Migraine

There are many different types of migraine with different root causes and etiology.

Genetics play a big role in migraine, and can make people more sensitive to changes in their environment that can bring on an attack.⠀

Gene-environment interactions relating to stress, high blood pressure, exercise (intolerance), blood sugar dysregulation (particularly hypoglycaemia), hormonal contraception, hydration, altitude and amine containing foods (histamine and tyramine) should be considered. 

Biogenic amines, including histamine, tyramine, dopamine and adrenaline are all deactivated (detoxified) by methylation ('MT' genes such as HNMT and COMT).

The TRPV1 gene modulates pain signalling, perception and tolerance in the context of migraine, as well as temperature regulation (hot flushes!) and sensitivity to spicy food!

Lifecode Gx Reports

The Nutrient Core report includes:

  • Genes impacting response to 'migraine trigger foods' - caffeine (CYP1A2), gluten (HLA) and dairy (LCT)
  • ACE and AGT genes which are involved in blood pressure regulation
  • Genes and nutrients that impact inflammation - TNF (tumour necrosis factor), IFNG (interferon gamma). Vitamin D (transport and sensitivity) and Omega fatty acids (FADs genes)
  • Oxidative stress - antioxidants - Vitamin C and Glutathione
  • Methylation (high level insights) - MTHFR (folate), and B12
  • Blood sugar regulation and diabetes risk - TCF7L2 (also in Metabolics report below)

The Methylation Report provides detailed analysis of genes involved in: 

  • synthesis of the (methyl) cofactors needed by 'MT' methyltransferase genes to deactivate and detoxify biogenic amines - histamine, serotonin, tyramine, dopamine and adrenaline synthesis, deactivation and detoxification
  • homocysteine excess which can be a factor in high blood pressure, cardiovascular disease and migraine - and impacted by many/ any genes involved in methylation, such as MTHFR
  • B12 deficiency - FUT2, TCN2 and MUT (which metabolises methyl-malonic acid - MMA).

The Histamine report details the pathways involved in Histamine degradation including:

  • HNMT - intracellular histamine, with particular impacts on respiratory systems (symptoms may include asthma, headaches etc)
  • DAO - extra cellular histamine, including gut/ GI with particular impacts on ingested histamine containing or liberating foods

The Metabolics report details pathways involved in glucose (sugar) metabolism, including:

  • TCF7L2 - defects in first phase insulin release, which can impact glucose uptake and risk of type two diabetes and gestational diabetes
  • IRS1 - insulin receptor substrate 1, which impacts sensitivity to insulin
  • Genes involved in the antioxidant cascade - FOXO3, NrF2, CAT, SOD and NOS, and inflammation - CRP, TNF and IL6.

The Hormones report, particularly in the context of menstrual migraines, which have been linked to oestrogen withdrawal for example in the late luteal phase, or in late perimenopause or menopause.

  • Oestrogen Receptors and their ability to adjust to fluctuations in oestrogen levels.
  • All genes involved in the Oestrogen lifecycle which contribute to high or low oestrogen, and therefore impact regulation and extent of fluctuation

The Nervous System Report shows your TRPV1 results and explains how nutrigenomics can help with migraine related pain and temperature regulation. 

You can also watch our free crowdcast on Migraines - centred around TRPV1 and the Nervous System here

Full details of all reports via https://www.lifecodegx.com/products


Research :

Brown, B. (2022) Migraine headaches: opportunities for management with precision nutrition. Nutr. Med. J., 1 (3), 117-152

https://www.nmi.health/migraine-headaches-opportunities-for-management-with-precision-nutrition/

Stanton, Angela A., Migraine Cause and Treatment (November 12, 2015). Available at SSRN: https://ssrn.com/abstract=2690927 or http://dx.doi.org/10.2139/ssrn.2690927

Did this answer your question? Thanks for the feedback There was a problem submitting your feedback. Please try again later.

Still need help? Contact Us Contact Us