migraine Archives - Page 2 of 3

Migraine, Diet, and Thiamine

Published on August 15, 2018

14399 views

In US population studies, the prevalence of migraine is approximately 18% in women and 6% in men. About 90% of sufferers have moderate or severe pain and 75% have a reduced ability to function during the headache attacks. One third require bed rest during an attack. A study at the Mayo Clinic showed the incidence in women increased 56% during the 1980s and 34% during the same period in men. Although the term “migraine” is often used to describe any severe headache, a migraine headache is the result of specific physiologic changes that occur within the brain leading to the characteristic pain and associated symptoms. They are usually accompanied by sensitivity to sound, light and odors and there may be nausea or vomiting. Typically, the headache involves only one side of the head but in some cases it may be bilateral. The pain is often described as throbbing, pounding and maybe made worse with physical exertion. Silent migraine is a variant where the patient may experience aura, nausea, vomiting and other nervous symptoms without headache.

Migraine headache is estimated to affect up to 28% of adolescents, most of whom are female. It has been associated with reduced quality of life and academic disruption due to missed school days. In 2014 the US Food and Drug Administration approved an existing medication called topiramate for prophylaxis in adolescents between the ages of 12 and 17 years. There are several possible adverse effects from this drug, some potentially serious. Prophylactic drugs are unpromising and unpredictable. A mild degree of prevention could be obtained from the use of acupuncture.

Migraine Precipitants

Of 171 patients who fully completed a survey, 49.7% reported alcohol as a precipitating factor of headache other than migraine. Only 8.2% reported aspartame and 2.3% reported carbohydrate. Patients with migraine were significantly more likely to report alcohol as a trigger. They also reported aspartame as a precipitant three times more often than those having other types of headache. Non-nutritive sweeteners, including aspartame, saccharin, sucralose, neotame, acesulfame-K and stevia have all been questioned as to their safety. Pregnant and lactating women, children, diabetics, migraine and epilepsy patients, represent the susceptible population. Although sucralose is not considered to be a migraine trigger, a patient was reported with attacks of migraine consistently triggered by this sweetener.

Hypoxia, Pseudo-hypoxia, and Migraine

Migraine with aura is prevalent in high-altitude populations, suggesting that hypoxia has a part to play in etiology. Of 15 patients with migraine headaches, artificially induced hypoxia triggered migraine attacks in eight patients.

Thiamine deficiency produces abnormal gene expression in brain exactly like that induced by true hypoxia. Migraine is a risk factor for thiamine deficiency and Wernicke encephalopathy (WE), the classic thiamine deficiency disease that affects the brain. Two female patients have been reported with chronic migraine. They also had clinical signs and laboratory support for WE. Both patients received intravenous thiamine supplementation, leading to improvement of both WE and the associated headache. The authors suggested that nausea and vomiting, occurring with migraine, may lead to the thiamine deficiency. However, headache, nausea, vomiting and loss of appetite are symptoms that occur in the early stages of WE, thus simulating migrainous features and the association is by no means clear. The authors suggest that thiamine supplementation might be a promising therapy in a subset of patients with chronic migraine.

Also, the range of pathologies associated with magnesium deficiency is staggering, including migraine, multiple sclerosis, glaucoma and many other disorders. It is important to emphasize once more that magnesium and thiamine work together in the cellular machinery that produces energy and deficiency of either is critical. Chronic recurrent nausea in childhood is a poorly described symptom and in a study of 45 affected children, 62% had migraine headaches. They also suffered from dizziness, anxiety, fatigue and sleep problems. The exact incidence of dizziness and vertigo during adolescence is not known. For those few adolescents who seek outpatient evaluation, the majority are diagnosed with migraine headaches and many suffer from postural orthostatic tachycardia syndrome (POTS), a condition that has been reportedly due to thiamine deficiency in some cases.

Autonomic Asymmetry

Normally there is a balance between the autonomic tone of the right and left half of the body. However, under stress or with hypothalamic instability this balance may be disrupted and result in the marked autonomic asymmetry seen in migraine. Abnormal regulation of the large cranial arteries appears to play a significant role in the mechanisms of migraine pain, also reflecting abnormal autonomic function.

Migraine and Diet

Attack frequency of migraine in children was associated with higher intake of high fat or sugar. The processing of both is dependent on thiamine. With these strong associations in the medical literature, it is impossible not to contemplate that the sweet sensory input from the tongue to the brain is an important trigger for migraine. There has been a steady increase in sugar consumption in America over the past few decades, suggesting the possibility that it represents the published increased incidence of migraine in the 1980s as mentioned above. It also suggests the possible implication of artificial sweeteners as migraine triggers.

The association of migraine with alcohol ingestion might be an important observation, since alcohol has long been known to be a cause of thiamine deficiency in the part of the brain that controls the autonomic nervous system. It has also long been known that beriberi, the classical thiamine deficiency disease, causes autonomic dysfunction in its early stages. One of the most important observations that I observed in practice was that a mild degree of this deficiency makes the brain extremely sensitive to many different input stimuli. It results in a high degree of sympathetic nervous system activity, hence so-called panic attacks that are really distorted fight-or-flight reflexes. Patients complain of constant anxiety, heart palpitations, unusual sweating, nausea, vomiting, dizziness and brief fainting attacks known as syncope. This collection of symptoms, thought by many physicians to be psychological in nature, is also referred to as postural orthostatic (positional) tachycardia (rapid heart) syndrome (POTS).

In a person who is in a marginal state of malnutrition, any mild stress such as a vaccination, a mild infection or some form of trauma may initiate POTS. A reader might conclude that this diversity of symptoms, that include the incidence of migraine, cannot be caused by a deficiency of a single nutritional element. In order to understand, it is necessary to be aware that a deficiency of energy in the brain resulting from a common form of malnutrition creates a multiplicity of cellular dysfunction according to the distribution of the deficiency. If this is the truth, it makes a mockery of the present medical model in which each described disease is thought to have a specific underlying cause. Hence, money is collected to find the cause of Alzheimer’s disease and is probably a pipe dream. It is well known a published association with thiamine metabolism strongly suggests that we should be looking for prevention rather than spending millions in trying to find a curative drug.

Conclusion

The clues that alcohol, sugar and artificial sweeteners are major triggers for producing migraine headaches are so strong, their avoidance would appear to be mandatory. However, it is almost certainly true that many sufferers know this, but make no attempt at avoidance, marking the taste of sweeteners as addictive. I became aware that there were millions of people in America suffering from symptoms that are constantly being unrecognized in medical clinics. Even if they are recognized as nutritional in nature, the doctor and patient are likely to ignore the appropriate prevention by adopting the consumption of an appropriate diet. Since most of the population is ingesting pills of one sort or another, perhaps advising the use of vitamin supplements as part of the dietary discretion might at least partially serve in the reversal of these common symptoms.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Photo by Mehrpouya H on Unsplash.

Trauma, Pain, and Complex Illness: A Battle for Survival

by MM

Published on June 11, 2018

3997 views

As a child, I endured every form of abuse. Both of my parents were mentally and emotionally abusive. I was beaten and experienced two severe head injuries that were never treated. One incident involved falling head first out of a moving vehicle. My brother grabbed my legs, but my head hit the pavement several times before he was able to pull me back in. The other incident was being thrown onto my parents’ waterbed and hitting the sharp corner of the bed frame.

I was sexually abused starting at the age of three.

I had my first period in third grade. My periods were painful with heavy flows that also came along with depression and anxiety. I was put on birth control at the age of 12 to try and control the menstrual symptoms.

At the age of 12, I was prescribed Prozac for the depression and within a couple of weeks of starting the medication, I had my first suicide attempt. Over the next 20 years, I was placed on almost every psychiatric drug there is – always resulting in a suicide attempt or a worsening of symptoms.

In high school, I started getting terrible headaches and went to a chiropractor for a few years. That chiropractor said that my neck curves the wrong way possibly caused by the head injuries as a child.

Also, in high school, my bladder started causing me a lot of distress. I pee a lot. Yes, women say they pee a lot. To this day I pee upwards of 30 times a day. The urologist in my hometown performed one of the most painful tests I have ever endured. They pumped me full of saline and waited until my bladder was full. I was in tears when it got to halfway full. Then they took x-rays as I tried to pee into a cup. The result was a diagnosis of overactive bladder. He said that my bladder was very strong, that when any urine hit my bladder it would spasm giving the feeling of needing to pee.

The menstrual issues continued to get worse. I would be debilitated during my periods. In my early 20s, we ran more tests on my bladder. They diagnosed me with interstitial cystitis and said that I had little to no capacity in my bladder. I cut back on caffeine and acidic drinks and /foods and upped my water intake.

Around this same time, I had a mental and emotional breakdown after a confrontation with my father. I was diagnosed with PTSD and went through EMDR therapy with great results.

In my mid-20s we did a laparoscopic surgery to determine why I was still having so many problems with menstruation and was told I had an excessive amount of blood vessels on my uterus. I was told that having children should help alleviate the symptoms. They sent me home before I was able to go to the bathroom. This led to one of the most painful nights I have ever had because I could not pee. I just sat on the toilet and cried. We went back to the hospital and they inserted a catheter and were bewildered. I was outputting way more than I was inputting. The doctors had no clue why this was happening or what could be done. Once I was able to urinate without the catheter, I was sent home and no further tests were run.

After a divorce and the death of my step-father, I married an abusive man. I had another breakdown and he had me institutionalized. While I was in the hospital they diagnosed me with Fibromyalgia. They put me on a cocktail of 40mg of Lyrica, Xanax, Valium, Trazadone, and Paxil. I was a zombie and within 3 weeks, I took all the pills in another suicide attempt. I was in the ICU for three days and came out a stronger person. I divorced my then husband and moved to the east coast.

I get regular sinus infections and bronchitis. I struggle with both falling and staying asleep. I have an amazing toolkit for managing anxiety and depression.

In 2010, during an MRI they discovered that I had 4 small nodules (under 1cm) on my thyroid. They diagnosed me with multinodular goiter.

I got pregnant in September of 2011 and it was brutal pregnancy. I ended up in the hospital with dehydration because I could not even keep water down. Thankfully Zofran helped me survive my pregnancy. I had a c-section in June of 2012 because I would not dilate. I was induced and after almost 48 hours of labor, I had only dilated ½ cm. I experienced severe postpartum depression but pushed through without medication.

In 2014, I got pregnant again and had another brutal pregnancy. I had gestational diabetes and was monitored closely. I had another c-section in August of 2014 followed by the worst infection I have ever endured. I went through five rounds of oral antibiotics and two weeks of IV antibiotics before the infection cleared up. Over the next few months, my husband and I became concerned with the increase in my bowel movements and swollen stomach. I saw a GI and he said it was most likely IBS and to try an elimination diet. I did and proceeded to lose 65 lbs. I cut out corn, wheat, rice, and only had minimal dairy. I also began working out regularly as well to improve my health. While this was going on I also started having increased pain with menstruation. I bled for three months non-stop. I saw several GYNs with no answers or help provided. I finally found an amazing GYN that discovered I had fibroids and cysts and we decided to try a partial hysterectomy. They removed my uterus and cervix in March of 2016. I had severe endometriosis and had scar tissue wrapped around my intestines. After surgery, I had another mental breakdown and he then regretted not taking my ovaries. He said he believed I have PMS disorder.

I also started to experience worsening headaches during this time but was able to manage with Tylenol, rest, etc. I was having significant shoulder and neck pain and my primary care doc ordered an MRI in August 2016 and we then discovered I had 9 thyroid nodules, two of which were over 1 cm in size. They were biopsied and found to be benign.

I broke my ankle in October of 2016 (first bone I have ever broken and had surgery to install a plate and six screws into my right ankle). I have permanent nerve damage and tendinitis in that ankle now. During the recovery from my ankle surgery, I noticed a high pitched and very loud ringing in my right ear. I was having difficulty hearing and felt very off balance (more so than usual). In January 2017, I went to an ENT and we discovered I have lost roughly 50% of the hearing in my right ear. They said it was Idiopathic Sudden Sensorineural Hearing Loss and I got a hearing aid to help. They performed an MRI and I was told there were no significant findings. I began having severe facial pain, headaches, and migraines. I began having severe issues sleeping. For almost a month, I was only averaging 3-4 hours of sleep a night and then went almost a full week with no sleep. I went to my primary care and she told me there was nothing she could do for insomnia and head pain but would treat the sinus infection I had with prednisone. This led to an acute psychotic break.

Over the next few weeks, I advocated for myself and made an appointment at a neurologist’s office and found a new primary care doctor. The nurse at the neurologist office I saw prescribed Imitrex. Which led to another adverse reaction and another hospitalization.

My new primary care doc ordered a CT scan of my sinuses and it appears I have a deviated septum with some sinus thickening. I went and saw an ENT and he advised me that I needed a competent neurologist but did not refer me to one.

A headache that began in January of 2017 continued with increased migraines. I began seeing a psychologist and learned mindfulness and cognitive behavioral therapy techniques. We did some neuro-biofeedback and EMDR.

The verdict is always the same – “this is complex” or “it’s all very biochemical”. We tried some blood pressure medication to help me sleep as well as some antipsychotics, but the side effects were worse than coping on my own.

We did a colonoscopy in July 2017, to investigate the stomach pain and distension I continue to have. While lying down I can often see the movement of my intestines. Looks like a baby moving around in my belly. The stomach distension comes and goes. Some days it’s normal and other days I look 6+ months pregnant. I also struggle with constipation and diarrhea. The GI specialist said that I had reflux but no other significant findings.

October of 2017, I saw the neurologist and he recommended Botox and neuro-biofeedback. I took a brain test on a computer and he did not perform any other tests. My GYN tried putting me back on birth control pills to see if the estrogen would help level me out. The results were BAD!!! I had an oophorectomy in December 2017. For a few weeks after the surgery, there was an improvement. I still had a never-ending headache, but migraines were less, and I felt strong enough to push through the head pain. Then it all came back with a vengeance. We lowered the estradiol from 1mg to .5mg and the neurologist gave me a sedative to try and break the migraine cycle. It helped but was brutal. The medication made me very suicidal and paranoid, but I pushed through!

After doing research on the Botox, I decided I did not want to proceed with that treatment.

I had a bit of a reprieve from the migraines after adjusting the estradiol and was just managing the headache. We did another thyroid ultrasound last month and there was significant growth on one of the nodules. They biopsied the largest nodule and it came back benign again.

Last week the migraine came back. We did two shots of 30mg of Toradol. It was better for a couple days and then came back again. We are going to shorten the time between changing the estradiol and see if that helps. I am researching and trying to find a headache clinic at the recommendation of my primary care. I practice self-care regularly and fight through a headache, joint pain, constant bladder pain and anxiety as best I can. I haven’t had a headache free day since January 2017. Please help.

Family History of Cancer:

Maternal Grandmother: Colon Cancer

Mother: Breast Cancer, Colon polyp that was removed w/ surgery

Father: Skin Cancer

Sister: Hodgkin’s Lymphoma Lung Cancer (age 14 – in remission)

Brother: Bile Duct Cancer (passed away in 2011)

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by inkoalseibua from Pixabay.

Migraine as a Metabolic Disease

by Angela A Stanton, PhD

Published on February 8, 2018

14985 views

Migraine is assumed to be a disabling neurovascular disease with various manifestations that affect the vasculature as well as the physiology of the brain. Migraine is categorized either as episodic headache (<15 pain days a month) or chronic (>15 pain days a month). It is also understood that migraine is associated with hyper sensory sensitivities and that about 15% of migraineurs suffer aura migraines. Migraine is strongly associated with metabolic disease^1-9. Based on many studies, migraine leads to metabolic disease—either because of migraine prevention medicines or because of dietary lifestyle. Genetic factors also strongly underlie why migraineurs end up with metabolic syndrome. Before we investigate what these genetic factors are and how a migraine sufferer can avoid metabolic syndrome, we first need to understand what migraine is.

So, What is Migraine?

The current scientific understanding of migraine ignores many key factors because most doctors only see migraineurs when they are in pain or have aura, and most research is, therefore, only focused on pain or aura. However, every single migraineur experiences migraines without pain—silent migraines. Silent migraines are usually associated with aura migraines but cyclic vomiting syndrome, irritable bowel syndrome (IBS), and restless legs syndrome (RLS) can also be present. These other syndromes are often precursors of the migraine-brain development (particularly in children) and they come without migraine-pain. If one can have pain-free migraines, it means the pain in migraines is only a symptom. A symptom of an underlying condition that my research and publications have been identifying and describing.

I have written many blogs about migraine and its genetic connections, see here and here and have published a book that details all genetic, neurovascular, and metabolic connections to migraine, which you can find here. In these publications, I discuss how even 2-year-olds can have migraines, how cyclical vomiting, IBS, RLS, and anxiety often precede the presentation of migraine pains by years. Because of this, migraine can appear as “not migraine” for many years and these seemingly independent symptoms may end up being treated separately. In my research, working with thousands of migraineurs over the years in my FB migraine group, I have found that nearly all of them have some form of insulin resistance (IR), which may be exhibited by hyperglycemia (HG) or reactive hypoglycemia (RH), all of which nearly always remain undiagnosed for a very long time. This is particularly important, since contrary to non-migraineurs with metabolic syndrome, migraineurs sport low blood pressure and are often very thin—meaning several commonly used key factors for the classification of metabolic syndrome are not present, based on which medical professionals would even consider testing for metabolic syndrome.

What is Metabolic Syndrome?

If three of the following five categories are met (based on the new revision of the ranges; see original article here), the person is said to have metabolic syndrome.

Waist circumference > 40 in (males) or >35 in (females)
Fasting glucose ≥ 100 mg/dl
Triglycerides ≥ 150 mg/dl
HDL cholesterol < 40 mg/dl (males) or <50 mg/dl (females)
Systolic blood pressure >130 mmHg or diastolic blood pressure > 85 mmHg

I repeat here the same in bold striked out the ones that migraineurs don’t typically have:

Waist circumference > 40 in (males) or >35 in (females)
Fasting glucose ≥ 100 mg/dl (true for a few)
Triglycerides ≥ 150 mg/dl (true for a very few)
HDL cholesterol < 40 mg/dl (males) or <50 mg/dl (females)
Systolic blood pressure >130 mmHg or diastolic blood pressure > 85 mmHg<.strike>

As you see, migraineurs don’t meet three (and often none) of the above to qualify for a metabolic syndrome examination. Yet, when I ask for an at-home 5-hour fasting blood glucose test, checking for blood sugar fasted, pre-breakfast, 30 minutes after breakfast, and then every 30 minutes after that for 5 hours, I find some very complex IR and RH cases. Below find two common examples:

Hyperglycemia (high glucose)—note that the “normal” may appear low to you but my migraineurs are on a low carbohydrate diet where the maximum blood sugar spike should not exceed 20 points. The above hyperglycemia graph shows both an overly large blood glucose spike and a significant delay in the spike, suggesting serious insulin resistance.

Reactive hypoglycemia is represented by blood glucose level that drops significantly after a meal.

Note that both of the above graphs come from people on a low carbohydrate diets, where breakfast is usually eggs with bacon with perhaps some raspberries with yogurt or a mix of nuts with cottage cheese. So the spike at the 2-hour mark usually represents the conversion of egg whites’ protein to glucose—hence, the spike at 120.00 minutes for the RH and a delayed spike for the HG. Some of the RH migraineurs ended up with such low blood glucose that they were close to fainting (two of them so far reached low 50s). Yet, because they don’t meet the “minimum three” criteria from the five listed above, many doctors flatly refuse to test them for metabolic syndrome. Some even disregard the at-home 5-hour blood glucose test as silly—not sure why, after all, there is no better method currently available. This just shows why migraineurs are never considered as having metabolic disease until it is late in the game, even though there are hundreds of academic articles showing the connection.

Given that migraineurs end up with metabolic syndrome (with most of the five points eventually) later in their lifetime, and since they are undiagnosed prediabetics for a very long time, could it be that migraine is actually a metabolic disease? Since IR, HG, and RH are part of metabolic syndrome and nearly all migraineurs have them from a young age, shouldn’t we investigate what the connection may be?

Observing that migraineurs end up with metabolic syndrome is one thing; finding if migraineurs have predisposition to metabolic diseases as a result of their genetics that includes metabolic gene variants within their migraine gene variants, would be an entirely different thing. Shall we go and find these genes?

The Genetics of Migraines

As a migraineur who is also a scientist, finding out as much as possible about migraines was easier for me than for those researchers who never had migraines. I knew what to ask and what to look for and could also tell what made sense and what didn’t. While most everyone’s first instinct is to say, “what works for one person may not work for another,” hold that thought! In the case of migraineurs this isn’t true. Over the many years of research, I found that migraineurs are like siblings. Nearly all of their symptoms and reactions to treatments are identical. If you want to fully understand why, you need to look at the genetic variances of migraineurs—all of these variances are identical or at least very similar to each other among migraineurs. How do I know this? Many migraineurs had genetic testing and shared their genetic data with me so I could compare their genetic variances with those “average” variances listed for migraine-genes.

True migraines start with a hormonal disruption as a result of overstimulation of the sensory neurons and end in electrolyte dysfunction that prevents action potential in some part(s) of the brain, which results in what is referred to as cortical spreading depression. This is well understood by studying the genetic template of migraine, where the first 30 or so genetic variances are all associated with ionic channels operating electrolyte management and maintenance. Other key genetic variants of importance among migraine genes are glucose transport, renin-angiotensin-aldosterone system (RAAS)¹⁰; see variants associated with RAAS as AGT, AGTR1, AGTR2 and BDKRB2 in the migraine genes and here the same associated with type 2 diabetes and here with hypertension, ATP binding, glucagon receptor, and several mitochondrial variants all with very high score in migraine genetic variances. These variants collectively lead to one key problem all migraineurs eventually face: metabolic syndrome^5,11. Is it possible then that migraine, while it is clearly genetic, with its metabolism and energy associated variances, is actually a sign (symptom) of metabolic syndrome? In other words, does the genetic makeup of migraineurs lead directly to metabolic syndrome? The answer to this is likely yes. The reason? When migraineurs change their nutritional regime by excluding or greatly reducing all carbohydrates, they reverse their metabolic health condition, achieve full remission, and with that their migraines also disappear.

Clearly, migraineurs’ genetic makeup is such that factors responsible for type 2 diabetes are major components of their migraines. What are those factors? Metabolic syndrome in migraine is not diagnosed until the migraineur had the disease for many years because as we described, migraineurs don’t carry three out of five typical metabolic syndrome traits. The one common variable is chronic insulin resistance (CIR). While academic literature is quite a war zone when it comes to the causes of CIR, in migraineurs the cause is very simple to determine and the condition is easy to reverse.

Reversing Chronic Insulin Resistance in Migraineurs

All people with chronic insulin resistance have common symptoms when they are late with a meal or skip a meal: feeling grumpy, nervous, ravenous, sometimes shaky, sweaty while cold, anxious, and may even faint. Feeling hungry when blood glucose levels are above the body’s preferred 99 mg/dl (about 1 teaspoon of glucose in the entire body) is not normal but those with hyperglycemia feel hungry even when their blood glucose levels are way over 100. To understand the importance of this, we should understand what hunger actually is. I am not covering the biochemical and hormonal elements of hunger. Hunger is a state in which the body is running short of glucose for whatever reason. If the blood glucose level is way above normal, feeling hunger is not warranted. This sort of hunger actually signals insulin resistance because while the blood has plenty of glucose to feed the organs that need glucose, glucose doesn’t get there. It cannot get there because insulin is resistant—meaning it is not sensitive enough to pick glucose up to carry it to the cells. Therefore, eating when hungry while the level of blood glucose is still high, causes more trouble and the hunger will not be sated.

Reversing this type of insulin resistance (hyperglycemia) is very simple: stop eating and keep on checking your blood glucose levels. My migraineurs are asked to not eat until their blood glucose levels dips well below 99 mg/dl—preferably between 70 and 95 mg/dl. Getting down to this low blood glucose may take several days of not eating! If a migraineur is not on any psychotropic or heart medicines, the ketogenic diet I specifically formulated for migraineurs is the best option.

If the migraineur has reactive hypoglycemia, fasting is not an option, since their blood glucose level can drop below healthy minimum levels, endangering their lives. In this case, the migraineur moves to the zero carbs diet (all meat and fat, ratio dependent upon certain factors). Without any exogenous easy glucose, the liver must convert glucose from protein for all of the body’s glucose needs and this reduces insulin, since insulin is not spiked by glucose in this case.

Normal hunger is *just hungry* and no urgency. Normal hunger is healthy, and you can continue being hungry for several days without eating without any problems. That’s normal. A normal hunger doesn’t affect your blood sugar in any shape or form, because the liver manufactures the proper amount of glycogen via gluconeogenesis and ketones for the ketogenic metabolic process. Migraine is 100% preventable by a metabolic process that doesn’t use carbohydrates at all or only in minimal amounts. Since a large body of science suggests that metabolic syndrome is driven by excess carbohydrate intake¹² (see here and here and here), and it is reversible by carbohydrate restriction (not caloric restriction), it follows that migraineurs recover from their migraines because they are able to reverse their genetic predispositions to carbohydrate intolerance and glucose sensitivity.

Since migraineurs are carbohydrate intolerant and glucose sensitive, they end up with metabolic syndrome if they continue to consume the – for them – offensive substances. This also suggests that each migraineur should be scrutinized by medical professionals to eliminate all opportunities for the development of metabolic syndrome by educating them to remove carbohydrates from their diet.

Support Hormones Matter

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Additional Sources

1 Bhoi, S., Kalita, J. & Misra, U. Metabolic syndrome and insulin resistance in migraine. The Journal of Headache and Pain 13, 321-326, doi:10.1007/s10194-012-0416-y (2012).

2 Casucci, G., Villani, V., Cologno, D. & D’Onofrio, F. Migraine and metabolism. Neurological Sciences 33, 81-85, doi:10.1007/s10072-012-1047-4 (2012).

3 Fava, A. et al. Chronic migraine in women is associated with insulin resistance: a cross-sectional study. European Journal of Neurology 21, 267-272, doi:10.1111/ene.12289 (2014).

4 Guldiken, B. et al. Migraine in metabolic syndrome. Neurologist 15, doi:10.1097/NRL.0b013e31817781b6 (2009).

5 Sachdev, A. & Marmura, M. J. Metabolic Syndrome and Migraine. Frontiers in Neurology 3, 161, doi:10.3389/fneur.2012.00161 (2012).

6 Salmasi, M., Amini, L., Javanmard, S. H. & Saadatnia, M. Metabolic syndrome in migraine headache: A case-control study. Journal of Research in Medical Sciences : The Official Journal of Isfahan University of Medical Sciences 19, 13-17 (2014).

7 Shaw, S. W., Johnson, R. H. & Keogh, H. J. Metabolic changes during glucose tolerance tests in migraine attacks. J Neurol Sci 33, 51-59, doi:10.1016/0022-510X(77)90181-2 (1977).

8 Sinclair, A. J. & Matharu, M. Migraine, cerebrovascular disease and the metabolic syndrome. Annals of Indian Academy of Neurology 15, S72-S77, doi:10.4103/0972-2327.100015 (2012).

9 Winsvold, B. S. et al. Migraine, headache and development of metabolic syndrome: An 11-year follow-up in the Nord-Trøndelag Health Study (HUNT). PAIN® 154, 1305-1311, doi:https://doi.org/10.1016/j.pain.2013.04.007 (2013).

10 Atlas, S. A. The Renin-Angiotensin Aldosterone System: Pathophysiological Role and Pharmacologic Inhibition. Journal of Managed Care Pharmacy 13, 9-20, doi:10.18553/jmcp.2007.13.s8-b.9 (2007).

11 Bhoi, S. K., Kalita, J. & Misra, U. K. Metabolic syndrome and insulin resistance in migraine. J Headache Pain 13, doi:10.1007/s10194-012-0416-y (2012).

12 Volek, J. S., Fernandez, M. L., Feinman, R. D. & Phinney, S. D. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 47, doi:10.1016/j.plipres.2008.02.003 (2008).

Migraine Brain as a Survival Advantage: Connecting the Dots with Angela A. Stanton

by Angela A Stanton, PhD

Published on February 1, 2017

7150 views

On February 2^nd, 2017, Thursday morning at 10 am Central time, I will be on ONE RADIO NETWORK (see schedule here). On this talk show I will present my views about the causes of migraines. The talk show invites advance emailed-in questions to email@oneradionetwork.com, as well as live call-ins during the show at: 888.663.6386. Here is the page where you can listen to the archived recording on the Internet (one hour talk show). If you are in Austin, Texas, you can listen on the radio.

Migraine Brain as a Survival Advantage

For a while we have known that the human body contains approximately 20 thousand genes, although this number seems to be a moving target as technology improves. The latest studies have reduced it to 19 thousand. From the 19 thousand, so far 1254 genes have been associated with migraines. Such a huge number of genes – associated with a condition that plagues nearly 30% of the population – begs for an explanation.

Could it be that migraine at one time in human history provided a survival advantage? A benefit that helped those endowed with this set of genes to survive? The answer to this question must be “yes” because the migraine-brain has survived in the population for so long. It has not been bred out of human populations over the millennia of our evolution. Health conditions disadvantageous for survival normally get deleted from our genome.

The question “why migraine hurts” has a simple answer based on this theory: pluck a group of people with a special adaptation from its natural habitat and place it into a different environment, and what was an advantage suddenly becomes a disadvantage. There are many examples for this in nature.

Greenland Inuit, Canadian Inuit and the Native American populations all have glucose (simple sugar into which all carbohydrates, including fruits and vegetables, grains, nuts, seeds, and some percent of proteins convert) intolerance genes. Fructose (a sweet substance that is approximately half of table sugar; found in fruits, vegetables, and syrups like honey, maple syrup, and of course high fructose corn syrup) can also be problematic. Many of us are born without the necessary enzymes to absorb fructose. The inability to digest sugar can cause diarrhea. In medical parlance, this is called “malabsorption” but the question remains: if so many people are born without the ability to absorb sugar, would that be considered a “malabsorption” or is sugar absorption an adaptation that occurred later in time? I am not the first one to ask this question.

Now returning to migraine: it is found in at least as large fraction of the population as it is for the inability to absorb sugars, like glucose or fructose. The set of adaptations for the more sensitized brain to danger (that migraineurs today still possess) at one time may have been present in all of our predecessors. Some percent of the ancient population likely never lost this highly sensitized brain adaptation because in the ancient environment it would have provided a survival benefit. However, in our modern life, the highly sensitized brain has become a painful burden, whereas a large percent of the population adapted to modern life, reduced their brain sensitivity and they feel no pain. This is likely similar to how the majority of the population adapted to digest and absorb sugar; only a minority retained their inability to do so, and they still experience painful health conditions as a result.

The cause of migraines is not the pain—the pain is one of many symptoms. Just like medicating children to be able to eat an ice cream makes little sense, so is medicating migraine pain by blocking certain brain functions makes little sense. That is the only thing that the medicines are able to do and they are dished out to migraineurs like candy. Here are three of the most common (and most dangerous) medications given to migraineurs as “preventive” and what they block: Propranolol (blocks cardiac and neuronal voltage-gated sodium channels), Topamax (blocks voltage gated calcium and sodium channels), Amitriptyline (blocks or initiates many channels out of sync, causing major heart damage and sometimes death). Would we put ourselves at these types of risks in order to be able to eat a piece of sugar if we lacked the enzymes to digest them? I think the real problem is the lack of understanding of the true nature of migraines.

Migraines and Salt

Migraine starts with prodromes that are signals of an impending migraine. These prodromes precede a cascade of events that lead to the pain, which starts with the initiation of an alarm status that leads to fight-or-flight from danger. A migraineur can easily be triggered into a migraine by noise, odor, a specific light intensity, and even taste that is above or below the norm. Migraineurs have hyper sensory organ sensitivities (1), more sensory neuronal connections than the norm (2), and this is how perfume can trigger a migraine because that scent is above the norm. A migraineur will start a migraine unless voltage is re-established. Why voltage? Migraineurs use more voltage (3, 4) as a result of the more sensitive sensory organs. Voltage is generated by the sodium/potassium pumps that are located in cell membranes, facilitating voltage differential exchanges between the inside and the outside of the cell. Since more voltage use requires more salt, migraineurs need to consume more salt (sodium chloride). Migraineurs tend to pass more sodium in their urine as a result (5).

The modern Western diet is forever reducing its salt recommendation for the general population, ignoring that a large percent of that population needs more salt than what is recommended. In general, I found that migraineurs need approximately 50% more salt in their diet than non-migraineurs.

Migraines and Sugar

Another factor is sugar. While there is no academic research on migraineurs lacking enzyme to absorb fructose or that they are genetically lacking glucose absorption (although there are many research papers hinting at their possibilities–here is a review of some), it seems, based on the several thousand migraineurs I studied, that migraineurs are either sugar intolerant or are hyper sensitive to sugar—and all forms of carbohydrates. Indeed, migraineurs usually become insulin resistant. It would be quite educational to provide genetic testing to all migraineurs to find out what may drive their intense reaction to carbohydrates. Most migraineurs can completely prevent all migraines by completely avoiding refined carbohydrates, reducing complex carbohydrates to near the low carbs high fat (LCHF) diet levels, and increasing dietary animal fats (not oils).

Myelin is made from fat and cholesterol; it is the white matter in the brain, responsible for insulating the neurons’ axons, the parts that transmit voltage. Since migraineurs transmit voltage more often, their myelin is more likely to get damaged. Glucose seems to aggravate nerves in general in all central nervous systems conditions. The ketogenic (high fat, very low carbohydrate) diet may be ideal for migraineurs since it appears to repair the myelin damage glucose causes. Myelin can be replenished by eating a proper, high in natural fat (not man-made oils) diet and by ensuring that a migraineur retains a healthy insulin response. As expected, migraine is highly correlated with the incidence of insulin resistance (6-8), diabetes mellitus (7), obesity (9), and cardiovascular disease (10).

If migraine were a true disease, dietary changes would not be able to change the brain response in a way that all migraines become preventable and abortable without medications. Since they can be prevented and aborted with the proper migraine-brain diet (an ancient type diet that is void of simple sugars and complex carbohydrates in excess), it follows that migraine is an unintended consequence of the modern Western diet and it is not a disease.

Sources:

Schwedt TJ (2013) Multisensory Integration in Migraine. Curr Opin Neurol:248-253.
Tso AR, Trujillo A, Guo CC, Goadsby PJ, & Seeley WW (2015) The anterior insula shows heightened interictal intrinsic connectivity in migraine without aura. Neurology:1043-1050.
Liu H, et al. (2015) Resting state brain activity in patients with migraine: a magnetoencephalography study. in The Journal of headache and Pain, pp 16-42.
Tessitore A, et al. (2015) Abnormal Connectivity Within Executive Resting-State Network in Migraine With Aura. Headache 55(6):794-805.
Campbell DA, Tonks EM, & Hay KM (1951) An Investigation of the Salt and Water Balance in Migraine. British Medical Journal:1424-1429.
Bhoi S, Kalita J, & Misra U (2012) Metabolic syndrome and insulin resistance in migraine. The Journal of Headache and Pain 13(4):321-326.
Guldiken B, et al. (2009) Migraine in Metabolic Syndrome. The Neurologist 15(2):55-58.
Sachdev A & Marmura MJ (2012) Metabolic Syndrome and Migraine. Frontiers in Neurology 3:161.
Bigal ME, Liberman JN, & Lipton RB (2006) Obesity and migraine: a population study. Neurology 66.
Tana C, et al. (2013) New insights into the cardiovascular risk of migraine and the role of white matter hyperintensities: is gold all that glitters? The Journal of Headache and Pain 14(1):9.

We need your help.

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Triptans ± SSRIs ± Migraines ± Depression: Flip a Coin!

by Angela A Stanton, PhD

Published on October 12, 2015

8391 views

Migraines and depression are understood to be neurological diseases though many consider them to be mental illnesses [1, 2]. Recent research sheds light on both conditions and shows us how much they have in common. Both migraines and depression can be stopped by voltage applied to the brain. In the case of depression, voltage has only been applied via open-brain surgical procedures as deep brain stimulation of the specific brain region, shown in the scanner as dark region [3-6]. For migraines the stimulation has been tried both outside of the brain [7, 8] and internally via deep brain electrical stimulation [9]. The cause inn both migraine and depression is seen in scanners [1, 10] as cortically depressed areas. These are dormant regions that have no observable electrical activity. When electrical stimulation is applied to a dormant brain region, it regains its function. Crucially for migraines, it has been demonstrated that a dormant area be shocked by a wave of electricity generated by the brain itself, called cortical spreading depression, energizing the dormant area to be able to create action potential again [11-14]. This is quite similar to a cardiac arrest patient receiving an electrical shock to the heart which restarts electrical activity. The difference is that in the case of the heart the electricity is applied externally by others, whereas in the case of the brain the electric shock is applied by the brain itself by using its functioning brain regions to energize nonperforming regions. Because neurons communicate to each other via neurotransmitters and are connected to each other, neurons that do not manufacture neurotransmitters and do not participate in communication exchange cannot hide. The healthy, energized regions send a wave of energy within the brain. However, this wave reaches the meninges where all pain sensory neurons are located [14] and hence migraine pain.

Similarly to how a cardiac arrest does not always get the heart to continue beating again, the electric shock of the spreading cortical depression may not awaken the dormant regions either. Energy for proper functioning of either the heart or the brain – or indeed for any living tissue – cannot be created from nothing. To continue to generate voltage after the initial shock, the proper minerals have to be available. One can only drive a car on fumes for so long. Interestingly we understand this very well when it comes to our cars but we tend to forget it when it comes to our body. Our body uses energy it receives from what we eat and drink. The energy is carried to the cells by electrolytes. Electrolytes are water mixed with vital nutrients. Electrolytes take up 55%-70% of our body per gender and age with salt about 9 grams per liter. Those brain regions that lack important nutrients will not function.

We now understand that brain regions that are starved of energy and that are not able to generate action potential cause abnormal synaptic transmissions [15, 16]. Yet rather than replenishing the brain by restocking it with nutrients, the current favorite treatment method is some form of serotonin medicine, such as triptans for aborting an ongoing migraine, or serotonin reuptake inhibitors (SSRIs or SNRIs) for prevention for both migraines and depression. Many unlucky migraineurs and depression patients also receive a voltage dependent calcium channel blocker, one of which I discussed in my last article. Given that these medications are so often prescribed, one would think that they actually work. But do they?

They actually don’t work for depression over 70% of the time. And for migraines? Well, that is another story as I am about to discuss. It is also important to note that where energy is needed, medicines that block energization via electrolytes actually work against recovery and dull the brain, using symptom management instead.

Why Triptans and SSRIs/SNRIs are Hit or Miss for Migraines

Serotonin for migraines only works sometimes and even then with tremendous side effects, often causing depression (see adverse reaction tables below), violence, and fatalities. Based on my migraine group where thousands of migraineurs have passed through over the years, the statistics show that 80% of those who join the group take some serotonin preventive, usually an SSRI or SNRI but they still need to take abortives, such as triptans, and yet they still have migraines! Not only does this show that serotonin does not work but also that there is a very dangerous practice of “more is better,” which may be followed by fatal consequences, such as serotonin syndrome. The dangerous practice is common because of five critical reasons:

Doctors should know better than to prescribe multiple serotonin medications to the same patient and if they don’t know what their patients take, they owe the courtesy to ask before they prescribe!
Pharmacies have records of all medicines a patient takes. If a doctor makes a mistake, it is the responsibility of the pharmacist to catch the mistake and warn the doctor and the patient. This has never happened in the entire history of my migraine group! I usually analyze their medicines and point out the pharmacological interactions and duplication that they print out and hand to their doctors. Only after the patient’s intervention will doctors initiate removal of dangerous medicines. Last time I checked: The patients are not responsible for the medicines they are being prescribed.
85% of the doctors do not recognize serotonin syndrome. The sad truth is that while 100% of the doctors can prescribe SSRIs and similar medications with a few scribbles, 85% of them do not recognize if it reaches toxic levels in their patients. I estimate that the majority of doctors are not familiar with the mechanisms of the medicines they prescribe; they cannot tell if one is a voltage dependent calcium channel blocker or a voltage dependent sodium channel blocker or both or neither.
This is the saddest of them all: financial incentives actually cause many doctors to be angry with patients who wish to reduce their medicines. Many members in my migraine group faced rude and angry doctors who placed them on such quick reduction from these highly “discontinuations syndrome” (politically correct for addictive) medicines that they were forced back on the medicines and of course that increased again the lunches and dinners or straight cash flow of the prescribing doctors—search out your doctor’s name and see what she/he has been earning on your medicines in 2014!
The side effects of many of these serotonin medicines are worse than the initial problem they are prescribed for; reduction is slow and painful. While the adverse effects hit all at once when starting a medicine, the very same adverse effects return in slow motion as the patients reduce. For example, they may not even realize that they had increased blood pressure, nausea, dizziness, and diarrhea all at once for a few days or weeks while starting the medication since these adverse effects showed up at once. But in reversing and stopping the medicine, each of these effects can last for weeks and is highly pronounced, frightening the patient. Furthermore, adverse effects are updated on the go by the FDA. Most users are not informed about these by their prescribing physicians.

I randomly picked two very common medications I see prescribed all the time. Zoloft, used for depression, is a selective serotonin reuptake inhibitor (SSRI), and Elavil, a tricyclic antidepressant (TCA), prescribed for migraines frequently. The list of side effects for Zoloft (Sertraline) is huge (Wikipedia). I must say that if I were not depressed before taking this medicine, I most certainly would be after reading this list:

Adverse effects: Fatigue, Insomnia, Somnolence (sleepiness), Nausea, Dry mouth, Diarrhea, Headache, Ejaculation disorder, Dizziness, Agitation, Anorexia, Constipation, Dyspepsia (indigestion), Decreased libido, Sweating, Tremor, Vomiting, Impaired concentration, Nervousness, Paroniria (i.e., depraved or morbid dreaming/nightmares), Yawning, Palpitations, Increased sweating, Hot flushes, Weight decrease, Weight increase, Myoclonus, Hypertonia, Bruxism (teeth grinding), Hypoesthesia, Menstrual irregularities, Sexual dysfunction, Rash, Vision abnormal, Asthenia, Chest pain, Paranesthesia, Tinnitus (hearing ringing in the ears), Hypertension (high blood pressure), Hyperkinesia, Bronchospasm, Esophagitis (swollen esophagus), Dysphagia, Hemorrhoids, Periorbital Edema, Purpura, Cold Sweat, Dry skin, Nocturia, Urinary Retention, Polyuria (excessive urination), Vaginal Hemorrhage, Malaise, Chills, Pyrexia (fever), Thirst, Pollakiuria, Micturition disorder, Salivary Hypersecretion, Tongue Disorder, Osteoarthritis, Muscular Weakness, Back Pain, Muscle Twitching, Eructation (belching), Dyspnea (air hunger), Epistaxis (nose bleed), Edema peripheral, Periorbital edema, Syncope, Postural dizziness, Tachycardia (high heart rate), Urticaria (hives), Migraine, Abnormal bleeding (esp. in the GI tract), Muscle cramps, Arthralgia, Depressive symptoms, Euphoria, Hallucination, Alopecia (hair loss), Urinary Retention (being unable to pass urine), Pruritus, Amnesia memory loss., Urinary incontinence, Eye pain, Asymptomatic elevations in serum transaminases, Abnormal semen, Melena (black feces due to a bleed in the stomach), Coffee ground vomiting, Hematochezia, Stomatitis (swollen mouth), Tongue ulceration, Tooth Disorder, Glossitis (soreness/swelling of the tongue), Mouth Ulceration, Laryngospasm, Hyperventilation (breathing more often than required to keep one’s blood sufficiently oxygenated), Hypoventilation (breathing less often than required to keep one’s blood sufficiently oxygenated), Stridor, Dysphonia (voice disorder), Upper Respiratory Tract Infection, Rhinitis (irritation/inflammation inside the nose), Hiccups, Apathy, Thinking Abnormal, Allergic reaction, Allergy, Anaphylactoid reaction, Face edema, Priapism, Atrial arrhythmia, AV block, Coma, Peripheral Ischemia, Injury, Vasodilation Procedure, Lymphadenopathy, Involuntary muscle contractions, Galactorrhea (lactation that is unrelated to pregnancy or breastfeeding), Gynecomastia (swelling of breast tissue in men), Hyperprolactinemia (high blood prolactin levels), Hypothyroidism (underactive thyroid gland), Syndrome of inappropriate secretion of antidiuretic hormone (SIADH), Pancreatitis (swollen pancreas), Altered platelet function, Hematuria (blood in the urine), Leukopenia (low white blood cell count), Thrombocytopenia (low blood platelet count), Increased coagulation times, Abnormal clinical laboratory results, Hyponatremia (low blood sodium), Conversion Disorder, Drug Dependence, Paranoia, Myocardial Infarction (heart attack), Bradycardia, Cardiac Disorder, Suicidal Ideation/behavior, Sleep Walking, Premature Ejaculation, Hyperglycemia (high blood sugar), Hypoglycemia (low blood sugar), Hypercholesterolemia (high blood cholesterol), Vasculitis, Aggressive reaction, Psychosis (hallucinations and delusions), Mania (a dangerously elated mood), Menorrhagia (an abnormally excessive amount of menstrual bleeding), Atrophic Vulvovaginitis, Balanoposthitis, Genital Discharge, Angioedema, Photosensitivity skin reaction, Enuresis, Visual field defect, Abnormal liver function, Dermatitis, Dermatitis Bullous, Rash Follicular, Glaucoma, Lacrimal Disorder, Scotoma, Diplopia, Photophobia, Hyphemia, Mydriasis, Hair Texture Abnormal, Neoplasm, Diverticulitis, Choreoathetosis, Dyskinesia, Hyperesthesia, Sensory Disturbance, Gastroenteritis, Otitis Media, Skin Odour Abnormal, QTc prolongation, Anaphylactoid Reaction, Allergic Reaction, Allergy, Neuroleptic malignant syndrome. A potentially fatal reaction that most often occurs as a result of the use of antipsychotic drugs. It is characterized by fever, muscle rigidity, rhabdomyolysis (muscle breakdown), profuse sweating, tachycardia, tachypnoea (rapid breathing), agitation, Stevens-Johnson syndrome a potentially fatal skin reaction, Toxic epidermal necrolysis another potentially fatal skin reaction, Torsades de pointes a potentially fatal change in the heart’s rhythm., Cerebrovascular spasm, Serotonin syndrome similar to neuroleptic malignant syndrome but develops more rapidly (over a period of hours instead of days/weeks for neuroleptic malignant syndrome), Bone fracture, Movement disorders, Diabetes mellitus, Dyspnea, Jaundice yellowing of the skin, mucous membranes and eyes due to an impaired ability of the liver to clear the haem breakdown by product, bilirubin, Hepatitis, Liver failure. This medicine can cause serotonin syndrome on its own.

For migraine I picked Elavil (Amitriptyline) which is a TCA. While it has fewer side effects (Wikipedia) than Sertraline (SSRI), one of its major side effects is headache. Why would a competent doctor prescribe a known headache causer to a migraineur?

Here are some of the other adverse effects: dizziness, headache, weight gain, delirium, confusion, anxiety, agitation, orthostatic hypotension (low blood pressure), sinus tachycardia, loss of libido, impotence, sleep disturbances such as drowsiness and insomnia. Most importantly, Amitriptyline inhibits sodium channels, L-type calcium channels, and voltage-gated potassium channels, and therefore acts as a sodium, calcium, and potassium channel blocker as well.

Recall my argument of a car only able to go on fumes for so long? This drug, by blocking all possible energizing channels, blocks the inflow of nutrients and the outflow of toxins. This car is not going anywhere!

Yet many migraineurs who join my group have been taking Elavil, which of course doesn’t work, so then they end up having to take several other medicines to replace activities the brain cannot do: they often receive prescriptions for other types of SSRIs, sometimes voltage dependent calcium blockers, barbiturates, NSADs, muscle relaxers, steroids and even triptans to come full circle, and add the very ingredient they blocked from being released the first place!

Does Serotonin Use Make Any Sense At All?

When a brain region is not able to generate action potential, as shown, lack of serotonin is not the cause. It is entirely possible that the particular neurons that cannot generate enough energy happen to be responsible for serotonin production, in which case adding serotonin will indeed take the pain away. However, it will not treat the underlying cause of not having enough energy for generating action potential. The fact that it is energy shortage rather than serotonin shortage that causes depression is clearly demonstrated by the deep brain stimulation experiments on live humans, where the voltage stimulation lifted their depression right there during the experiment without any serotonin. The patients were able to explain what they felt and how their depression lifted during the procedure [4-6, 17]. It all sounds very simple actually since we know what generates action potential in the brain: salt.

So why do migraine and depression sufferers keep on getting serotonin medications knowing that serotonin has absolutely nothing to do with migraines? This is a great question that I would like to ask many physicians! Habits are hard to break but eventually they must!

Concluding Thoughts

There is only a small chance that triptans or SSRIs will work for your migraines or depression but it is 100% certain that adverse effects will prevent your brain from working properly. In the long run, these drugs cause permanent damage. Do yourself a favor and learn what migraines are and how to prevent them. Since migraines and depression have the same cause as seen in the scanners, why not try the same solution? Many who joined my migraine group with depression and migraine are now free of both, as well as all their medicines! Join the movement for healthy life without medicines.

Sources

Gasparini, C.F., H.G. Sutherland, and L.R. Griffiths, Studies on the Pathophysiology and Genetic Basis of Migraine. Current Genomics, 2013. 14(5): p. 300-315.
Young, W.B., et al., The Stigma of Migraine. PLoS ONE, 2013. 8(1): p. e54074.
Holtzheimer, P.E., et al., Subcallosal Cingulate Deep Brain Stimulation for Treatment-Resistant Unipolar and Bipolar Depression. Jama Psychiatry, 2012: p. 150-158.
Lozano, A.M., et al., A multicenter pilot study of subcallosal cingulate area deep brain stimulation for treatment-resistant depression. J Neurosurg, 2012: p. 315-322.
Mayberg, H.S., et al., Deep brain stimulation for treatment-resistant depression, in Neuron. 2005. p. 651-60.
Taghva, A.S., D.A. Malone, and A.R. Rezai, Deep brain stimulation for treatment-resistant depression. World Neurosurg., 2013: p. 826-831.
Aurora, S.K., et al., Transcranial magnetic stimulation confirms hyperexcitability of occipital cortex in migraine, in Neurology. 1998. p. 1111-4.
DaSilva, A.F., et al., tDCS-Induced Analgesia and Electrical Fields in Pain-Related Neural Networks in Chronic Migraine. Headache: The Journal of Head and Face Pain, 2012. 52(8): p. 1283-1295.
Tepper, S.J., et al., Acute Treatment of Intractable Migraine With Sphenopalatine Ganglion Electrical Stimulation. Headache: The Journal of Head and Face Pain, 2009. 49(7): p. 983-989.
Hadjikhani, N., et al., Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proceedings of the National Academy of Sciences, 2001. 98(8): p. 4687-4692.
Charles, A.C. and S.M. Baca, Cortical spreading depression and migraine. Nat Rev Neurol, 2013: p. 637-44.
James, M.F., et al., Cortical spreading depression and migraine: new insights from imaging? TRENDS In Neuroscience, 2001: p. 226-271.
Lauritzen, et al., Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury, in J Cereb Blood Flow Metab. 2011. p. 17-35.
Bolay, H., et al., Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med, 2002. 8(2): p. 136-142.
Pietrobon, D., Insights into migraine mechanisms and Ca(V)2.1 calcium channel function from mouse models of familial hemiplegic migraine. The Journal of Physiology, 2010. 588(Pt 11): p. 1871-1878.
Vecchia, D., et al., Abnormal cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans. Front. Cell. Neurosci., 2015: p. epub ahead of print.
Lozano, M. and N. Lipsman, Probing and regulating dysfunctional circuits using deep brain stimulation, in Neuron. 2013. p. 406-24.

Migraines and Hormones: Behind the Curtain

by Angela A Stanton, PhD

Published on December 15, 2014

10778 views

Before puberty, migraines are three times more frequent in males than in females but after puberty the tides turn and females are more likely to suffer from migraines than males. An Oxford study found that females are twice as likely to have migraines and that

“brains are deferentially affected by migraine in females compared with males. Furthermore, the results also support the notion that sex differences involve both brain structure as well as functional circuits, in that emotional circuitry compared with sensory processing appears involved to a greater degree in female than male migraineurs.”

The overwhelming belief is that the connection is clear: the hormones kick in for women at puberty and that must be the reason. This begs the questions: 1) Do males have the same hormonal problems before puberty as females do after puberty? If hormones are at root of the problems, then there must be some similarities, right? 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? 3) Do migraines cease when hormones stop changing after menopause? 4) What about pregnancy or postpartum, how do hormones impact women then? And finally, 5) Do men stop having migraines after puberty?

Some of the answers to these questions will surprise you and may make you wonder if hormones have anything to do with migraines at all. In this post, I show you that while there are some connections between hormones and migraine they might not be the primary drivers of migraine. The relationship between hormones and migraine is not in the presence of hormonal changes but what those changes require in terms of brain energy, the lack of which causes migraines.

First, I would like to respond in quick the five questions I asked earlier: 1) Do males have the same hormonal problems before puberty as females do after puberty that causes them migraines? The answer to this is no. 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? The answer to this also is no. 3) Do migraines stop after menopause? Many women have more migraines and some even start migraines in their menopause, so the answer is no. 4) Do migraine increase or decrease during pregnancy or postpartum? The answer is no during pregnancy, but yes postpartum. 5) Do men stop having migraines after puberty? No they do not.

It is not obvious that the cause of migraines must have anything to do with female monthly cycles and their associated hormones. Given also that many women have migraines after puberty, we are safe to assume that some other factors may play a role. It would be hard to envision a world full of children in which our evolutionary road took women to necessarily experience migraines with their menstrual cycles. So what is the connection to hormones; how do women end up with migraines; and why?

Rather than listing all the hormones that activate throughout the monthly cycle of a woman, let’s take a look at what is happening in the body of that woman backstage, during the hormonal changes. First, in a small review I cover in a few sentences what a migraine is.

Migraine is a collection of symptoms that have an underlying physiological mechanism based on chemical (ionic) imbalance in the brain. Migraine is a neurovascular event that Dr. Charles at UCLA called “spectacular neuro-physiological event” that changes the neurophysiology or chemistry of the brain itself. This can be seen using fMRI technology where oxygenation of brain regions shows where activity occurs during migraine—albeit this does not show why it occurs. The same article also suggests that though medications are available to treat the pain associated with migraines, half the sufferers do not receive any pain relief benefit from the drugs. I find this statement alone interesting because if migraine was truly understood, the pain medication would work for all. This clearly is not the case. To understand what is happening, we must think out of the box and leave behind the hormonal theory of migraines.

Moving Beyond the Hormone Migraine Theory

We now visit the female body all through a month. Let’s start two days after her menstrual cycle has ended. As female, we feel great, no pain, no bleeding, life is awesome. But what we don’t see works hard in the background using up important energy: the brain. Our hormonal changes are happening every moment of the day only we don’t feel it—hormonal changes are directed by the brain. Because we don’t feel the changes, we are ill-prepared for the inevitable day when it reaches a threshold point of not enough brain energy and the migraine starts. This typically happens 2-4 days prior to menses. I do not think migraines are caused by hormones, but rather they are triggered by the lack of energy available to the brain as the hormones cycle. When the brain runs out of energy, a wave of cortical depression begins in some part of the brain. This is what we feel as a migraine.

What actually happens that uses all that energy? After the menstrual cycle is over, the female body immediately prepares for the next menstrual cycle. There is no downtime for rest. The brain turns off one group of hormones and turns on others thereby manipulating how women see the world prior to and during estrus (fertile time). After a menstrual cycle is over, the brain turns on the estrogen to do a few things:

Prepare the uterus with a new fertile lining to accept the fertilized egg should one arrive and start a new life.
In order to make such fertilized egg happen, the egg must be prepared in the ovaries so hormones initiate the ripening of a new egg.
The woman’s body goes through amazing visible changes at this time of the month. If she had pimples, they magically disappear. If she was bloated, her bloating goes away. Her face becomes the most symmetrical it possibly can; the more symmetrical the more sexually appealing she becomes to the opposite sex.
She becomes extremely attracted to high testosterone males requiring her pheromones to change and to be able to sense a high testosterone pheromone male’s presence. This high testosterone attraction changes after estrus to attraction to low testosterone males for the safety of the child, should mating end in a baby.

With all this activity going on in the female body that she cannot feel, she is in danger of exceeding the threshold of brain energy-shortage without prior notice or preparation. The cost of all of these activities behind the curtains in the female body is very high in terms of brain energy and hydration. These are sex-hormonal functions that only exist for a certain period of time during the female life. Females are known to be born with all of their eggs they will ever ripen for possible babies. Only these eggs are not “ripe” at birth. Every month one egg ripens in one of two ovaries (sometimes in both and sometimes in none). This egg breaks out of the ovary and starts its journey down the ovarian tube where it either gets fertilized by a sperm or not. If the egg is fertilized, it attaches to the wall of the uterus lining—later to become the placenta of the baby—and a new life cycle begins in the mother-to-be. If however there is no sperm able to penetrate the egg, while it descends in the ovarian tube, the egg will have to be cleared from the uterus together with the nutritious blood vessel rich lining created. This happens with the menstrual bleeding. This we can see and feel.

My Theory: Why Hormone Changes are not the Cause of Migraines

As shown earlier, migraines are not equally present in everyone’s life. Other factors, such as genetic predisposition to sensory organ hyper sensitivities (SOHS) that require more energy, may be the cause. Recent research hints at ionic balance (meaning energy available for use) is crucial in maintaining optimal function and the slightest imbalance can cause major problems (Wei et al.).

When the body is tasked with demanding activities the cells responsible for completing those extra tasks are doing extra chores and need extra energy. The brain regulates the creation of extra hormones for the menstrual cycle. The brain manages the clearing of the uterus after the fertile layer was not used.

By the third day after the cycle, the brain is ordering an egg to ripen—this takes extra energy. This is a once a month event. The brain must have extra energy to complete this task. Ever tried to run a marathon on empty or run your car the extra mile without fuel in your tank? Not possible. Something must break. The brain is the logical one for those who are predisposed to SOHS. If their brain runs out of energy, the neurons cannot generate voltage and stop creating neurotransmitters that instruct the production of hormones in the body. This leads to cortical depression and migraine.

Migraine during Pregnancy

Hands up: how many of you had migraines during pregnancy? Up to 75% of migraineurs do not have migraines during pregnancy. Why you may ask? There is more than one reason for this. The first and most important reason is that while the mom-to-be is pregnant, she has no menstrual cycles so the brain has no monthly cyclical job and it need not use extra energy. Even if the pregnancy comes with a menstrual flow here and there—as it sometimes happens—there is no egg that ripens and there is no uterus layer to remove. It is only a bit of bleeding but no extra energy was needed by the brain for this menstrual flow.

The second important factor is that during pregnancy the mom-to-be seems is more cognizant of what her and her baby-to-be needs. She eat more, tends to eat what she craves and is less likely to be good-looking-body conscious during this time. Pickles with ice cream are famous cravings of women. All the nutrients the brain craves for re-creating energy and feed the brain to prevent migraines: salt, calcium, magnesium, and fat that converts to sugar in the brain.

Migraine during Postpartum

After giving birth nearly, nearly all women immediately revert to eating for a good looking body, lose all the baby fat, and get back into the size zero genes. They stop eating brain-healthy after pregnancy (they never realized they ate brain healthy the first place). Nearly all women return to their migraines postpartum as they return to their old dietary habits.

Post-Menopausal and Menopausal Migraines

We are often told that after we enter menopause or are post-menopausal, our migraines will disappear. Yet, I talk to many women, who have more migraines after their fertile period of life has passed. I am one of those women who experienced more migraines in menopause than in early life. Thus, being no longer fertile, no longer ‘hormonal’ does not mean that we become migraine free; further pointing to the lack of connection of migraines to hormonal fluctuations. In menopause, many women are still very body conscious and watch their dress size more than their health. Others, however, recognize the value of a body supporting diet that may not create a body to fit into such small jeans but may be healthier for an older woman. This second group probably stops experiencing migraines (like I did) whereas the first group remains dehydrated and lacks brain nutrition to work those SOHS brains. They end up continuing their migraines as they had them before.

Of course, we already know from my previous posts that migraines are genetic so not everyone abusing her body will end up as migraineur. To be migraine free, everyone, male or female, must follow the rules of brain fuel.

Fuel for Migraines (Hormonal or Not)

What exactly is the fuel for migraines of any kind? I am leading you back to the first post on migraine that tells you what nutrition the brain needs to return to energy and fuel-filled comfortable homeostasis. The brain works on electricity, which requires specific charge differences inside and outside the cell’s membrane. This voltage is created by salt (sodium and chloride) in ample supply. Sodium also retains water inside the cells for hydrations and opens the sodium-potassium gate to allow nutritional exchange. I am also linking you back to the second post on migraines that explains the anatomy of migraines and what actually happens when the brain in not in homeostasis. How a migraine starts is now visible in fMRI. If you follow the posts I linked to and read the book on how to prevent and fight migraines, chances are, you may never have to face another migraine in your life.

Sources:

Fighting the Migraine Epidemic; A complete Guide. An Insider’s View by Angela A. Stanton, Ph.D. Authorhouse, February 2014. https://www.amazon.com/Fighting-Migraine-Epidemic-Complete-Migraines/dp/154697637X/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=1518636023&sr=8-1
Why Women Suffer More Migraines Than Men by Patty Neighmond, NOR April 16, 2012 3:17 AM ET http://www.npr.org/blogs/health/2012/04/16/150525391/why-women-suffer-more-migraines-than-men
Her versus his migraine: multiple sex differences in brain function and structure by Maleki et al. BRAIN. 2012: 135; 2546–2559, http://brain.oxfordjournals.org/content/brain/135/8/2546.full.pdf
Hormones & desire Hormones associated with the menstrual cycle appear to drive sexual attraction more than we know. American Psychological Association By Bridget Murray Law. March 2011, Vol 42, No. 3 Print version: page 44 http://www.apa.org/monitor/2011/03/hormones.aspx
Human Oestrus by Steven W Gangestad, Randy Thornhill. The Royal Society, Proceedings B May 2008 http://rspb.royalsocietypublishing.org/content/275/1638/991
Ovulating Women are STRIPPING Men of their Money. Cal Poly Bio 502 class lecture notes article. A blog about human evolution, economics, and sexual physiology. Why do strippers make more money at different times of the month? By Hayley Chilton http://physiologizing.blogspot.com/2013/01/ovulating-women-are-stripping-men-of.html
Migraine and Children. Migraine Research Foundation http://www.migraineresearchfoundation.org/Migraine%20in%20Children.html
Prevalence and Burden of Migraine in the United States: Data From the American Migraine Study II; Richard B. Lipton, MD; Walter F. Stewart, MPH, PhD; Seymour Diamond, MD; Merle L. Diamond, MD; Michael Reed, PhD. Journal Headache; 646:657
Population-based survey in 2,600 women. Karli et al., The Journal of Headache and Pain October 2012, Volume 13, Issue 7, pp 557-565 http://link.springer.com/article/10.1007%2Fs10194-012-0475-0
Multisensory Integration in Migraine Todd J. Schwedt, MD, MSCI. Curr Opin Neurol. Jun 2013; 26(3): 248–253
Unification of Neuronal Spikes, Seizures, and Spreading Depression. Wei et al., The Journal of Neuroscience, August 27, 2014 • 34(35):11733–11743 • 11733

The Anatomy of a Migraine

by Angela A Stanton, PhD

Published on November 17, 2014

12789 views

What is the anatomy of a migraine? Do migraines have an anatomy, a location map, in the same way heart disease does? Sure, migraine happens in the brain and we feel the pain in our head if there is pain – not all migraines come with pain, but does the pain guide us to a causative anatomy of the migraine the same way a heart attack does to the heart? No, it does not; at least not in the same way a blocked artery points to the cause of heart attack. The symptoms of migraines correspond to no specific regions of the brain, except in the case of the aura migraine, which points at the visual cortex. Only about 15% of those with migraines have auras. For 85% of the cases, we do not have the anatomical location of the migraine understood. Most science seems to consider aura and non-aura migraine different in nature and cause. Are they? Maybe not.

Most migraines are not connected to the symptoms we feel (nausea, dizziness, IBS, RLS, anxiety, nausea, vomit, etc.) and because of the variety of symptoms, there is nothing to guide us, such as a scan of the arteries for heart or a stroke. Another contributing factor is that there are no pain sensing nerves in the brain. All pain is felt by the trigeminal neuron receptors that are located on the meninges of the brain. That is, the pain we feel as migraineurs is disconnected from the actual location that causes migraines. To find the anatomy of a migraine, we need to go beyond the symptoms and the pain of the disease, beyond the visible disturbance of the eye in the aura, to the underlying cause for these symptoms.

For much of recent history, migraine research has revolved around two discrete theories of migraines: vascular and non-vascular mental illness. The two schools of thought were merged into what is now called neurovascular disease. But the latest findings suggest that there is more to migraines than neurovascular disease.

Migraine as Vascular Disease

For much of the 20^th century, migraine was considered to be a vascular disease. This meant that migraine pain was caused by cranial blood vessel dilation or constriction. Still today we can see many over-the-counter migraine drugs that constrict blood vessels with caffeine in order to constrict the vascular structure of the brain (and the heart and the rest of our body). Alternatively, many doctors still prescribe beta blockers that reduce blood pressure and loosen arteries for easier blood flow and reduced constriction. If migraine is a disease of vascular nature, what causes the cranial vasodilation changes, particularly if these changes do not affect the heart or other parts of the body? This is the first clue that migraines are something more than just vascular in nature.

Migraine as Non-Vascular Mental Illness

The second prominent theory in migraine research attributes migraine pain to alterations in neurotransmitters, specifically, serotonin. Research is confusing on whether migraineurs have less or more serotonin than non-migraineurs. The possible serotonin connection brought us the many prescription drugs containing, increasing, or decreasing serotonin in the brain (triptans, SSRIs and others). Today, most migraineurs receive at least one serotonin enhancing drug; some I know receive serotonin blocking drug but that represents the minority. I was one of the millions of migraine patients who received serotonin enhancers (triptan) and also one of the millions of migraineurs for whom these medications did not work.

Again, I must ask, if there is a serotonin deficiency or overflow in migraineurs, what causes it? And if it is a deficiency as is proposed to be the case for most migraineurs, isn’t this the same proposed deficiency as in depression? Why then don’t most who are depressed also suffer from migraines or why do those who suffer migraines as a result of lack of serotonin not suffer depression? It is not clear to me that there is any connection between serotonin and migraine since most migraineurs I know are not at all depressed and most depressed do not have migraines. This tells me that something is not right with the concept of identical treatments for such two completely different illnesses.

Serotonin is created by a normally functioning brain. Why it is deficient, or in some cases, elevated in the brain of migraineurs has always puzzled me. It still puzzles me that others didn’t ask why neurons cannot produce the right amount of serotonin on their own or why physicians so easily prescribed drugs to add or enhance what the brain was not making. Should we not find out why the neurons are not producing serotonin in the first place? Wouldn’t this help us better treat and maybe even cure migraines?

Migraine and New Research

The most recent theory about migraines involves the aberrant electrical discharges associated with migraine and a phenomenon called cortical spreading depression:

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. (Lauritzen et al., J Cereb Blood Flow Metab)

Researchers have linked CSD to the eminent onset of migraine pain. Such a rapid change in brain ion homeostasis can affect changes in neurotransmitter concentrations, causing cranial vascular dilation and ionic imbalance with depolarized regions. These changes can evoke what migraineurs sense as pain but one has to ask by what mechanisms are these ionic brain changes initiated and by what pathways do they elicit the pain. For the first question, let us return to the concept of neural dehydration and salt deficiencies as possible instigators.

A Unified Theory of Migraine Pain

A new report shows migraines, seizures and strokes are all about ion (sodium, potassium, chloride, magnesium, and oxygen) homeostasis. These particular models looked at how changing potassium ion concentration affects brain activity and how seizures and migraines have similar underlying mechanisms. Potassium’s job is to work both inside and outside of the neurons helping to balance homeostasis by ensuring that potassium ions are in the correct place all the time. Potassium is a diuretic substance and helps in the removal of excess or used water from the cell. If there are too many potassium ions inside or outside of a neuron, with all else remaining constant, the neuron will end up dehydrated because of the osmotic gradient.

The overabundance of potassium and a depletion of both extra-cellular sodium chloride reduces water, and changes the pH balance (acidic level) of the neuron (Costa et al., The Journal of Headache and Pain). Recall from my earlier post: Dehydration and Salt Deficiency Trigger Migraines, that channels on the membrane of the neuron allow for leaks using osmotic gradient to balance the internal and external ionic content. Because ionic homeostasis balance is required for a healthy brain, the ionic balance must be true for all electrolyte elements, including sodium as well. Not enough sodium can cause a potassium overabundance that can trigger migraines because the neuron is not able to generate electricity or retain water.

In Dehydration and Salt Deficiency Trigger Migraines, I talked about the importance of hydration and explained how that works at the cellular level. I introduced the sodium-potassium pumps and their role in keeping the cell hydrated. Through the sodium-potassium pumps sodium ions and potassium ions head in and out of the neuron when proper electric currents are established. For the electric current, the ionic balance of sodium and chloride is essential so that the pumps can open and close. There are also osmotic channels through which leakage of ions may happen depending on higher or lower levels of ions inside versus outside the cell—the osmotic gradient.

The phenomenon of cortical spreading depression is a slow spreading electrical surge corresponding to depolarized regions of migraine initiating locations. It is initiated by ion imbalance where the normal homeostasis has been lost. Here the sodium-potassium pumps do not function properly; the channels leak too much potassium and water, magnesium and oxygen out from the neuron. If these ions cause imbalance, trouble ensues. Even a small, unnecessary increase in potassium outside the cell can lead to seizures and by association to migraines.

It’s All About the Ions

So, beneath the vascular and non-vascular definitions of migraine, the neurotransmitter imbalances and the hyper-excitability of neurons in the certain brain regions associated with migraine, are simple variations in ionic balance, responsible for the onset of migraine and the possibility of vasoconstriction or relaxation changes as a consequence. Too much or too little of one or more ions, evokes changes in brain’s electrical activity that can lead to migraines or seizures. Where in the brain those changes occur determines the type of symptoms a migraineur experiences. For example, with aura migraine the anatomical initiating migraine location is the visual cortex. The migraineur sees the aura with eyes also closed. So what the migraineurs sees is happening inside the brain and not outside. The visual cortex’s function is to translate the light signals it receives into meaningful images of objects. The CSD is an electric storm that the visual cortex interprets as aura. The aura usually starts with a blind spot. It is my belief that the blind spot represents the region of neurons that is the cause of the migraine; the depolarized region that the CSD is trying to activate.

Concluding Remarks

The overall neuron-behavior is very complex but today we can say with a high degree of conviction that:

Migraines are caused by malfunctioning neurons as a result of ion imbalances.
Ion imbalance can be visualized by regions of depolarization.
Depolarized regions demonstrate the anatomy of the disturbance.
Hydration and maintaining proper ionic balance (correcting salt deficiency, magnesium deficiency, potassium excess or deficiency) is important for migraineurs since the slightest ionic imbalance can cause a migraine.

From my perspective, I am glad to see the most recent attempts at understanding physiological problems in the brain behind the migraine. This is a very important shift in migraine research – looking beyond the symptoms for a cause. Nevertheless, I am still looking for answers. How does the ion balance become so disturbed that it initiates a migraine? Why does this happen for some folks and not others? Those are the questions, researchers and clinicians need to address. My theory is that the depolarized regions of the brain result from disturbances in homeostasis and ion balance which are precipitated by dietary deficiencies. We need to determine the proper amounts of each mineral and micronutrient required for the well-functioning brain to reduce migraine.

Sources:

Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury. Martin Lauritzen, Jens Peter Dreier, Martin Fabricius, Jed A Hartings, Rudolf Graf, and Anthony John Strong; J Cereb Blood Flow Metab. Jan 2011; 31(1): 17–35. Published online Nov 3, 2010. doi: 10.1038/jcbfm.2010.191 PMCID: PMC3049472
Cortical spreading depression as a target for anti-migraine agents. Cinzia Costa, Alessandro Tozzi, Innocenzo Rainero, Letizia Maria Cupini, Paolo Calabresi, Cenk Ayata and Paola Sarchielli1; Costa et al. The Journal of Headache and Pain 2013, 14:62
Interpreting fMRI data: maps, modules and dimensions. Hans P. Op de Beeck, Johannes Haushofer & Nancy G. Kanwisher Nature Reviews Neuroscience 9, 123-135 (February 2008)
Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Hadjikhani N1, Sanchez Del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RB, Sorensen AG, Moskowitz MA. Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4687-92. Epub 2001 Apr 3.
Unification of Neuronal Spikes, Seizures, and Spreading Depression. Yina Wei, Ghanim Ullah, and Steven J. Schiff ; The Journal of Neuroscience, 27 August 2014, 34(35): 11733-11743; doi: 10.1523/JNEUROSCI.0516-14.2014

Please Folks – Migraine Is NOT A Headache

by Nancy Bonk

Published on August 22, 2013

12132 views

We continually make strides in migraine disease and headache disorders education but we still have much work to do. As we succeed to reduce the stigma that surrounds migraine and headache, it’s time for a definitive name for migraine. Once migraine is qualified as a disease, its stigma will be reduced and patients will be taken more seriously and most likely receive an accurate diagnosis sooner. In order to do this we need to use the correct terminology when discussing migraine disease and headache disorders; call migraine a migraine and headache a headache. After all they are two very different things.

A Migraine is not a Headache

The majority of people including many in the medical community continue to use ‘migraine headache‘ when discussing migraine disease. This is problem because migraine is a genetic neurological disease that impacts the entire body; migraine is a primary disorder – a disorder by itself. Headache may be either a primary disorder or secondary disorder, and may be a symptom that is caused from another disorder. Migraine disease is not caused by any other disease or condition. It’s not a symptom of any other disease or condition. To that end, many advocates, myself included become extremely aggravated when we hear the term ‘migraine headache.’

Dr. Oz and the TV ‘Experts’

A recent Dr. Oz show entitled The New Science to Reverse Aging included a segment on how to treat ‘migraine headaches‘ holistically. One of the first problems I notice are they talking about migraines or headaches? Neurologist Dr. Majid Fotuhi (who isn’t a board certified doctor in headache medicine from the United Council of Neurological Subspecialties) was one of the featured guests and talked about the various foods can help reduce ‘migraine headache’ pain. To his credit, Dr. Fotuhi said the most important “weapon against frequent ‘headaches‘ is prevention, prevention, prevention.” I’m fairly certain at this point he means migraines – so why not use the correct term? Dr. Fotuhi goes on to say the best way to prevent ‘headaches‘ is exercise, avoid trigger foods that trigger ‘headaches’ and monitor the foods you eat because certain foods may be able to reduce the frequency of certain types of ‘headaches.‘ Trigger identification and management along with exercise are important pieces of any migraine management plan. For some exercise will trigger a nasty migraine attack.

Terminology Matters

At this point in the show, neither doctor has taken the time to distinguish the difference between migraine disease and headache disorders. Dr. Oz goes on to explain ‘migraine headache’ pain occurs on one side of the head, with nausea and light sensitivity. Many times this is true, but not always. Migraine pain can occur on both sides of the head, be mild to moderate and/or severe to debilitating. An attack can last from 4- 72 hours, sometimes longer, and not everyone will experience nausea.

Dr. Fotuhi reports that foods high in riboflavin which is vitamin B2 can “help reduce certain types of headaches and migraine headache.'” Mushrooms, asparagus, quinoa, milk are indeed high in B2 and it’s used for migraine prevention, but again, some of these foods may be strong migraine triggers for certain people. The doctors continue to interchange migraine and headache.

‘Hormonal headache’ and foods used to prevent them include those rich in magnesium like sweet potatoes, spinach, chard and bananas Dr. Fohuti goes on to say. But eating these foods may be a strong migraine trigger for some. He continues to report that eating these foods can help reduce ‘menstrual headaches‘ and even suggests taking 450 mgs of magnesium will help prevent ‘hormonal headache. No mention here of checking with your doctor before you take the supplement. According to International Headache Society’s International Classification of Headache Disorders – III, 3rd edition, beta version or ICHD-III 3rd ed., beta version there is no diagnosis of ‘hormonal headache‘ or ‘menstrual headaches‘. However, pure menstrual migraine without aura, menstrually related migraine without aura and non-menstrual migraine without aura can all be found in it. Let me stress again how important correct terminology is.

Dr. Oz then describes tension type headache (a real diagnosis) as a “dull pain, band around the head, and the muscles behind your temples are contracting.” Eating foods with high levels of Coenzyme Q10 such as eggs, broccoli, cauliflower, tuna, organ meats and salmon may be beneficial for tension headache according to Dr. Fohuti – or they can be strong migraines triggers for some people. Dr. Fohuti says to avoid a tension type headache it’s imperative to get eight hours of sleep each night and practice daily relaxation. The truth of the matter is it’s more important to go to bed and wake up at the same time every day, seven days a week, then get various eight hour pockets of sleep.

The doctors went over “cold or flu headache” which doesn’t exist in the ICHD-III 3rd edition, beta version. Dr. Fotuhi said when we have a cold we can become dehydrated, so eating foods that have a high water content include strawberries, pineapples, watermelon and cantaloupe will help with that. Becoming dehydrated is not a good idea at any point for people with migraine and can certainly trigger a migraine attack.

Dr. Fotuhi goes on to say not to take aspirin, ibuprofen and/or acetaminophen more than once a week when you have a ‘headache‘ or you may get medication overuse headache or moh, formerly called rebound headache. In part he is correct, but the reality is if we use pain relievers, whether over-the-counter and/or prescription or migraine abortive medication, more than two to three times a week we may get moh. He never discusses how many ‘headaches‘ are too many or when to see a doctor, intimating that we should be able to handle our head pain with these vitamin rich foods and supplements. This is neither true nor accurate.

In my opinion, when discussing migraine disease prevention and treatment, it would be nice to hear from an expert, someone who is board certified in the related field and really knows what they are talking about.

Resources

“Dr. Oz offers holistic help for headaches and migraines.” Examiner.com, July 22, 2013.

“Foods Solutions to Ease Headache Pain, Part I.” The New Science to Reverse Aging. The Dr. Oz Show. August 15, 2013.

migraine - Page 2

Migraine Precipitants

Hypoxia, Pseudo-hypoxia, and Migraine

Autonomic Asymmetry

Migraine and Diet

Conclusion

We Need Your Help

Related posts:

You might be interested in

We Need Your Help

Related posts:

You might be interested in

So, What is Migraine?

What is Metabolic Syndrome?

The Genetics of Migraines

Reversing Chronic Insulin Resistance in Migraineurs

Support Hormones Matter

Additional Sources

Related posts:

You might be interested in

Migraine Brain as a Survival Advantage

Migraines and Salt

Migraines and Sugar

Sources:

We need your help.

Related posts:

You might be interested in

Why Triptans and SSRIs/SNRIs are Hit or Miss for Migraines

Does Serotonin Use Make Any Sense At All?

Concluding Thoughts

Sources

Related posts:

You might be interested in

Moving Beyond the Hormone Migraine Theory

My Theory: Why Hormone Changes are not the Cause of Migraines

Migraine during Pregnancy

Migraine during Postpartum

Post-Menopausal and Menopausal Migraines

Fuel for Migraines (Hormonal or Not)

Sources:

Related posts:

You might be interested in

Migraine as Vascular Disease

Migraine as Non-Vascular Mental Illness

Migraine and New Research

A Unified Theory of Migraine Pain

It’s All About the Ions

Concluding Remarks

Sources:

Related posts:

You might be interested in

A Migraine is not a Headache

Dr. Oz and the TV ‘Experts’

Terminology Matters

Resources

Related posts:

You might be interested in