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Why Are We So Scared of Salt?

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Over the past several decades, the general consensus of health professionals has been to recommend that all people lower their salt intake. Without the recognition of the effects of lifestyle and dietary choice differences, this avalanche of low salt advice hit the general public and as a direct result many became ill. Differences in individual genetic, lifestyle, and dietary factors have completely been ignored in the broad-brush campaign for lowering salt intake. Today, it is unmistakably obvious that a large segment of the population followed the low salt regimen with disastrous consequences.

The professionals who first introduced and propagated the low salt diets had good intentions. They did not know any better. Now we do know better and there is no excuse for not revising a failed treatment regimen in the face of new countervailing evidence. The process of correction needs to begin on a large scale. My work is part of this very much needed correction.

Why Are We Scared of Salt?

In the 1960’s, scientific studies linked salt consumption to hypertension and obesity. I am not quite sure why it was salt they picked on as “enemy number one.” I suspect the reason was the proliferation of precooked and canned food, all of which were salt preserved. To me, it was not logical that only salt was picked on. There were many other dangerous food items that could have been singled out: sugar, margarine, preservatives, pesticides, etc. The American Heart Association still has some of these salt reduction articles on their website. Even today, when waiting for an appointment at my medical institution, the forever-on TV was showing how to cut salt out of kids’ daily lunch to be “healthy.” Indeed, once something is ingrained in our brains, it is habit forming. Habits are very hard to break, particularly when the medical research relied upon showed that salt is something dangerous that may kill you.

Is Salt or Sugar the Enemy?

The problem is that hypertension and obesity are not and have never ever been caused by salt! They are caused by sugar—I am saving the sugar discussion for my next article.

Why not salt? Consider: human fetuses are floating in salt water and are typically not born with heart attack or hypertension. Our bodies are made of over 7% salt, our brains, heart, and all of our cells use salt to function. Humans have always consumed salt. Do they all have hypertension and heart attacks? No, they don’t. In fact, for some time now, studies have been surfacing suggesting that reduced salt does not eliminate the chances for hypertension and heart attack but may even contribute to the problem.

It is scientifically irresponsible to analyze biological processes in the human body involving salt without accounting for the effects of sugar and sugar substitutes and the amount of water consumed.

Probably not many of you have the handbook “Harrison’s Manual of Medicine” (18th edition McGraw Hill Medical by Longo et al.,) but I do. Page 4

…serum Na+ [sodium] falls by 1.4 mM for every 100-mg.dL increase in glucose, due to glucose-induced H2O efflux from cells.

Let me explain this sentence for you: Sodium is part of salt. Salt is Sodium (Na+) and Chloride (Cl-) where the + and – represent the ionic state in which there is either one extra or one fewer electron (electrons have negative charge) and so the atom is looking for another atom it can attach to and form a bond creating a molecule. According to the medical handbook, Na+ drops if glucose, which is blood sugar, increases. If you eat glucose, it causes “H2O efflux from cells” which means that sugar attracts water to the point that it pulls it out of the cells, thereby emptying the cells of sodium, and thus, the cells are dehydrated.

Sugar causes a very serious problem that can result in hypertension and heart attack. The volume of blood inside the cells reduces by dehydration of the sugar and higher pressure is required to pass the dehydrated blood to traverse the same route and be able to oxygenate organs at the same rate as hydrated blood cells. Think of a water hose when suddenly the pressure drops (unfortunately we cannot replicate reduced water molecule size the same way dehydrated cells become smaller). You instinctively squeeze the hose end to increase pressure so the water can continue to reach to the same distance. You have just given a hypertension to your water hose!

Note that if sodium (page 3 in same book) falls below 135 mmol/L, it is an electrolyte abnormality whose symptoms include “nausea, vomiting, confusion, lethargy, and disorientation”; if Na+ falls below 120 mmol/L it is a life threatening emergency that may cause “seizures, central herniation, coma, or death.” Not having enough salt (sodium) in the body is called hyponatremia and is “primarily a disorder of H2O homeostasis” meaning too much water and not enough salt. In common parlance, this is called water toxicity. Water toxicity can be caused by drinking too much water—e.g. drinking only water.

Interestingly, in the same book under the section of hypertension (page 834-835), the causes of hypertension are listed. Increased salt (or sodium) is not mentioned at all, but glucose intolerance is. However, under treatment, on page 836, it recommends lifestyle modifications that include lowering salt intake. So increased salt did not cause hypertension but lowering will cure it? I do not understand. Do you? Seems the authors of even this highly respected medical reference book could not escape the fallacy of the low salt campaign. Hypertension is clearly listed to be caused by sugar under the causes. So for heaven’s sake, if something is caused by sugar, treat it with removing sugar from our diet and not salt.

Confusion in the Ranks

In recent years a major fight started between the academic groups, not-for-profit organizations, and the government. Test after test shows that earlier hypotheses were all wrong about salt. Not only is added salt not hurting us, reduced salt does. Even the American Heart Association (AHA) and other heart organizations are in complete confusion. Next to the article of “lower your salt for health” are articles saying “that is all wrong and increase your salt.” I find this kind of funny. Here is an article from the AHA suggesting to increase salt. Here is another from the HealthAffairs organization; one from the American Journal of Hypertension, one from the Journal of the Association of American Medical Colleges, and there are now dozens more proving that indeed, reduced salt is actually bad for you.

How Bad is Reduced Salt on Health?

This particular article is my favorite because it shows how bad reduced salt diets really are on the heart. In detail, for a healthy individual reduced salt diet reduces BP by 1% (that means your systolic BP of 120 just dropped to oh my 118.5!!! gasp) and in patients with hypertension it reduced their BP by 3.5% (that is if it is say 160 systolic, which is high, it is reduced by a whopping 5.6 to 154.4! gasp again) but at the same time triglycerides, which contains the accurate measure of the sticky type of bad cholesterol in the LDL increased by 7% in people with hypertension (triglyceride should be less than 149). So if an individual with hypertension and triglyceride levels at 150 went on a low salt diet, that low salt diet would increase their triglycerides by 10.5 to 160.5, which is a significant jump for bad cholesterol. In a healthy individuals, the triglycerides jumped by 2.5%. Armed with such details, do you still believe that salt is bad for you?

Which Would You Rather Eat?

If I handed you 2 teaspoons: one was full of table sugar and the other full of table salt, which would you chose? For taste, we all would choose the sugar. What happens to our salt levels when we eat sugar? Refer back to the Harrison’s Medical Manual I mentioned earlier: eating glucose drops salt in our body because it sucks up all water and dehydrates. Eating a teaspoon of sugar will effectively dehydrate you and put you at risk of hyponatremia. By contrast, what will happen if you chose the teaspoon of salt? You will be thirsty, drink a couple of glasses of water and will feel like you are on top of the world.

My Recommendation

Stop being scared of salt and start being scared of sugar!

Sources

Longo et al., Harrison’s Manual of Medicine; 18th Edition, 2013; McGraw Hill Medicine

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This article was first published on June 13, 2015.

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Hydration, Thirst, and Drinking Water

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drinking water, hydration

Most of us equate the expression “hydrate extra” with drinking more water but – unfortunately – this is incorrect. In any online dictionary “to hydrate” means to create “…a substance that is formed when water combines with another substance…” In other words, water alone is not a hydrating fluid but it must be combined with something to become one. We do not have water in our body on its own; we have a substance we call electrolyte. I wrote substantially on the topic of hydration, mixing water with minerals, as part of the protocol that prevents migraines. However, a new problem has surfaced: when to drink water? Several articles have recently published water drinking instructions on the internet. Most of these articles consider it bad practice to drink water when one is not thirsty and recommend drinking water only when thirsty. There are several serious flaws with this argument.

Sweat

The first flaw is that most research is aimed at athletes, but athletes are not representative of the majority of the population. Furthermore, athletes should not be drinking “water” to hydrate. Drinking water cannot be absorbed by cells without adequate sodium to hold onto it. When athletes sweat, the content of sweat is not water but electrolyte. Many sports drinks aim at re-hydrating athletes but their problem is their sugar or sugar substitute content, defeating the purpose — see how much sports drink one needs to drink to make up the content of sweat for an athlete. Then add up the sugar in a typical sports drink: 1 teaspoon of sugar is 4 grams of carbs. An average serving of a typical sports drink provides between 14 grams to 54 grams of carbs, all sugar, which converts to 3.5 to 13.5 teaspoons of sugar per serving. Drinking sugar substitutes is even worse because sugar substitutes fool the body like it is receiving glucose so insulin spikes but there is no glucose. This creates insulin overflow in the blood causing you to become hungry! Sugar substitutes may lead to obesity and metabolic syndrome. Drinking sports drinks with sugar substitutes actually reduces muscle energy.

Moreover, anything that converts to glucose in the body removes both water and sodium from the cells1 so drinking/eating sugar with sodium (salt is the form in which sodium is available to us) and water is worse than not drinking anything at all. Many athletes have smartened up and drink pickle brine rather than water. Pickle brine is great, assuming the brine is of salt and water and not vinegar. Vinegar is fermented ethanol (alcohol). Thus, drinking vinegar-processed pickles will dehydrate further. Look for pickles made with salt rather than vinegar.

Best Hydrating Fluid

Whole milk is an ideal hydrating fluid because it has a perfect electrolyte balance in sodium, potassium, water, blood sugar (lactose), calcium, phosphorus, magnesium, and protein. Whole milk is THE perfect electrolyte. Some athletes drink water and take salt pills (also called electrolyte pills). That is also a great option, particularly since they are easy to carry around and take when needed.

The second flaw in the argument of “drink water when thirsty” is that many people feel thirst after eating sugar when it is the least advisable to drink water. Since about half of sugar converts to glucose, and glucose pulls water and sodium out of the cells1, if one is thirsty after eating sugar and drinks water, the metabolic process will remove more water from the cells. This can cause edema. Although most articles today blame salt for causing edema, the opposite is true.

While sodium retains water inside the cell, glucose removes water and sodium from the cell and forces the water to be retained in extracellular space2. Eating salt when one has edema reduces edema by the sodium bringing water back into the cell. This was easily demonstrated by a previous article showing how this works.

The problem with most studies that blame salt on retaining water is that no studies have ever controlled for both salt and sugar at the same time in the same experiment. All studies I could find only looked at the effects of salt on the body regardless of the amount of sugar, water, or protein the subjects had consumed before the experiment. Since the body can easily be tipped out of balance and is never in a vacuum for a pristine controlled experiment, one cannot say with certainty that one element makes a particular change without looking at what else is affecting the body. No such studies exist except in my migraine group where we control for all variables. We found that being thirsty often means the person does not have enough salt to keep water where it belongs3. A migraineur should never drink water when she is thirsty, particularly not if carbohydrates were consumed.

The final problem with only drinking water when thirsty is the population of people who have diabetes 2; they are always thirsty. Being thirsty can be a sign of diabetes mellitus and not the need for more water.

Should You Wait Until You Are Thirsty Before You Drink?

Absolutely not, and for sure drinking water alone will not get you hydrated. How much water you should drink is a question I will address in another article. Drinking the minimum 8 glasses of water is a myth; people vary in size, age, and activity, implying that each person needs a different amount of water. Many online water calculators go into detail of weight, climate, activity, altitude, your health, pregnancy, nursing, etc. For each person the amount of water and thus hydration needed (not just water) will differ and for that hydration level you need to make sure you drink adequate amounts of water as part of your hydration protocol.

Sources

  1. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison’s Manual of Medicine 18th Edition. New York: McGraw Hill Medical; 2013.
  2. Millar T. Biochemistry Explained: A Practical Guide to Learning Biochemistry. Vol reprint edition: CRC Press; 2002.
  3. Stanton, Angela A. Fighting The Migraine Epidemic: A Complete Guide: How To Treat & Prevent Migraines Without Medicine

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

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Angela Stanton, PhD

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:

  1. 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!
  2. 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.
  3. 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.
  4. 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!
  5. 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

  1. 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.
  2. Young, W.B., et al., The Stigma of Migraine. PLoS ONE, 2013. 8(1): p. e54074.
  3. Holtzheimer, P.E., et al., Subcallosal Cingulate Deep Brain Stimulation for Treatment-Resistant Unipolar and Bipolar Depression. Jama Psychiatry, 2012: p. 150-158.
  4. 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.
  5. Mayberg, H.S., et al., Deep brain stimulation for treatment-resistant depression, in Neuron. 2005. p. 651-60.
  6. Taghva, A.S., D.A. Malone, and A.R. Rezai, Deep brain stimulation for treatment-resistant depression. World Neurosurg., 2013: p. 826-831.
  7. Aurora, S.K., et al., Transcranial magnetic stimulation confirms hyperexcitability of occipital cortex in migraine, in Neurology. 1998. p. 1111-4.
  8. 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.
  9. 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.
  10. 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.
  11. Charles, A.C. and S.M. Baca, Cortical spreading depression and migraine. Nat Rev Neurol, 2013: p. 637-44.
  12. James, M.F., et al., Cortical spreading depression and migraine: new insights from imaging? TRENDS In Neuroscience, 2001: p. 226-271.
  13. 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.
  14. Bolay, H., et al., Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med, 2002. 8(2): p. 136-142.
  15. 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.
  16. 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.
  17. Lozano, M. and N. Lipsman, Probing and regulating dysfunctional circuits using deep brain stimulation, in Neuron. 2013. p. 406-24.

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Sweet Death by Sugar

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Angela A Stanton,Ph.D.

We all know that sugar is bad for us but we cannot resist it. Why not? Expert Robert Lustig MD, reasoned on 60-Minutes that for humans in nature all sweet tasting things are edible and not poisonous. There are no toxins in nature that taste sweet, and thus, evolutionarily speaking, favoring sweet things is predetermined in our genes; we are born liking sweets. All of this is true with one major exception: sugar, the natural substance, can become poisonous when modified.

Sugar and Ethanol

Consider the simple modification of squeezing a fruit for its juice. The modification is not chemical: we merely separated the sugary liquid from the insoluble fiber in the fruit–some soluble fibers may remain. This little change makes no difference for most fruits or our taste buds, but it modifies how our body metabolizes sugar in it. According to Lustig’s book Fat Chance (a must read!), when we eat the fruit with insoluble fiber attached (typically the skin), the fructose in the fruit (most sugar in fruit is fructose) bypasses our metabolic digestive process (insoluble fibers are not digestible) and heads straight to the gut where the good bacteria digest the fructose as their food from the fibers, thereby producing more nutrients for us. But if we drink the juice alone without any insoluble fiber, the same amount of fructose now gets into the metabolic cycle and by a complicated process turns into ethanol and gets stuck in the liver. Ethanol is a toxin. Ethanol is an alcohol we also use to improve car mileage. Ethanol causes non-alcoholic “alcoholic” liver disease. In fact, ethanol is alcohol and those drinking apple juice (thinking of kids now) are in fact drinking alcohol in terms of the likely outcome of the metabolic process, as per Dr. Lustig.

So we all thought that feeding our kids fresh fruit juices is a good thing but we also knew that they should not be getting too much sugar because their behavior changes from it. Now it is clear why their behavior changes: the part of sugar that turns into ethanol is alcohol. The other parts of the fruit juice that do turn into digestible sugars (glucose and sucrose) do something else to the body.

What is Glucose?

Glucose is “blood sugar” meaning the sugar our body can use. Sucrose converts to glucose as well. What happens to the glucose?

Some stores sell glucose in a liquid gooey form—thicker than honey—that I recommend you taste. Take a small teaspoon, fill it with glucose and swallow. The first thing you will notice (yes, I did the tasting test) is that it is not that sweet. The second thing you will notice is that the moment you swallow it, you cannot count till 5 and you are hot. So you take your sweater off. Then you have the urge to do something—paint the house? Mow the grass? If you are a kid: bounce off the walls and drive the people around you nuts. This is normal. This is what glucose feels like.

Note, however, that when you eat a teaspoon of table sugar, you will neither feel so hot, nor will you have so much energy. What is the difference? What happens when you drink a diet drink or eat sugar substitutes? You will neither be hot nor have any energy. The difference in feeling hot and having energy versus not feeling hot and not having energy represents the difference in the metabolism of glucose versus fructose and the fake sugar stuff.

The Metabolism of Glucose versus Fructose

I will not get into deep chemical equations or models; for that please watch the video below by Dr. Lustig. Rather, I will reduce all complexity and simply tell you the end of the story with as minimal of the underlying process as possible.

When food arrives into the body, insulin is released to convert the food into fat and deposit it for later use as glucose. Glucose is used by our brain and muscles for energy. After insulin has done its conversion, all insulin is used up. When the brain is hungry, it fetches the hormone leptin to get some energy. Thus, leptin grabs a hold of the available glucose and serves it to the brain (this is highly simplified!). The brain is happy and full of energy.

Now consider the situation when the only food we eat is glucose. Insulin is released but it has nothing to convert. It is already in the final form (glucose for the brain) and so the glucose goes straight to the brain, the kids are popping off the wall, and you suddenly find yourself painting the house. Note, however, that the insulin is in the blood and it is waiting for the food to arrive so it can work and convert it to fat. But there is no food; we only ate glucose and it is already being used by the brain! So what is insulin in the blood to do? Insulin stays in the blood, circles around looking for food. It finds none. By staying in the blood, over time this is a “cry wolf” scenario and the body starts ignoring insulin announcing the arrival of food that isn’t there. This is how insulin resistance starts.

Now consider that instead of glucose, you drink a glass of apple juice. It has natural sugar in it, some vitamins (very little), no fiber, no protein. The sugar of fruit is mostly fructose but a small part of it is also sucrose. So insulin releases again to match the size of the apple juice drink we just had, but again, it faces a problem. While sucrose becomes glucose in our body and can be converted and stored as fat, fructose is not seen as sugar. So once again, insulin is looking for food but finds none; it keeps on circling in our blood looking for food. It is ignored and insulin resistance begins.

The Metabolism of Glucose versus Sugar Substitutes & “Natural” Sugars like Stevia

Now consider you eat a diet something—by diet I mean sugar substitutes with reduced or zero calories. It certainly tastes sweet (very sweet indeed) but again, there is no glucose or sucrose in it and while it does not become alcohol in the liver, it certainly makes insulin run around in circles looking for food to convert to fat and deposit. Cry wolf again and the insulin is ignored. Insulin resistance begins. Why is this important? Because insulin resistance is type II diabetes!

The Famine

Now let’s continue about the peril of our non-toxic sweets. The fact that insulin is out looking for glucose also signals leptin that energy is incoming! Leptin is a hormone that is in charge of messaging the brain that glucose is available. In the case when insulin is running around in our blood in search of food it can convert to fat for later use as glucose but there is no food to be found, leptin finds no glucose. Thus, leptin tells the brain that famine is here.

Famine for the Brain is Obesity for Your Body!

The famine message to the brain means one thing: conserve energy. It reduces all non-essential activities, and literally, will not let you get up from that couch! This is highly simplified of course, but pay attention to the outcome. You are actually eating and drinking and at the same time your brain is getting the message of famine. What will that lead to? When the brain thinks it is famine time, it is famine time. The fact that you are eating and drinking sugar or sugar substitutes with lots of calories is not noticed by the brain. As far as it is concerned, there is no glucose available so it must slow your metabolism. A slow metabolism leads to obesity.

Sugar Anyone?

So, while there are many people who think nothing of having sweets or a soda, consider what it does to your body! Consider that it slows down your activity and forces you into famine state even though you are well fed! Consider that it makes you obese and sets you up for type 2 diabetes.

Now tell me if you still think that sweets are not toxic poisons for us! They are. And there is one more thing to add to the story that no one talks about. I mention this because I deal with a group of migraineurs—I was one of them until I figured things out and wrote a book about it and several articles about it on Hormones Matter.

Consider this quote from the Harrison’s Manual of Medicine:

…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells. (page 4)

Na+ is sodium ion. Sodium is part of sodium-chloride, which is salt. Glucose-induced H2O efflux from cells represents water exiting the cells as a result of an increase of glucose. Why is that, you may ask? The answer is very simple: sugar is an amazing water soak-up device. It pulls water from everywhere it can. It holds onto water like its life depended upon it. Unfortunately for the body, sugar pulls the water from the cells leaving the cells empty on the inside and a lot of fluid tied to sugar on the outside. As long as that sugar is there, the cells are not able to hydrate in any fashion until the level of Na+ is increased beyond a threshold level where Na+ can take water away from the glucose. Na+ also attracts water. In fact, all saline electrolyte liquids provided by IV or for drinking in hospitals are Na+ heavy to rehydrate the cells.

Thus, sugar not only starts and enhances diabetes II and obesity; it also shuts down cell hydration. This may cause headaches or migraines depending on your propensity.

In conclusion, if someone asks you if you would prefer to eat a teaspoon of sugar or a teaspoon of salt, while your taste buds will undoubtedly scream for sugar, you should know better!

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References

  1. Sugar: The Bitter Truth https://www.youtube.com/watch?v=dBnniua6-oM
  2. Longo et al., Harrison’s Manual of Medicine. 18th edition. McGraw Hill. 2013.
  3. Artificial sweeteners could cause spikes in blood sugar by By Brady Dennis September 17, 2014
  4. Washington Post: http://www.washingtonpost.com/national/health-science/study-suggests-sweeteners-could-contribute-to-obesity-and-diabetes/2014/09/17/c3c04ea6-3dc2-11e4-b03f-de718edeb92f_story.html
  5. Artificial sweeteners could lead to obesity, diabetes. By Michelle Castillo CBS NEWS July 10, 2013, 4:28 PM
  6. CBS News: http://www.cbsnews.com/news/artificial-sweeteners-could-lead-to-obesity-diabetes/
  7. Artificial sweeteners may promote diabetes, claim scientists
  8. The Guardian: http://www.theguardian.com/science/2014/sep/17/artificial-sweeteners-diabetes-saccharin-blood-sugar
  9. Do Artificial Sweeteners Really Cause Diabetes? By Published: June 7, 2013 By Jessica Chia
  10. Women’s Health Magazine: http://www.womenshealthmag.com/health/artificial-sweeteners-cause-diabetes
  11. Could artificial sweetener CAUSE diabetes? Splenda ‘modifies way the body handles sugar’, increasing insulin production by 20% by Rachel Reilly Published: 12:27 Est, 30 May 2013 | Updated: 12:27 Est, 30 May 2013
  12. The Daily Mail: http://www.dailymail.co.uk/health/article-2333336/Could-artificial-sweetener-CAUSE-diabetes-Splenda-modifies-way-body-handles-sugar-increasing-insulin-production-20.html
  13. How To Starve Cancer To Death By Removing This One Thing From Your Diet
  14. Organic Health: http://organichealth.co/starve-cancer-to-death-by-removing-this/
  15. Is sugar a toxin? Experts debate the role of fructose in our obesity epidemic By Tamar Haspel, September 2, 2013
  16. Washington Post: http://www.washingtonpost.com/national/health-science/is-sugar-a-toxin-experts-debate-the-role-of-fructose-in-our-obesity-epidemic/2013/08/30/58a906d6-f952-11e2-afc1-c850c6ee5af8_story.html
  17. Scientific team sounds the alarm on sugar as a source of disease. By Barbara Sadick Chicago Tribune
  18. The Chicago Tribune: http://www.chicagotribune.com/lifestyles/health/sc-health-1210-sugar-metabolic-syndrome-20141205-story.html#page=1

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Migraines and Hormones: Behind the Curtain

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Angela A Stanton,Ph.D.

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:

  1.  Prepare the uterus with a new fertile lining to accept the fertilized egg should one arrive and start a new life.
  2. 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.
  3. 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.
  4. 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:

  1. 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 
  2. 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
  3. 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
  4. 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
  5. Human Oestrus by Steven W Gangestad, Randy Thornhill. The Royal Society, Proceedings B May 2008  http://rspb.royalsocietypublishing.org/content/275/1638/991
  6. 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
  7. Migraine and Children. Migraine Research Foundation http://www.migraineresearchfoundation.org/Migraine%20in%20Children.html
  8. 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
  9. 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
  10. Multisensory Integration in Migraine Todd J. Schwedt, MD, MSCI. Curr Opin Neurol. Jun 2013; 26(3): 248–253
  11. Unification of Neuronal Spikes, Seizures, and Spreading Depression. Wei et al., The Journal of Neuroscience, August 27, 2014 • 34(35):11733–11743 • 11733

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The Anatomy of a Migraine

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Angela A Stanton,Ph.D.

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 20th 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:

  1. 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
  2. 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
  3. 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)
  4. 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.
  5. 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

 

 

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