Migraine: Do We Have It All Wrong?

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Migraine brain
The combined APS (American Physiological Society) and EB (Experimental Biology) conference was full of excitement for me. This was my first migraine-associated presentation to scientists, MDs, and premed students. I have never presented a poster at any conference—I have usually given lectures. I was concerned. Will my posters catch any interest? Then I arrived at Chicago’s McCormick Conference Center and was shocked by its size and the size of this conference. There were 1500 poster boards, each with new posters every day for three days, in addition to booths and lectures. I took a deep breath.

Here I share with you what I presented and some of the questions attendees asked, answers I provided, and offer a more comprehensive explanation of what migraine is. I am also including one of the two posters I presented.

The first day I presented a poster under the EB session so most visitors were curious about the biological aspects of migraine. The second was presented under the Electrolyte Homeostasis session, which brought very different visitors and very different questions. I find it important to define what migraine is and then continue with my hypothesis, which is drawn in the middle of the poster, and I highlight it here for easier viewing.

What is Migraine?

The answer is not pain. I found that the majority of those who have no migraines or never met anyone with migraines know migraine as a pain in the head. The truth is pain is just one – and not even mandatory – aspect of migraines. For me, presenting the real definition of migraines equals to explaining the conclusions of my many years of research.

Migraine is the manifestation of an energy (voltage) shortage in the brain, caused by insufficient electrolyte quality. This actually makes migraine into a symptom. The insufficient electrolyte mix is caused by certain genetic variances that result in some electrolyte mineral deficiency. Therefore, the electrolyte imbalance is also a symptom. The direct cause of migraine lies hidden in critical genetic variances that should operate the voltage gated channels of neurons but cannot. Why not? This is the heart of migraine: migraineurs are glucose sensitive with a brain that lacks capability to handle the huge electrolyte disruption when glucose enters the brain cells. As we know, adaptation is an important part of evolution. It seems that a very large percentage of the human population was able to adapt to the dietary circumstances of contemporary life but people with the migraine-brains could not. I call the migraine brain an ancient brain that is not able to utilize glucose. Modern carbohydrate-rich diets overload this ancient brain with glucose. Migraineurs are not the only ones with this problem. People with seizures, multiple sclerosis, Alzheimer’s disease, and many more conditions, have very similar—if not the same—problem. Not every human can eat birthday cakes, potatoes, and toast for breakfast. Migraineurs cannot.

The Migraine Brain Difference

sensory neuron comparison

Image copyright by Angela A. Stanton, Ph.D.©

Figure 1. Neuron: non-migraineur vs migraineur

The top image represents a single neuron in an average human brain, highlighting an enlarged section showing the receptors and the neurotransmitters in the circled region. The bottom image is the same for a migraineur. The two are obviously very different—look at the density of the receptors and neurotransmitters (the layer of black dots under red). The questions one must ask:

  1. Why do the migraineur’s neuron contain so many more receptors and neurotransmitters?
  2. Does that have anything to do with pain? And if so how and why?

A migraine brain’s sensory neurons are hyper sensitive (1) and hyper alert in comparison to the sensory neurons of a non-migraine brain. More alertness is explained by the more receptors (2) and neurotransmitters. But why do migraineurs have more receptors and hyper sensory brains? To answer this question I present a few hypotheses:

Hypothesis 1: If you look at many mammal species in the wild, you find they are always on alert for predators. If they are not on alert, they are likely to become food. For these species the hyper-sensory alert brain is the default. The migraine-brain is a hyper-sensory alert brain.

Hypothesis 2: If hyper-sensory brain can be the default then such a brain, the migraine-brain, is the default mammalian brain that all human ancestors must have had at one time. Since this brain is still very prevalent in the human population (15%), it must have represented a significant survival advantage in ancient times. Today, however, the majority of humans do not have this brain type.

Hypothesis 3: While the majority of humans were able to adapt to more modern lifestyles and food supply, some could not; their brain remained unchanged, still holding onto the ancient traits and retained hyper sensory organs. These then are today’s migraineurs.

Hypothesis 4: The tendency for electrolyte imbalance is a sign that the migraine-brain is greatly compromised under modern nutritional challenges. While the majority of humans adapted to the use of carbohydrates for fuel during our recent evolution, migraineurs did not. Up until about 15,000 years ago carbohydrates formed minimal part of the human diet.

Hypothesis 5: The ancient brain (in some of its traits) may go back as far as the Euarchontoglires (100 million years ago), the first common ancestor to all mammals and primates. The early mammals had a few special traits that appear to be connected to migraine-brain. Two of these are the Ehlers-Danlos Syndrome (EDS) and Raynaud’s Syndrome. Both of these are highly connected to migraine and to each other and are ancient traits that some small mammals still carry today—and apparently a very large percentage of migraineurs do as well, although in the general population the percentage is minuscule.

Hypothesis 6: Migraine is a neurovascular condition (not a disease) that is an evolutionary throwback. Neuro because it is neuron voltage energy generation problem and vascular because of the different vascular structure migraineurs have from non-migraineurs. Both EDS and Raynaud’s are vascular in nature and EDS is also associated with hyper mobility and being disjointed, which was a very important adaptation in early mammals and still are in many, such as cats, often referred to as floating shoulders. Having a different vascular system allows for more flexibility without vascular damage.

Hypothesis 7: Migraineurs have a very different vascular system from non-migraineurs. I propose the vasculature segments are shorter and more numerous. This can often be seen on the skin of people with EDS because they also have very thin and transparent skin. Shorter vascular regions allow for more flexibility along with the hyper flexibility of those afflicted with EDS.

Hypothesis 8: Migraine brain is of the era when being disjointed and having different vascular system was an evolutionary benefit. From evolutionary throwback perspective then it makes sense that migraineurs are glucose sensitive and carbohydrates intolerant, since at that time, carbohydrates and glucose were not consumed.

Support for the Hypotheses

Support for these hypotheses come from genetics, which shows us that the migraine brain has different voltage gated ionic channels for calcium, ATPase, the sodium/potassium pump, sodium channel, and potassium pump, implying that all electrolyte modulation for a migraineur is different from a non-migraineur, in addition to glucose and insulin regulatory variances. See below the top few genetic variances. I used GeneCards database to find all gene variance associated with migraines—sorted by importance called “score”—and removed some that are not relevant to my point:

GeneCards Migraine Genes
GeneCards Migraine Genes

I only listed 16 gene variances from the 1293 currently associated with migraines (highlighted important words), though as more research is conducted, this number is certain to grow. Some variances that have low score—such as insulin resistance—will likely move to higher scores since migraineurs are associated with a very high incidence of metabolic disorders, specifically migraine is associated with insulin resistance (3) as a result of being glucose sensitive.

Migraines, Drugs, Nutrition

Pharmaceutical companies have spent much of their migraine-allocated time developing drugs that block migraineurs’ voltage gated channels that are different from that of the standard population, without any concern why they are different. As a result, these channels cannot work at all when medicated. Of course, just as there is no point in medicating blue eyes, a genetic variance, so is medicating a type of voltage gated channel is futile. It takes a bit of understanding why. At the conference I spent eight hours a day for two days explaining this to doctors, scientists, and even representatives of big pharma. It took me 10 years to figure it out.

Since “…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells” (4) (page 4), you can immediately see that as glucose enters the cells, sodium (Na+) falls and water (H2O) leaves the cell, causing major electrolyte disruption.

Regular human brains that have adapted and are able to reset electrolyte homeostasis with ease have no trouble. The migraine brain cannot because all associated voltage gated ionic pumps and channels are in their ancient forms, where carbohydrate consumption was too minimal to matter in electrolyte dysregulation. The long epoch in which the hyper sensory mammalian brain was still the dominant variant of humanity, sugar and grains were not part of the diet at all and very little if any carbohydrates were consumed.

The migraineurs’ exaggerated reactions to carbohydrate consumption shows that they have a problem with glucose metabolism. With this major negative, is there a way to prevent migraines without the use of any medicines? Absolutely. Before I detail the proper migraine nutrition, I would like to answer a question I received from some doubters during the conference. Facing a skeptic is great, it forces the scientist to come up with the appropriate answers.

The most common comment (particularly from those representing pharmaceuticals) was that “whatever is done without medicine must be placebo”. This was extremely easy to defend by the simple logic that goes as follows:

If A > B AND B > C then A > C 

This applies to pharmaceuticals since their clinical trials for medicines are placebo tested. Therefore, migraine medicines, M, are proven to be better than placebo, P. M > P. The medicine-free treatment available is MF. Given that the MF treatment has been successful for thousands of migraineurs who also quit taking all their migraine medicines and remained migraine free, we can state the following:

If MF > M AND M > P then MF > P – that is medicine free is better than placebo.

Medicine & Migraine Free

So what is medicine free and migraine free? It is quite simple: since migraineurs cannot use glucose as energy and if they try they end up with major electrolyte disruption as a result, it implies that by stopping the consumption of carbohydrates migraines can be prevented. Certain amount of protein also converts to glucose (gluconeogenesis) so controlling protein amount is also important but less critical.

Can migraineurs eat any carbohydrates? Yes, they can but minimal and highly fibrous. Carbohydrates of up to 5 net carbs grams (total carbs – fiber = net carbs grams) per meal seems to be tolerable by all migraineurs. For example, a migraineur can eat green leafy salads, cucumbers, zucchini, avocado, and many similar foods. However, she cannot eat a slice of bread, an apple, or drink smoothies, fruit juices, or soft drinks. See below the poster I showed in Chicago, summarizing what I just wrote and also showing what a migraineur should or should not be eating.

Image copyright by Angela A. Stanton, Ph.D.©

Conclusion

So we are dealing with a brain that is not used to eating carbs and this leads to glucose sensitivity, leading to major reaction to glucose with edema and sodium leaving cells. This leads to electrolyte dysregulation. Migraineurs on the Stanton Migraine Protocol®, LCHF, or the ketogenic diet, slowly taper off their medicines, their insulin reverts to normal and migraines typically vanish.

Sources

  1. Schwedt TJ (2013) Multisensory Integration in Migraine. Curr Opin Neurol:248-253.
  2. Wei Y, Ullah G, & Schiff SJ (2014) Unification of Neuronal Spikes, Seizures, and Spreading Depression. The Journal of Neuroscience:11733-11743.
  3. Fava A, et al. (2014) Chronic migraine in women is associated with insulin resistance: a cross-sectional study. European Journal of Neurology 21(2):267-272.
  4. Longo DL, et al. (2013) Harrison’s Manual of Medicine 18th Edition (McGraw Hill Medical, New York).

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13 Comments

  1. Dear Angela,

    Thank you for sharing your work. It is grabbing my attention. You may also wish to consider the contribution of TRP receptor genes to the migraine process. I believe TRPM variations probably predict who may benefit from magnesium glycinate in migraine prevention. Another interesting gene might be FMO3. I believe Variations in this gene have some implication for tyramine and xenobiotic degradation.

    I cope with cervicogenic headaches, weather change headaches and menstrually related headaches. Some of these headaches are migraines. I am diagnosed with c-EDS, Hashimotos and mast cell related issues. Lack of a gall bladder and genetic variations in the PPAR-A and FADS genes make ketogenic diets an impossibility. My Interesting CYP450 variations make supplements and medications hard to dose. I’m trying to figure out how to eat, supplement and medicate. Perimenopause has really created havoc for me. I am having success taking 1/8 tsp of Himalayan salt before 12 oz of water upon awakening and before bed. Any other suggestions for diet considerations?

    Warm Regards,
    Robin

    PS For multiple reasons, I’m unable to Facebook. So, I miss out on resources there.

    1. Hi Robin,

      Migraineurs usually benefit from magnesium but that alone doesn’t solve any of the problems. Magnesium, as you probably know, provides the “key” to open the voltage gated pumps attached to an ATP molecule so that Na and K can come and go. But if there are not enough Na or K, they can have as much magnesium as possible and nothing will happen. I recommend to all migraineurs to take the maximum RDA of magnesium (400 mg) daily, and I recommend a combination of glycinate, malate, taurate, and citrate. So far, I found this combination seems to work flawlessly for most everyone.

      In terms of FMO3, I have not found that on the migraine genetics literature (I use Genecards) and no migraine-associated degradation of tyramine or xenobiotic discussion anywhere in literature.

      I believe migraine is now very clearly understood (at least by me if not yet by the scientific and medical industries). I am presenting my findings next month at the AAAS (American Association for the Advancement of Science) that is based on Ionic Channelopathy as the cause of migraine, with genetic variances of highest score among nearly all possible ionic channels that operate electrolyte management for action and resting potential. Once the reason for the electrolyte imbalance is stopped, the ionic channels need not work extra and all migraine issues vanish.

      In terms of the ketogenic diet–gallbladder is of no concern since that is only bile storage. One can train the liver for quick bile manufacturing–I have been on the ketogenic diet for over 2 years without gallbladder for over 6 years. PPAR-A and FADS can cause problems–assuming they have been expressed. Having genetic testing done and finding variances (homozygous or heterozygous but autosomal dominant) doesn’t mean you have the condition since epigenetics dictates whether you will or will not express the trait. The best way to test that is to get an NMR lipid profile test, which looks at your particle sizes and can truly see if you have expressed or not your lipid profile that would prevent you from the ketogenic diet.

      In terms of salt: what you are doing is great except if I may recommend you replace Himalayan salt with purified table salt or kosher salt for 2 reasons.

      1) Since you have Hashimoto’s disease, even minimal amount of iodine can be harmful and Himalayan is not without iodine
      2) Himalayan is an ancient fossilized rock salt that under pressure of the weight of the mountain, as it lifted out from under the sea, has collected a mired of heavy metals that are harmful. See the article I wrote on this earlier here and in greater detail here. The radioactive materials in there a definite negative as well.

      I wish you good luck and all the best!
      Angela

      1. Dear Angela,

        Thank you for your guidance.

        I’m also trying to understand the possible link between having reduced TRPM3 receptors and pain. This is too simplistic, but I’m Wondering if having fewer TRPM3 receptors causes more sodium to leave cells, leading to more vasodilation, igniting a neurogenic pain process. Presently, reduced TRPM3 receptors are implicated in chronic fatigue/ME.

        1. Hi Robin,

          The TRMP3 receptors appear to be related to calcium entering and leaving the cells–calcium has a major connection to pain but not because of what you are thinking. Let me first quote from NIH the definition of the TRMP3 gene: “The product of this gene belongs to the family of transient receptor potential (TRP) channels. TRP channels are cation-selective channels important for cellular calcium signaling and homeostasis. The protein encoded by this gene mediates calcium entry, and this entry is potentiated by calcium store depletion. Alternatively, spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008]” that you can find here.

          Therefore, rather than having the TRMP3 gene have sodium leave, the sodium may not be able to let enough calcium in or it may let in too much calcium–dependent upon the sodium-potassium homeostasis, which is Independent from the TRMP3 gene as per the definition above. Rather we need to look at what calcium does in the neuron and how it signals to pain sensors and then look at why this happens to understand it. It is complex and fascinating by the way!

          The role of calcium in the cell is to kick neurotransmitter out of the neuron. Neurotransmitters collect in little vesicles in the base of the neuron in the “feet” that we call terminal buttons. This of each vesicle as little sacs that are full of neurotransmitters. In the “communication in the brain” are the neurotransmitters. However, the communication must be constant because if one neuron stops communicating, the connecting neurons prune their connections (called synaptic pruning) and connect to other neurons instead–assuming there are any communicating. If there are no nearby neurons that communicate, much synaptic pruning may occur and this may be permanent if there is no action taken. Luckily the brain is resilient and adaptive in most cases.

          Now let’s look at how calcium kicks the neurotransmitters out of a neuron. Voltage dependent calcium channels are high voltage channels. This high voltage suggests that there needs to be enough sodium entering the neuron all through the length of the axon with every single voltage dependent sodium and potassium channels and pumps working perfectly–this is called a spike train as the voltage jumps from node to node (Nodes of Ranvier) between sheath of myelin on the neuron.

          At each node of Ranvier sodium must enter the cell to generate action potential, followed by potassium entering at the same node to induce resting potential. While a particular pump starts a resting potential, all sodium moves from that area to the next node and enters there to create an action potential and so forth. This is a “train” of action potential carried from the top of the neuron all the way to the bottom and when it reaches the bottom, the terminal buttons, calcium must enter that area and with high voltage literally kick the neurotransmitters out. So, the importance of calcium is at the end of the spike train as the neurotransmitters release. There are two possibilities here:

          1) the voltage is large enough and all neurotransmitters are released in a timely fashion. This is a healthy brain with healthy response so neither pain nor fatigue or depression follows.
          2) somewhere along the spike train some sodium and potassium pumps and channels were not working and voltage stopped short of reaching the terminal buttons. This is a problem because if there is not enough voltage, neurotransmitters are not released from that neuron. When a range of neurons are experiencing the inability of releasing neurotransmitters, the range is experiencing cortical depression (CD).

          If you are an aura migraineur, the blind spot you see is the area that is in CD.

          The problem starts here. Since neurons communicate, when a region goes offline like this, the other areas of the brain send a large voltage wave called cortical spreading depression (CSD), which is a wave of energy that travels at the speed of 2-5 mm per minute and if this voltage wave reaches the dura (meninges), that is where the pain sensors are located. This CSD is also what is the aura, which is the visualization and touching of every neuron as it passes by, exciting it into action. Should the CD region awaken from this electrical shock, the wave stops and the pain is averted.

          So now you can understand the role of calcium’s main function associated with neurons in general. The way this connects to chronic fatigue is similar to migraine only without having the migraine brain, which is architecturally built different from a non-migraine brain. Thus, the very same phenomenon also causes chronic fatigue and also depression. In the case of depression, the brain region involved in lack of activation is deep within the brain and is very specific to mood whereas chronic fatigue is a general area and migraine is a general area but with a genetically specific migraine brain.

          I hope this helps you see that it is not any one thing–it is not just the TRMP3 gene but how all functions neurons must do interrelate and any one step missing causes chaos.

          Hope this helps!
          Angela

  2. Hi, I am suffering from very intense headaches with my perimenopause symptoms. This also happened when I was in the first trimester of pregnancy. The headaches last for days and seem like migranes to me. I’ve always thought of them as such, but they are not one-sided, rather, behind the eyes and at the base of the head. It feels like my whole CNS is in pain, and my whole body has been run over by a bus, with some digestive upset as a kind of mean-spirited cherry on top.

    What I am trying to figure out is the link between fluctuating hormones and headache. Why, and I mean in the body specifically, what happens to cause hormones to trigger a migrane? What is the connection between what your research is showing and hormone triggered migranes? There is absolutely no doubt in my experience that these headaches are related to my hormone shifts.

    I have explored the Paleo diet for a couple of year, at the end of which my hormones were more out of balance than ever and I was experience worse headaches. So, I am confused at to how all this research fits together and I hope you can point me in a direction to clarify the situation.

    Thank you for your great work,
    warmly
    N. Sparrow

    1. Dear Naomi,

      Very sorry to hear about your suffering. It seems there are a few possibilities in terms of what your headache is. Since it starts in the back of your head, it appears to be starting as a cervicogenic headache, which is not a migraine, but which can morph into one if care is not taken. Cervicogenic headaches are caused either by a pinched nerve in your upper back, shoulders, or neck, or bad posture, a bad move, holding your head in a bad position from stress, etc. This is a “postural” headache. Cervicogenic headache need not be on one side.

      When the pain arrives into your eyes, that tells me that it can also be occipital neuralgia (ON), also not a migraine, but a permanent damage of the nerve that goes from the eye to the occipital cortex (in the back of your head). ON can be caused by many things, among them having taken quinolone antibiotics, such as Cipro or Levaquin–all antibiotics that have “floxa” in the generic name like Cipro generic is Ciprofloxacin, can cause ON. These antibiotics are now labeled with a warning box that includes ON in addition to a few other things.

      Pain in the eye, if “stabbing” like pain can also be cluster headaches. So the cervicogenic headache may also morph into that. If you have cluster headaches, it feels like someone is constantly stabbing you in your eye(s). It is also called “ice pick” or “suicide” headaches… for good reason. They are the most painful. For most, cluster headache is also only on one side but I suppose there are no rules in that one.

      There is a great overlap between migraine, cervicogenic, and cluster headaches–not so much ON. It seems that many people with cluster headaches or ON are misdiagnosed so if you have the stabbing eye pain, please visit your doctor. Cluster headaches benefits from oxygen use right as the first pain occurs. ON requires a different treatment, usually nerve block. Though given that you have this only once a month, I don’t believe you have ON.

      Cervicogenic headache will morph into other headache types if not stopped on the spot. Many people benefit from a very deep (nearly painful) massage of the back of the head and neck. Some people take simple OTC medicines and they stop a cervicogenic headache before it becomes a monster. Once you let it pass onto the front of your head, it is not that easy to stop the pain! Your upset stomach hints at the depth of the pain–it is probably quite intense.

      In general, hormonal cycles initiate all kinds of pains–including headaches and those with migraine-brain, migraines. To get a migraine one needs to have a migraine-brain. Since migraine always has prodromes and you don’t, and since your pain is on both sides, we can exclude migraine. However, the preparation for your PMS is important no matter what causes your pain. Pain can be caused by eating too much cabs (grains, nuts, seeds, fruits, vegetables, juices, smoothies are all carbs not just sugar and sweets!), and, of course, at PMS times women always crave sweets. The craving hints at voltage energy need in the brain (salt and water) so at the time of craving sweets, have a piece of aged cheese or olives or just salt and water. This will help you prevent the pain. I have an article written up on this that you can find here. You may find it helpful.

      I wish you well and have a nice weekend,
      Angela

  3. This is all fascinating! My daughter has suffered chronic migraines for 17 years. Her favorite food is a sandwich and diet ginger ale. How do I help her with her diet?? Thank you for all your hard work!! She has mentioned giving up. She is worn out with the fight. I just pray each morning she will wake up. It all began around puberty. Is there a connection. She also suffers from vertigo.

    1. Dear Jenny,

      Very sorry to hear that your daughter has been suffering for so long. Glad to help.

      Unfortunately her favorite food is a problem–and probably other foods as well. Because migraine brain is such that glucose causes energy shortage, the brain–not knowing any better–craves more glucose. This is normal since for most people glucose is the main energy source for the brain. Sandwich is unfortunately made from bread and bread (of any kind) is instant glucose and is void of all nutrition. Most migraineurs do much better by stopping all grains–including gluten free alternatives. Unfortunately grains are extremely addictive, more so than sugar. They are very hard to give up. Grains also represent a very large percent of the calories in an average modern diet so one is left without fully understanding of what to even eat once grains are stopped.

      Diet drinks are also a very bad choice since 1) some sugar substitutes can trigger migraine and 2) they lead to obesity and insulin resistance, something migraineurs are predisposed to already. They also mislead the brain by tasting sweet and so the brain expects carbohydrates, which doesn’t come and so diet drinks, in some ways, are worse than sugary drinks.

      There are a few alternative nutritional methods but they all start by having to quit refined carbohydrates, sugar substitutes, and reduce other carbohydrates as well. There are many medical groups online that can help but they are not free.

      If she needs guidance on how to change her lifestyle, a migraine group, such as one of mine can help and is free. This is my “starter” migraine group that helps migraineurs change their lifestyle and which has been extremely successful. From this there are many choices for those who need further dietary changes–I also offer a ketogenic process specifically for migraineurs–also free.

      Please reassure your daughter that there are thousands of migraineurs like her (I am one of them), who managed to overcome and become migraine and medicine free by a modification of lifestyle. She needs help by guidance and support on how to, and given your help and support, she can overcome. Thank you for reaching out in her name for help! <3 Please recommend her to read to article and to join us in our free Facebook group for guidance. We are glad to help her.

      Best wishes,
      Angela

  4. I think it is also very important to consider the comorbidity of ion channel disorders also disrupting the electrolyte balances causing migraines. Diagnosed with a considered rare ion channelopathy of potassium channels I suspect I may actually have several. Possibly a second one in the sodium channels. I have chronic fatigue well beyond the original injuries that seemed to trigger it. My body reacts to minor shifts in my potassium level. High sodium intake as well triggers pots sudden muscle weakness and even paralysis attacks. I was considered neurotic and suffering somatoform symptoms. Curiously connective tissues also are a known comorbidity and happens quite frequently in those with ion channel disorders. I am hoping to receive my genetic data and have educated myself on the mutations that I could be carrying. Insulin surge is known to cause potassium drops that are manageable by those with out serious ion channel disorder but can prove disastrous for many with one of the periodic paralysis disorders.Three female relatives died from cardiac arrythmias while treating diabetes with insulin injections.

    1. Hi Karen,

      Your comment is correct about the ion channels–this is what the article is about. Sodium channels are included under Na+ (there are many sodium channels and several are affected by genetic variances). In terms of insulin surge and potassium: you stated it backwards. Increased insulin production (insulin surge) or administration (by pumps) can cause a state of hyponatremia (not enough sodium) as a result of glucose entering the cells, removing Na+ and water. You can see this in this quote form my medical manual: “…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells” (Harrison’s Manual of Medicine, 18th edition, page 4–citation #4 in the article). Potassium is usually inside the cells whereas sodium is outside and sodium enters to generate action potential. Thus high glucose causes leaching of the cells and they cannot create action potential. Potassium is responsible for resting potential, which returns the cell to a brief refractory period of no action at all–the period that is the most dangerous. If there is a voltage gated sodium ionic pump failure and not enough sodium can enter, the cell cannot snap out of refractory mode at that particular point.

      As you likely know, a neuron is not a one-shot game but Nodes of Ranvier break up the surface of the axon. It is only at these Nodes that sodium and potassium can shake hands in one coming and the otehr going. There are many such pumps. The failure of many of these pumps at any one Node can cause the entire cell from being able to continue to generate action potential. This knowledge has yet to be visualized by scientists and doctors although big pharma has its handle on it perfectly well–hence the many ionic channel blockers migraineurs are given to take. The thought is likely that “it is different so we must turn it down” to prevent a migraine attack. The ensuing shutting down of the brain seems inconsequential.

      So, to continue, those with insulin problems (and this includes migraineurs) have an ionic imbalance. This is why increasing sodium is necessary.

      There are many comorbidities but ion channelopathy is not one of them since migraine seems to be one of the kings of ion channelopathy itself–it is not a comorbidity. This is shown in the table where I have 16 genetic variances shown–there are more at that database. They are all but a couple reflect ionic channel variances. So migraine IS a form of channelopathy.

      There are comorbidities with other health conditions that I didn’t mention but often appear together: chronic fatigue, depression, seizures, fibromyalgia, and many more. The reason why I mentioned only a couple because most neurological health conditions are, in some way or another, connected to ionic channel problems, electrolyte disruption, and myeling sheath damage. It is worthy to mention that many people with such comorbidity manage extremely well on the Stanton Migraine Protocol®, LCHF, or the ketogenic diet. The trick is reducing carbohydrates such that a particular threshold is reached. This I call carbs-threshold and some people I test with it but not all–this is not used in the ketogenic diet approach.

      I highly recommend all migraineurs to test their glucose since the question is “when” rather than “if” insulin resistance will knock on the door unless they completely honor the brain they have–as described in the article. To date over 4000 migraineurs have responded extremely well to the Stanton Migraine Protocol®, and recently I started a “keto mild for migraine” group that specifically addresses how to apply the ketogenic diet to migraineurs.

      If you have ion channel health conditions, I highly recommend you do invest in a blood glucose testing kit. They are cheap and very telling. I find that fasting blood tests are not very useful once one is on the LCHF diet or one that even eat less carbs, because the Dawn Effect of hormonal surge uses insulin receptors, causing an increase in glucose reading (glucose backs up until those hormones are cleared) and also with the liver “dumping” glycogen as a result of fasting, which can end up showing a high fasting glucose as a result, giving misleading information about your health condition.

      The cardiac arrhythmia you refer to (or if death I would call that atrial fibrillation or a-fib) are caused by hyponatremia rather than hypokalemia. Many new studies are coming out now showing how our reduced sodium diet is hurting us. If you are predisposed to a-fib, keeping to proper electrolyte balance is vital. Since I am very much subject to this as well, I can also share that every time I had an episode in which I landed in ER, my electrolytes showed way low sodium (not potassium). So be careful what is low. Do get frequent blood tests including the electrolyte panel to ensure you are where you should be. I also recommend you invest in a home blood pressure device since that is very telling what you need!

      Hope this helps answer some of your concerns.
      Angela

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