extract, Thymoquinone, in Pancreatic Cancer Cells.” HPB : The Official Journal of the International Hepato Pancreato Biliary Association, vol. 11, no. 5, Aug. 2009, pp. 373–81. PubMed Central, https://doi.org/10.1111/j.1477-2574.2009.00059.x.
Chiang, Chia-Chun, and Amaal J. Starling. “OnabotulinumtoxinA in the Treatment of Patients with Chronic Migraine: Clinical Evidence and Experience.” Therapeutic Advances in Neurological Disorders, vol. 10, no. 12, Dec. 2017, pp. 397–406. PubMed Central, https://doi.org/10.1177/1756285617731521.
—. “OnabotulinumtoxinA in the Treatment of Patients with Chronic Migraine: Clinical Evidence and Experience.” Therapeutic Advances in Neurological Disorders, vol. 10, no. 12, Dec. 2017, pp. 397–406. PubMed Central, https://doi.org/10.1177/1756285617731521.
Christ, Pia, et al. “The Circadian Clock Drives Mast Cell Functions in Allergic Reactions.” Frontiers in Immunology, vol. 9, July 2018, p. 1526. PubMed Central, https://doi.org/10.3389/fimmu.2018.01526.
Daubert, Elizabeth A., and Barry G. Condron. “Serotonin: A Regulator of Neuronal Morphology and Circuitry.” Trends in Neurosciences, vol. 33, no. 9, Sept. 2010, pp. 424–34. PubMed Central, https://doi.org/10.1016/j.tins.2010.05.005.
Deen, Marie, et al. “Low 5-HT1B Receptor Binding in the Migraine Brain: A PET Study.” Cephalalgia: An International Journal of Headache, vol. 38, no. 3, Mar. 2018, pp. 519–27. PubMed, https://doi.org/10.1177/0333102417698708.
Demarquay, G., et al. “Olfactory Hypersensitivity in Migraineurs: A H(2)(15)O-PET Study.” Cephalalgia: An International Journal of Headache, vol. 28, no. 10, Oct. 2008, pp. 1069–80. PubMed, https://doi.org/10.1111/j.1468-2982.2008.01672.x.
—. “Olfactory Hypersensitivity in Migraineurs: A H(2)(15)O-PET Study.” Cephalalgia: An International Journal of Headache, vol. 28, no. 10, Oct. 2008, pp. 1069–80. PubMed, https://doi.org/10.1111/j.1468-2982.2008.01672.x.
Di Lorenzo, C., et al. “Migraine Improvement during Short Lasting Ketogenesis: A Proof-of-Concept Study.” European Journal of Neurology, vol. 22, no. 1, Jan. 2015, pp. 170–77. PubMed, https://doi.org/10.1111/ene.12550.
Dodick, David W., et al. “Effect of Fremanezumab Compared With Placebo for Prevention of Episodic Migraine: A Randomized Clinical Trial.” JAMA, vol. 319, no. 19, May 2018, pp. 1999–2008. PubMed, https://doi.org/10.1001/jama.2018.4853.
Drummond, P. D. “Tryptophan Depletion Increases Nausea, Headache and Photophobia in Migraine Sufferers.” Cephalalgia: An International Journal of Headache, vol. 26, no. 10, Oct. 2006, pp. 1225–33. PubMed, https://doi.org/10.1111/j.1468-2982.2006.01212.x.
Durham, Paul L. “Diverse Physiological Roles of Calcitonin Gene-Related Peptide in Migraine Pathology: Modulation of Neuronal-Glial-Immune Cells to Promote Peripheral and Central Sensitization.” Current Pain and Headache Reports, vol. 20, no. 8, Aug. 2016, p. 48. PubMed Central, https://doi.org/10.1007/s11916-016-0578-4.
—. “Diverse Physiological Roles of Calcitonin Gene-Related Peptide in Migraine Pathology: Modulation of Neuronal-Glial-Immune Cells to Promote Peripheral and Central Sensitization.” Current Pain and Headache Reports, vol. 20, no. 8, Aug. 2016, p. 48. PubMed Central, https://doi.org/10.1007/s11916-016-0578-4.
—. “Diverse Physiological Roles of Calcitonin Gene-Related Peptide in Migraine Pathology: Modulation of Neuronal-Glial-Immune Cells to Promote Peripheral and Central Sensitization.” Current Pain and Headache Reports, vol. 20, no. 8, Aug. 2016, p. 48. PubMed Central, https://doi.org/10.1007/s11916-016-0578-4.
Ebrahimi-Monfared, Mohsen, et al. “Use of Melatonin versus Valproic Acid in Prophylaxis of Migraine Patients: A Double-Blind Randomized Clinical Trial.” Restorative Neurology and Neuroscience, vol. 35, no. 4, 2017, pp. 385–93. PubMed, https://doi.org/10.3233/RNN-160704.
Evans, E. Whitney, et al. “Dietary Intake Patterns and Diet Quality in a Nationally Representative Sample of Women with and without Severe Headache or Migraine.” Headache, vol. 55, no. 4, Apr. 2015, pp. 550–61. PubMed, https://doi.org/10.1111/head.12527.
Foods Highest in Tryptophan. https://nutritiondata.self.com/foods-000079000000000000000.html. Accessed 3 Sept. 2021.
García-Martín, Elena, et al. “Diamine Oxidase Rs10156191 and Rs2052129 Variants Are Associated with the Risk for Migraine.” Headache, vol. 55, no. 2, Feb. 2015, pp. 276–86. PubMed, https://doi.org/10.1111/head.12493.
Gasparini, Claudia Francesca, et al. “Genetic and Biochemical Changes of the Serotonergic System in Migraine Pathobiology.” The Journal of Headache and Pain, vol. 18, no. 1, Feb. 2017, p. 20. PubMed Central, https://doi.org/10.1186/s10194-016-0711-0.
—. “Genetic and Biochemical Changes of the Serotonergic System in Migraine Pathobiology.” The Journal of Headache and Pain, vol. 18, no. 1, Feb. 2017, p. 20. PubMed Central, https://doi.org/10.1186/s10194-016-0711-0.
—. “Genetic and Biochemical Changes of the Serotonergic System in Migraine Pathobiology.” The Journal of Headache and Pain, vol. 18, no. 1, Feb. 2017, p. 20. PubMed Central, https://doi.org/10.1186/s10194-016-0711-0.
Goadsby, Peter J., et al. “Pathophysiology of Migraine: A Disorder of Sensory Processing.” Physiological Reviews, vol. 97, no. 2, Apr. 2017, pp. 553–622. PubMed Central, https://doi.org/10.1152/physrev.00034.2015.
—. “Pathophysiology of Migraine: A Disorder of Sensory Processing.” Physiological Reviews, vol. 97, no. 2, Apr. 2017, pp. 553–622. PubMed Central, https://doi.org/10.1152/physrev.00034.2015.
—. “Pathophysiology of Migraine: A Disorder of Sensory Processing.” Physiological Reviews, vol. 97, no. 2, Apr. 2017, pp. 553–622. PubMed Central, https://doi.org/10.1152/physrev.00034.2015.
Gonçalves, Andre Leite, et al. “Randomised Clinical Trial Comparing Melatonin 3 Mg, Amitriptyline 25 Mg and Placebo for Migraine Prevention.” Journal of Neurology, Neurosurgery, and Psychiatry, vol. 87, no. 10, Oct. 2016, pp. 1127–32. PubMed, https://doi.org/10.1136/jnnp-2016-313458.
Heatley, R. V., et al. “Increased Plasma Histamine Levels in Migraine Patients.” Clinical Allergy, vol. 12, no. 2, Mar. 1982, pp. 145–49. PubMed, https://doi.org/10.1111/j.1365-2222.1982.tb01633.x.
“How to Check for Histamine Intolerance Genes.” Genetic Lifehacks, 13 Apr. 2021, https://www.geneticlifehacks.com/histamine-intolerance-genetics-part-2/.
John, P. J., et al. “Effectiveness of Yoga Therapy in the Treatment of Migraine without Aura: A Randomized Controlled Trial.” Headache, vol. 47, no. 5, May 2007, pp. 654–61. PubMed, https://doi.org/10.1111/j.1526-4610.2007.00789.x.
Karimi, Narges, et al. “The Efficacy of Magnesium Oxide and Sodium Valproate in Prevention of Migraine Headache: A Randomized, Controlled, Double-Blind, Crossover Study.” Acta Neurologica Belgica, vol. 121, no. 1, Feb. 2021, pp. 167–73. PubMed, https://doi.org/10.1007/s13760-019-01101-x.
Kayama, Yohei, et al. “Functional Interactions between Transient Receptor Potential M8 and Transient Receptor Potential V1 in the Trigeminal System: Relevance to Migraine Pathophysiology.” Cephalalgia, vol. 38, no. 5, Apr. 2018, pp. 833–45. PubMed Central, https://doi.org/10.1177/0333102417712719.
Key, Felix M., et al. “Human Local Adaptation of the TRPM8 Cold Receptor along a Latitudinal Cline.” PLoS Genetics, vol. 14, no. 5, May 2018, p. e1007298. PubMed, https://doi.org/10.1371/journal.pgen.1007298.
Kilinc, E., et al. “Effects of Nigella Sativa Seeds and Certain Species of Fungi Extracts on Number and Activation of Dural Mast Cells in Rats.” Physiology International, vol. 104, no. 1, Mar. 2017, pp. 15–24. akjournals.com, https://doi.org/10.1556/2060.104.2017.1.8.
Koyuncu Irmak, Duygu, et al. “Shared Fate of Meningeal Mast Cells and Sensory Neurons in Migraine.” Frontiers in Cellular Neuroscience, vol. 13, Apr. 2019, p. 136. PubMed Central, https://doi.org/10.3389/fncel.2019.00136.
Krueger, J. M., et al. “Sleep. A Physiologic Role for IL-1 Beta and TNF-Alpha.” Annals of the New York Academy of Sciences, vol. 856, Sept. 1998, pp. 148–59. PubMed, https://doi.org/10.1111/j.1749-6632.1998.tb08323.x.
Latremoliere, Alban, and Clifford J. Woolf. “Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity.” The Journal of Pain : Official Journal of the American Pain Society, vol. 10, no. 9, Sept. 2009, pp. 895–926. PubMed Central, https://doi.org/10.1016/j.jpain.2009.06.012.
Lin, Qi-Fang, et al. “Association of Genetic Loci for Migraine Susceptibility in the She People of China.” The Journal of Headache and Pain, vol. 16, 2015, p. 553. PubMed, https://doi.org/10.1186/s10194-015-0553-1.
Liu, Hua, et al. “Association of 5-HTT Gene Polymorphisms with Migraine: A Systematic Review and Meta-Analysis.” Journal of the Neurological Sciences, vol. 305, no. 1–2, June 2011, pp. 57–66. PubMed, https://doi.org/10.1016/j.jns.2011.03.016.
Liu, Ruozhuo, et al. “MTHFR C677T Polymorphism and Migraine Risk: A Meta-Analysis.” Journal of the Neurological Sciences, vol. 336, no. 1–2, Jan. 2014, pp. 68–73. PubMed, https://doi.org/10.1016/j.jns.2013.10.008.
—. “MTHFR C677T Polymorphism and Migraine Risk: A Meta-Analysis.” Journal of the Neurological Sciences, vol. 336, no. 1–2, Jan. 2014, pp. 68–73. PubMed, https://doi.org/10.1016/j.jns.2013.10.008.
Magalhães, Elza, et al. “Botulinum Toxin Type A versus Amitriptyline for the Treatment of Chronic Daily Migraine.” Clinical Neurology and Neurosurgery, vol. 112, no. 6, July 2010, pp. 463–66. PubMed, https://doi.org/10.1016/j.clineuro.2010.02.004.
Masruha, Marcelo R., et al. “Urinary 6-Sulphatoxymelatonin Levels Are Depressed in Chronic Migraine and Several Comorbidities.” Headache, vol. 50, no. 3, Mar. 2010, pp. 413–19. PubMed, https://doi.org/10.1111/j.1526-4610.2009.01547.x.
“Mast Cell Diseases: MCAS, Genes, and Solutions.” Genetic Lifehacks, 24 Apr. 2020, https://www.geneticlifehacks.com/mast-cells/.
McKemy, David D. “TRPM8: The Cold and Menthol Receptor.” TRP Ion Channel Function in Sensory Transduction and Cellular Signaling, edited by Wolfgang B. Liedtke and Stefan Heller, CRC Press/Taylor & Francis, 2007. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK5238/.
—. “TRPM8: The Cold and Menthol Receptor.” TRP Ion Channel Function in Sensory Transduction and Cellular Signaling, edited by Wolfgang B. Liedtke and Stefan Heller, CRC Press/Taylor & Francis, 2007. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK5238/.
Meyer, Melissa M., et al. “Cerebral Sodium (23Na) Magnetic Resonance Imaging in Patients with Migraine – a Case-Control Study.” European Radiology, vol. 29, no. 12, Dec. 2019, pp. 7055–62. PubMed, https://doi.org/10.1007/s00330-019-06299-1.
Meza-Velázquez, R., et al. “Association of Diamine Oxidase and Histamine N-Methyltransferase Polymorphisms with Presence of Migraine in a Group of Mexican Mothers of Children with Allergies.” Neurología (English Edition), vol. 32, no. 8, Oct. 2017, pp. 500–07. www.elsevier.es, https://doi.org/10.1016/j.nrleng.2016.02.012.
“Migraine Aura.” Mayo Clinic, https://www.mayoclinic.org/diseases-conditions/migraine-with-aura/multimedia/migraine-aura/vid-20084707. Accessed 3 Sept. 2021.
“Migraine Intensity, Frequency Linked to High Cholesterol.” National Headache Foundation, 21 Oct. 2015, https://headaches.org/2015/10/21/migraine-intensity-frequency-linked-to-high-cholesterol/.
Moon, Debbie. “Disease Prevention Topic Summary.” Genetic Lifehacks, 18 Oct. 2020, https://www.geneticlifehacks.com/disease-prevention-topic-summary/.
—. “Tyramine Intolerance: MAOA and Cheese Effect.” Genetic Lifehacks, 21 Dec. 2018, https://www.geneticlifehacks.com/the-cheese-effect-and-your-genes/.
Mulder, Elles J., et al. “Genetic and Environmental Influences on Migraine: A Twin Study Across Six Countries.” Twin Research and Human Genetics, vol. 6, no. 5, Oct. 2003, pp. 422–31. Cambridge University Press, https://doi.org/10.1375/twin.6.5.422.
Parohan, Mohammad, et al. “The Synergistic Effects of Nano-Curcumin and Coenzyme Q10 Supplementation in Migraine Prophylaxis: A Randomized, Placebo-Controlled, Double-Blind Trial.” Nutritional Neuroscience, vol. 24, no. 4, Apr. 2021, pp. 317–26. PubMed, https://doi.org/10.1080/1028415X.2019.1627770.
Peatfield, R. C. “Relationships between Food, Wine, and Beer-Precipitated Migrainous Headaches.” Headache, vol. 35, no. 6, June 1995, pp. 355–57. PubMed, https://doi.org/10.1111/j.1526-4610.1995.hed3506355.x.
—. “Relationships between Food, Wine, and Beer-Precipitated Migrainous Headaches.” Headache, vol. 35, no. 6, June 1995, pp. 355–57. PubMed, https://doi.org/10.1111/j.1526-4610.1995.hed3506355.x.
Pogoda, Janice M., et al. “Severe Headache or Migraine History Is Inversely Correlated With Dietary Sodium Intake: NHANES 1999-2004.” Headache, vol. 56, no. 4, Apr. 2016, pp. 688–98. PubMed, https://doi.org/10.1111/head.12792.
Ran, Caroline, et al. “Implications for the Migraine SNP Rs1835740 in a Swedish Cluster Headache Population.” The Journal of Headache and Pain, vol. 19, no. 1, Nov. 2018, p. 100. BioMed Central, https://doi.org/10.1186/s10194-018-0937-0.
Rodriguez-Acevedo, Astrid J., et al. “Genetic Association and Gene Expression Studies Suggest That Genetic Variants in the SYNE1 and TNF Genes Are Related to Menstrual Migraine.” The Journal of Headache and Pain, vol. 15, Oct. 2014, p. 62. PubMed, https://doi.org/10.1186/1129-2377-15-62.
Savi, LT, et al. “Prophylaxis of Migraine with Aura: A Place for Acetylsalicylic Acid.” The Journal of Headache and Pain, vol. 14, no. 1, Feb. 2013, p. P195. Springer Link, https://doi.org/10.1186/1129-2377-14-S1-P195.
Sazci, Ali, et al. “Nicotinamide-N-Methyltransferase Gene Rs694539 Variant and Migraine Risk.” The Journal of Headache and Pain, vol. 17, no. 1, Oct. 2016, p. 93. PubMed Central, https://doi.org/10.1186/s10194-016-0688-8.
Schoenen, J., et al. “Effectiveness of High-Dose Riboflavin in Migraine Prophylaxis. A Randomized Controlled Trial.” Neurology, vol. 50, no. 2, Feb. 1998, pp. 466–70. PubMed, https://doi.org/10.1212/wnl.50.2.466.
Schürks, Markus, et al. “A Candidate Gene Association Study of 77 Polymorphisms in Migraine.” The Journal of Pain, vol. 10, no. 7, July 2009, pp. 759–66. PubMed, https://doi.org/10.1016/j.jpain.2009.01.326.
Silva-Néto, R. P., et al. “Odorant Substances That Trigger Headaches in Migraine Patients.” Cephalalgia: An International Journal of Headache, vol. 34, no. 1, Jan. 2014, pp. 14–21. PubMed, https://doi.org/10.1177/0333102413495969.
Sintas, Cèlia, et al. “Replication Study of Previous Migraine Genome-Wide Association Study Findings in a Spanish Sample of Migraine with Aura.” Cephalalgia: An International Journal of Headache, vol. 35, no. 9, Aug. 2015, pp. 776–82. PubMed, https://doi.org/10.1177/0333102414557841.
—. “Replication Study of Previous Migraine Genome-Wide Association Study Findings in a Spanish Sample of Migraine with Aura.” Cephalalgia: An International Journal of Headache, vol. 35, no. 9, Aug. 2015, pp. 776–82. PubMed, https://doi.org/10.1177/0333102414557841.
Stuart, Shani, et al. “The Role of the MTHFR Gene in Migraine.” Headache, vol. 52, no. 3, Mar. 2012, pp. 515–20. PubMed, https://doi.org/10.1111/j.1526-4610.2012.02106.x.
Talebi, Mahnaz, et al. “Relation between Serum Magnesium Level and Migraine Attacks.” Neurosciences (Riyadh, Saudi Arabia), vol. 16, no. 4, Oct. 2011, pp. 320–23.
Terrazzino, Salvatore, et al. “Brain-Derived Neurotrophic Factor Val66Met Gene Polymorphism Impacts on Migraine Susceptibility: A Meta-Analysis of Case–Control Studies.” Frontiers in Neurology, vol. 8, May 2017, p. 159. PubMed Central, https://doi.org/10.3389/fneur.2017.00159.
“Treximet Prices, Coupons & Savings Tips.” GoodRx, https://www.goodrx.com/treximet. Accessed 3 Sept. 2021.
van Oosterhout, Wpj, et al. “Chronotypes and Circadian Timing in Migraine.” Cephalalgia: An International Journal of Headache, vol. 38, no. 4, Apr. 2018, pp. 617–25. PubMed, https://doi.org/10.1177/0333102417698953.
von Luckner, Alexander, and Franz Riederer. “Magnesium in Migraine Prophylaxis-Is There an Evidence-Based Rationale? A Systematic Review.” Headache, vol. 58, no. 2, Feb. 2018, pp. 199–209. PubMed, https://doi.org/10.1111/head.13217.
Wells, Rebecca Erwin, et al. “Meditation for Migraines: A Pilot Randomized Controlled Trial.” Headache, vol. 54, no. 9, Oct. 2014, pp. 1484–95. PubMed, https://doi.org/10.1111/head.12420.
Yılmaz, Ibrahim Arda, et al. “Cytokine Polymorphism in Patients with Migraine: Some Suggestive Clues of Migraine and Inflammation.” Pain Medicine, vol. 11, no. 4, Apr. 2010, pp. 492–97. Silverchair, https://doi.org/10.1111/j.1526-4637.2009.00791.x.
—. “Cytokine Polymorphism in Patients with Migraine: Some Suggestive Clues of Migraine and Inflammation.” Pain Medicine, vol. 11, no. 4, Apr. 2010, pp. 492–97. Silverchair, https://doi.org/10.1111/j.1526-4637.2009.00791.x.
Zhang, X. C., and D. Levy. “Modulation of Meningeal Nociceptors Mechanosensitivity by Peripheral Proteinase-Activated Receptor-2: The Role of Mast Cells.” Cephalalgia: An International Journal of Headache, vol. 28, no. 3, Mar. 2008, pp. 276–84. PubMed, https://doi.org/10.1111/j.1468-2982.2007.01523.x.
Zhang, Xichun, et al. “Activation of Meningeal Nociceptors by Cortical Spreading Depression: Implications for Migraine with Aura.” The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, vol. 30, no. 26, June 2010, pp. 8807–14. PubMed, https://doi.org/10.1523/JNEUROSCI.0511-10.2010.




Author Information:   Debbie Moon
Debbie Moon is the founder of Genetic Lifehacks. She holds a Master of Science in Biological Sciences from Clemson University and an undergraduate degree in engineering from Colorado School of Mines. Debbie is a science communicator who is passionate about explaining evidence-based health information. Her goal with Genetic Lifehacks is to bridge the gap between the research hidden in scientific journals and everyone's ability to use that information. To contact Debbie, visit the contact page.