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Deep Dive

Migraine: energy crisis in the brain?

 

The world of migraine research has been buzzing for decades, and it’s showing no signs of slowing down. This complex disorder continues to puzzle experts, with old myths needing correction, new hypotheses awaiting discovery, and a huge unmet need to fix the challenges the condition brings.

While groundbreaking discoveries have been made over the years – such as the 2016 revelation of specific genetic variations linked to increased migraine risk – much remains unknown about the precise causes and mechanisms underlying migraines. One prevailing and durable theory among researchers is that brain energy supply plays a pivotal role in triggering migraine attacks. Preventive measures targeting this brain energy shortage often bring about noticeable improvements. Recent findings have shed light on peculiarities in a specific brain energy production process that could have a significant impact on migraine occurrences.

 

Mitochondria: powerhouses of our cells

In the body’s energy game, mitochondria take center stage. These tiny organelles within our cells are responsible for producing ATP (adenosine triphosphate), the universal carrier of energy in our bodies – essentially, the ‘currency' fueling all biological processes. The body strives to maintain its energy balance, ensuring that ATP production matches its consumption over time. However, when an energy deficit occurs, it spells trouble for the brain – which is the body’s biggest energy consumer, yet lacking energy reserves to draw on if there’s a shortage.

 

Ailing powerhouses and oxidative stress

When the brain faces an energy supply crisis, a migraine attack can strike. Current understanding suggests that the attack serves as a protective mechanism. As the brain becomes overwhelmed by the energy shortage, oxidative stress builds up. Cell detoxification processes are unable to cope, potentially leading to cellular dysfunction. The migraine attack then acts as a 'last resort,' forcing the entire organism to rest. The body uses this respite to ‘restore power’ and refill its energy reserves.

Mitochondria, alongside the cell nucleus, are the only cell components that have their own DNA. Just like nuclear DNA, mitochondrial DNA can develop minute changes, also known as mutations. Some mutations are harmless, while others can lead to disorders and diseases.

Scientists have uncovered dozens of genes in mitochondria and hundreds in the cell nucleus that harbor mutations capable of causing illness. When our cellular powerhouses malfunction, a condition known as mitochondrial disease can result. The mitochondria are unable to produce ATP, which is the primary transporter of energy in our bodies, as effectively as before. The resulting symptoms can be incredibly diverse, typically affecting organs with high energy demands, such as the brain, heart, and skeletal muscles. Mitochondrial diseases are some of the most commonly inherited causes of illness.

 

Detecting sick mitochondria

As with many other diseases with an inherited component, diagnosing mitochondrial diseases starts with a thorough familial medical history. This can help find clues suggesting inherited risk factors. The next step is specialized laboratory tests focusing on energy metabolism, followed by stress tests and neurological examinations. If suspicions arise, recently developed molecular biology and molecular genetics techniques come into play. Scientists employ techniques like sequencing to determine the exact composition of the DNA in mitochondria and muscles, and examine the DNA using PCR (polymerase chain reaction, a method that gained fame in COVID-19 diagnostics). Screening also includes carefully examining the function of all organs that might be affected by mitochondrial disease.

 

Mitochondrial disease and migraine

Recent research has shed light on the significant link between impaired energy metabolism due to mitochondrial dysfunction and migraine development. When oxidative stress consistently exceeds nerve cells' capacity to counteract it, the delicate energy balance collapses, triggering a migraine attack. Scientific studies reveal that individuals with mitochondrial diseases are more likely to get migraines. While migraines affect 11–14% of the general population, this figure doubles in individuals with mitochondrial diseases. Certain genetic configurations of mitochondrial energy metabolism can even raise this prevalence to over 50%. These recent findings affirm studies from the 1970s hinting at mitochondrial diseases' potential causative role in migraine development.

 

Preventing migraine by avoiding energy deficits

For those whose migraines stem from mitochondrial dysfunction, understanding preventive strategies and integrating them into daily life is crucial. Central to this approach is avoiding energy deficits in the brain, primarily through suitable nutrition. Consistent intake of carbohydrates and sufficient hydration form the foundation for adequately fueling the brain – the top energy consumer without its own reserves.

Additionally, research explores the impact of specific micronutrients on mitochondrial performance. Studies show that a proper supply of vitamin B2 (riboflavin), coenzyme Q10 (ubiquinone), and magnesium can help support and stabilize mitochondrial function. Further extensive scientific inquiry is needed to equip healthcare professionals and patients with more effective preventive strategies in the future.

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    Duffner K. Energiemangel im Gehirn – ein Schlüssel zur Migräne (Energy shortage in the brain - a key to understanding migraine)? Ars Medici 2007; 14: 683-685

    Gantenbein AR, Sandor PS, Fritschy J, Turner R, Goadsby PJ, Kaube H. Sensory information processing may be neuroenergetically more demanding in migraine patients. Neuroreport. 2013 Mar 6;24(4):202-5. doi: 10.1097/WNR.0b013e32835eba81. PMID: 23381352.

    Gormley P, Anttila V, Winsvold BS, Palta P, Esko T, et al. Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine. Nat Genet. 2016 Aug;48(8):856-66. doi: 10.1038/ng.3598. Epub 2016 Jun 20. Erratum in: Nat Genet. 2016 Sep 28;48(10 ):1296. PMID: 27322543; PMCID: PMC5331903.

    Klopstock T, Priglinger C, Yilmaz A, Kornblum C, Distelmaier F, Prokisch H: Mitochondrial disorders. Dtsch Ärztebl Int 2021; 118: 741–8. DOI: 10.3238/arztebl.m2021.0251.

    Oka F, Lee JH, Yuzawa I, Li M, von Bornstaedt D, Eikermann-Haerter K, Qin T, Chung DY, Sadeghian H, Seidel JL, Imai T, Vuralli D, Platt RM, Nelson MT, Joutel A, Sakadzic S, Ayata C. CADASIL mutations sensitize the brain to ischemia via spreading depolarizations and abnormal extracellular potassium homeostasis. J Clin Invest. 2022 Apr 15;132(8):e149759. doi: 10.1172/JCI149759.

    Sacconi S, Trevisson E, Salviati L, Aymé S, Rigal O, Redondo AG, Mancuso M, Siciliano G, Tonin P, Angelini C, Auré K, Lombès A, Desnuelle C. Coenzyme Q10 is frequently reduced in muscle of patients with mitochondrial myopathy. Neuromuscul Disord. 2010 Jan;20(1):44-8. doi: 10.1016/j.nmd.2009.10.014. Epub 2009 Nov 27. PMID: 19945282.

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    Website:

    https://schmerzklinik.de/kann-die-ernaehrung-bei-migraene-eigentlich-auch-zur-therapie-werden/

    Accessed 02 May 2024

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