As a migraine sufferer myself since childhood, I have searched for a solution that helps to prevent or reduce the frequency and severity of my migraines all through my young adult life, by visiting doctors and by trying to get “better care”. As a scientist, I did not focus on finding a solution, because my field of science was not in migraines. However, when my doctor prescribed a medicine that was off-label (“experimental drug” is a better name for it), I refused and decided to find a solution. I retired from my teaching job and dedicated myself to migraine research for about ten years. I read every single research paper and book I could find on migraines, as well as related physiology and genetics. The more I read, the wider the field of interest became. While some research used the framework that migraine is a neurological disease, others focused on its vascular aspects. In general, I found that both research and suggested treatments addressed only the symptoms of migraines. After a while, it became apparent that there had been no dedicated, comprehensive research about the causes of migraines.
Understanding migraines requires several fields of expertise, and to find the cause, one must connect many dots. I emerged from my multi-year study and experimentation with a clear understanding of migraine cause. I became patient #1 for applying my findings. After successfully testing my method with a number of relatives and acquaintances as well, I summarized everything in a book “Fighting the Migraine Epidemic” (currently in its 2nd edition), and also opened a Facebook migraine group Migraine Sufferers who Want to be Cured by the Stanton Migraine Protocol. In the group, thousands of migraineurs have applied my n=1 process, which by now developed into a successful protocol.
Basically, I concluded that migraine can fully be prevented by doing two things:
1. Reduce or eliminate carbohydrates from diet
2. Greatly increase salt in diet
At the time I discovered this, I was not yet aware of the benefits of ketosis. That discovery came after I entered ketosis by accident. One day, I didn’t have time to eat and I found myself in ketosis. However, I also found myself with a serious migraine, so clearly that was not a great experience. I spent the next two years experimenting with a variety of ways one can reach and stay in ketosis and what it takes to do so without migraines.
Thus, ketosis was a later addition to the migraine solution. It soon became clear that reaching ketosis was different for migraineurs than for people without migraine. The genetic migraine brain influences how the whole body behaves and responds to its environment. So, the standard nutritional recommendations for ketosis, be it the ketogenic diet, the carnivore diet, or just fasting, has to be modified to work for migraineurs.
Definition of Migraine
I look at migraine as a condition rather than a disease. If we can stop migraine from hurting, and also stop all its other symptoms such as dizziness, nausea, aura, foggy brain, tingles, vertigo, etc., and if we can prevent these from happening again, are we left with a disease? No, I don’t believe so. Migraine is a condition caused by several genetic variances. Once we understand the true nature of migraine, we can completely control and prevent it.
There are two very important conclusions can be drawn:
· If we can prevent it, we know what causes it
· If we can prevent it, it is not a disease
Migraine is a channelopathy (see here, here, and here). Channelopathy is a condition in which ionic channels don’t function properly. In searching the human genome database, one may enter “migraine” into the keyword search to have all known gene variants (SNPs) show up in order of importance (I already searched for migraine here). You really need not go past the first three variants: voltage gated sodium/potassium pump (ATP1A2 ATPase Na+/K+), voltage gated calcium channel (CACNA1A), and voltage gated sodium channel (SCN1A) are the three most important variants. These are the pumps and channels where channelopathy can occur, and indeed, it does.
The connection of how dietary carbohydrates initiate ionic channel failure and why increased dietary salt helps prevent channel malfunction is a subject for a separate article because of its complexity, but part of the explanation can be read here and here. In brief: migraineurs have hyperexcited brains with a significantly larger number of sensory neuronal connections than people without migraines. As a result, migraineurs need to generate a lot more voltage for communication among neurons, and that requires more sodium (Na+). Glucose entering cells (from carbohydrates) removes sodium and water from the cells, causing a sodium shortage, which can lead to migraine.
Reduction of Carbohydrates
Clearly, there is a benefit from reduction of carbohydrates if carbohydrates are part of the migraine problem. The reduction of carbohydrates leads to an increase in the consumption of fats and proteins. Depending on the degree to which one removes carbohydrates from the diet, it may be called the Low Carbs High Fat diet (LCHF), ketogenic diet (keto), MAD (Modified Atkins Diet — a form of ketogenic diet), carnivore diet (CD), or zero carbs diet (ZC). With any one of the above diets, the metabolic process of the body may switch to ketosis — this is dependent upon the amount of carbohydrates consumed. Often the LCHF diet contains up to 150 gr carbs a day, and that may be too much for ketosis to start in most people. In the LCHF program for the migraineurs, the amount of carbs has to be 50–70 gr for women and 65–85 for men. At this level of carbohydrates, many migraineurs enter very low-level ketosis — although not all. It appears that migraineurs are able to handle this amount of carbohydrates, with special care, well enough to remain migraine and medicine free.
Further reduction of carbs to below 30 gr a day initiates ketosis in every person — this is the keto diet. Complete removal of all plant matter in CD or ZC will lead to ketosis.
The Migraineur Difference with Carbohydrate Reduction
Being a migraineur means that there is a great likelihood of having metabolic syndrome, such as insulin resistance (a level of Type 2 Diabetes (T2D)). While research shows that the ketogenic diet is ideal for reversing T2D, my experience with the thousands of migraineurs is that they end up with serious hypoglycemia, sugar crash, and reactive hypoglycemic events, and also extremely high blood ketones, β-hydroxybutyrate (BHB). These conditions lead to major migraines that may last for multiple days. Thus, switching to an “out of the box” keto does not work for most migraineurs very well.
The best carbohydrate reduction plan for migraineurs is to cut carbohydrates completely and increase fat and protein consumption, so that gluconeogenesis can help alleviate the dangers associated with sugar crash. A few minutes of brisk walk, climbing the stairs, or a few squats can also help bring glucose levels into normal range, thereby reducing BHB levels to nutritional ketosis range. Such carbohydrate reduction leads directly to CD or ZC. Migraineurs usually do extremely well with dairy; dairy is a perfectly balanced electrolyte. The separation between CD and ZC is that the CD incorporates dairy.
To monitor the reversal of insulin resistance, migraineurs are strongly encouraged to measure their blood glucose and BHB levels regularly in their induction phase — and preferably much longer. Reduced carbohydrate diets seem to require more salt and water than what other diets need. One of the reasons for this is the burning of stored fat, which are triglycerides — meaning three fatty acids held together by a glycerol cap. The conversion of triglycerides to ketones, referred to as lipolysis, releases water, so more water leaves the body than normal, and water and salt leave together via the kidney. Hence, because of the loss of electrolytes, more salt and water need to be replaced. This is especially true for migraineurs.
While many people on the CD or ZC only eat meat, fat, and water, this is not a very good choice for migraineurs. Because the migraine brain uses much more salt than the brain of non-migraineurs, a diet without salt leads to migraines even in a carbohydrate-free diet.
Fasting and Migraine
The ability to fast without hunger is one of the benefits of the reduced carbohydrate or carbohydrate-free diets. However, because migraineurs are so sensitive to blood glucose drops and BHB increase, fasting can lead to migraines and sugar crashes, particularly when the migraineur is not yet keto adapted. Keto adaptation can take as little as one day to as long as two years for a migraineur — this length is greatly dependent on medication and migraine history and metabolic health at the start. In addition, migraineurs who switch from a plant-based diet to CD or ZC have an extended period of adjustment.
I have found that the best way to initiate fasting for a migraineur is to slowly spread time between meals over a period of weeks. This allows for stopping and reversing, should a migraine pop up. Fasting is only recommended after sugar crashes and reactive hypoglycemia have been cured by using CD or ZC. For migraineurs, using the keto diet as a metabolic cure is not a viable solution.
A concern in fasting by a migraineur is the insufficient electrolyte concentration. It is important to continue to drink lots of water and take lots of salt while fasting. Although the body is not receiving external nutrients, it is burning internal nutrients (fats), while water evaporation and salt use are actually increased. Some people are able to practice water-free fasting but not migraineurs. Migraineurs should drink plenty of water and add salt during fasting. I also take magnesium while fasting. As the migraine-brain uses more salt for voltage generation, more magnesium is also used by the voltage activated sodium/potassium pumps.
A serious concern during long-term fasting is heart rate and blood pressure. Migraineurs usually have very low blood pressure — unless medications they take increased their blood pressure. Long-term fasting, meaning longer than two days of fasting, should only be completed under continuous supervision by a healthcare provider, if such is possible, or at least a family member or friend, armed with a digital portable cuff-type blood pressure monitor, checking blood pressure and heart rate regularly. My blood pressure dropped into the range of 80/50 with pulse in the 50s. This is not a range of good health. I immediately broke fast and recovered very quickly. I did have supervision at all times — this is necessary, in case your heart rate drops too low. There is a serious danger of passing-out.
Ketosis and Migraine Medicines
Unfortunately, migraineurs are prescribed many dangerous medicines, some of which have known interactions with ketosis. Topiramate (Topamax) has a black box label by the FDA not to be used while in ketosis. While other drugs have not yet received official warning, my personal and group experience show that most migraine preventive medicines interact with ketosis:
· Anti-seizure medications — voltage gated calcium channel blockers
· Selective Serotonin Reuptake Inhibitors (SSRIs, SNRIs)
· Simple serotonin meds (triptans, antidepressants)
· Beta blockers, and ACE inhibitors — heart medications
· Opioids, narcotics, and barbiturates
Although there has not yet been research on understanding why there are interactions, I hypothesize that the reason has to do with drug clearance difficulties as a result of the different metabolic process from what the drugs were designed to work in. It is important that migraineurs consult with their doctors and work out a plan of safe reduction.
I trust this summary of the do’s and don’ts of ketosis for migraineurs will help to evaluate how to manage a well-designed program to ketosis. I am glad to respond to anyone asking for clarifications and more information.
1 Longo, D. L. et al. Harrison’s Manual of Medicine 18th Edition. (McGraw Hill Medical, 2013).
2 Rainero, I., Govone, F., Gai, A., Vacca, A. & Rubino, E. Is Migraine Primarily a Metaboloendocrine Disorder? Current Pain and Headache Reports 22, 36, doi:10.1007/s11916–018–0691–7 (2018).