The Migraine Hypotension Connection
Ever wonder why migraines, or cluster headaches, happen?
Well, you’re not alone, 30+ million others get bad headaches too. The search for why your head hurts, and what to do about it, yields nearly zilch, until you read this article…
Few, if any sources, offer explanation of why migraines happen. Our goal here was to connect the dots – your headache, your stress and your probable low blood pressure:
- Why you get migraines;
- Why stress triggers migraines;
- Suggest actionable protocols to address cause.
Believe it or not there are two mature publications that when taken together explain why most people get migraines – and suggest a nutrient and oxygen therapy model to address the cause. If you like to study you will need to dig up:
- Research In Physiopathology as a Basis of Guided Chemotherapy – Emmanuel Revici
- Oxygen Multistep Therapy – Manfred von Ardenne
The analysis that follows interprets these two seminal references into a functional explanation of migraines and low blood pressure that leads to a method for fixing the causes.
The Migraine Connection / Hypotension
Hypotension or low blood pressure is caused by loss of vascular tone and usually results from one or more of the following conditions:
- Insufficient oxygen to arterial smooth muscle to maintain tone
- Dysfunction of brain area that controls Blood Pressure
- Inhibition of vagus nerve
- Toxic Shock where one or more toxins disrupt tissue oxygen delivery
- Traumatic Shock where one or more events disable metabolism
- Acute dehydration which results in blood volume loss or excess salts which prevent oxygen solubility and oxygen delivery
- Severe blood loss
The body uses two mechanical processes to control blood pressure:
- Heart Rate and Force to force blood to move blood;
- Vascular tone to direct blood where needed through vascular system.
Hypotension from a weak heart is rare because usually diagnosed as heart disease. Low blood pressure usually results from failure in vascular tone maintenance.
You don’t have to have low blood pressure for low brain oxygen – but it’s typical. If you have normal or high blood pressure, then it means something else is causing your brain NOT to get enough oxygen to work right.
Even if you don’t have low blood pressure your brain can not get enough oxygen from:
- Not enough oxygen in your blood
- Blood cannot transfer oxygen to brain
- Deficiency in transfer nutrients
- Deficiency in CO2 from fatigue
- Blood cannot flow through brain
- Vascular inflammation in the brain inhibits blood flow
- Blood is too thick (sludged) to flow through the brain
By the way – all of these factors also apply to people with hypotension. Any combination of either set of factors can cause your brain NOT to get enough oxygen.
Stress and Flow
Arterial smooth muscle tension limits blood flow, and preserves pressure. Squeezing arteries directs blood where needed by restricting flow to areas where it is not needed.
Weak arterial tone inhibits the body’s ability to regulate blood flow. Likewise, systemic hypoxia, that triggers an entire-body vasodilator reflex, can also result in hypotension.
Breakdown in the vascular tone is the dominant underlying cause of low blood pressure. Loss of vascular tone causes limits blood and oxygen delivery to high demand areas in the body.
Flow-control failure causes poorly supplied tissues under-perform, exhibit functional weakness produce excess lactic acid. This transient under-performance results in a wide range of syndromes and symptoms ranging from benign to severe and degeneration.
Hypotension is both a cause and an effect of vascular tone loss. When tissues that control oxygen delivery do not get enough oxygen. This is positive feedback.
It evidences a durable and recurring pattern which limits stress adaptive responses.
The Migraine Connection
Migraine-like symptoms nearly always present with reduced systolic blood pressure (below 105), or with a sudden relative drop in blood pressure prior to the migraine onset. Although this connection is weakly documented in medical literature, it is easily verified.
Several theories describe migraine cause, Depolarization, Vascular, Neural and Unifying. Curiously, none of these theories suggests that tissue oxygen deprivation as a trigger or cause for migraine.
Hypoxia conditions, relating to capillary performance, and functional oxygen delivery, are fully hidden in medical evaluation methods, except in advanced cases where the arteries are sufficiently degenerate and show occlusion or aneurysm.
A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early migraine stages.
A disabled hypothalamus, controls blood flow, both victim and cause of poor oxygen during a migraine.
The victim/cause pattern makes complicates recovery and explains why migraines tend to last a long time 4-72 hours.The depression wave model results from the spreading hypoxic distress of brain tissue.
We assert that the hypoxic (stress) triggers a portion of the brain to enter anaerobic glycolysis which causes local acidosis, which further inhibits the aerobic metabolism of nearby brain area, causing expansion of the distressed region.
In simple terms, a migraine is a brown-out that affects part of the brain – that grows.
As the “wave effect” expands, more brain tissue enters distress. This model describes migraine onset as triggered by a blood-plasma desaturation event, from a toxin or other stress.
This failure causes a drop in usable oxygen delivery to brain, directly or by triggering capillary swelling in the brain, when capillaries bloat and narrow due to cellular sodium accumulation.
The drop below the migraine-trigger-threshhold causes a cascade effect of distress processes including potentially neurotransmitters, hormones, inflammation and so on, involving the hypothalamus gland, which in turn controls blood pressure.
This network of factors reinforces the distress pattern, which enables migraines to persist for days.
Both Manfred von Ardenne and Dr. Emanuel Revici developed methods that reduce the severity and incidence of migraines, though different, but complementary mechanisms:
- Manfred von Ardenne documented Oxygen Multistep Therapy, p- 251, 259, 282, which reduced migraine incidence and severity by restoring capillary blood flow;
- Dr. Revici and associates found that n-Butyl alcohol was sufficient to control migraines a strong majority of cases. The author asserts that this effect resulted from an unknown role as a Vasoregulator which aids restoration of normal blood flow to the brain after a migraine trigger.
Physiology Models
Hypotension is weakly defined in most medical literature. It generally reflects the inability of the body to regulate blood flow due to an absence of vascular tone. Cardiac insufficiency is outside this description.
| Lack of oxygen to Brain Controls | |
 Damage or trauma to the back of the head can establish conditions which inhibit signal generation that prevents proper blood flow.Hypoxic trauma establishes durable blood flow reduction because of capillary swelling at the root of the vagus nerve.See von Ardenne.Inhibited blood flow prevents normal regulation of sympathetic nervous system, including blood pressure. Leads to sympathetic/parasympathetic imbalances. |
|
| Autonomic Nervous System Imbalance | |
 See Vasovagal Syncope. Trauma or stress that that exceeds the current adaptive range of the autonomic nervous system causes an imbalance where either the sympathetic or parasympathetic branch of the autonomic nervous system dominates.Sympathetic dominance produces hypertension, high blood pressure, while parasympathetic produces hypotension, low blood pressure.Chronic stress tends to create a durable and usually recurrent pattern of sympathetic or parasympathetic dominance.Episode recurrence reflects the normally progressive depletion metabolic agents which enable balance.Principle agents which support autonomic balance:
Agents which inhibit autonomic balance:
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| Lack of oxygen to artery smooth muscles | |
_-en.svg) Secondary hypoxia is a medically unrecognized condition. While vascularized tissue receives oxygen from capillary networks, non-vascularized tissue is supported by solubility and diffusion processes in blood plasma.Secondary hypoxia occurs when nutrient and oxygen delivery from plasma fails to meet the demands from non-vascularized tissue. Smooth muscle cells in arteries are non-vascular and receive oxygen from plasma.When plasma oxygen concentration decreases below the vascular tone threshold, the smooth muscles cannot squeeze, resulting in hypotension. Vascular dilation of a known effect of hypoxia except in the lungs, which respond with vasoconstriction, which further limits oxygen absorption. |
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| Shock Cascade | |
 Shock is the sequence of events which leads to systemic failure. It reflects the process of metabolic breakdown resulting from progressive hypoxia occurring when the effects described above exceed durability. |
Hypoxic Degeneration
Loss of oxygen to non-vascularized tissue enables degeneration.Degeneration non-vascular tissue normally indicates durable decrease in secondary oxygen delivery. oxygen and likely nutrients to the degenerate tissue.
Degeneration of non vascular tissue at soluble oxygen transport is degenerate to. This is a typical cause of many sorts of degeneration:
- Decreasing Vision (lens of eye)
- Vascular (arteriosclerosis)
- Connective tissue (cartilage, ligaments & tendons)
Protocol Model
Since the several models of hypotension reflect chronic stress effects, hypotension can be viewed as stress response pattern with dominant prevalence of the parasympathetic branch of the ANS.
This means that the sympathetic response is inhibited or parasympatheticactivation is elevated, or both.Stress compensation performance reflects collateral performance in body systems:
- Systemic and local oxygen delivery performance
- Stress tolerance cofactors (neutralization & elimination)
Oxygen performance is a result of several factors (von Ardenne):
- Adaptive delivery to demand variant tissues;
- Unimpeded blood flow to vascularized tissue;
- Plasma saturation for delivery to non-vascularized tissue;
- Available reserves of oxygen delivery nutrient substrates;
Stress Tolerance Cofactors
- Availability of Group 6 Chalcogen Nutrients Sulfur & Selenium / (Revici)
- Oxygen Transport Cofactors, including B Vitamins & Oxygenic Minerals, Mg
- Vascular Tone Modulators, n-Butyl & glycerol
The goal of this protocol is to optimize support of underlying compensation systems. There are several functional methods:
- Optimize oxygen availability to regulatory structures / Hypotension (Requires strong heart)
- Nutrients that support Oxygen Transport
- Detoxification of agents which inhibit oxygen transport (Primary and Secondary)
- Optimize oxygen availability to vascular structures / 36h
- Supplement Nutrients that support Vascular Tone
Therapeutic Agent Overview
This provides concurrent maintenance of primary systems which result in failure to maintain vascular tone:
- Oxygen to brain to support areas that control blood pressure with Oxygen Multistep Therapy and Mitochondria Nutrients;
- Nutrients which aid in transfer of oxygen from blood to tissue;
| Component | Role |
|---|---|
| Vitamin Cofactors for oxygen delivery | |
| Magnesium aids oxygen use by cells and desaturation | |
|
Thiamine (Vitamin B3)
|
Mobilizes bile and activates liver detoxification |
| Vasoregulator aids dilation response. Provides NO substrate for vasoregulation and CN detoxification pathways. |
Toxins which bind to hemoglobin sites on red blood cells limit oxygen transport.
- Glycated Hemoglobin from chronic elevated glucose reduces oxygen binding sites on blood cells;
- Elevated plasma ureas result from under-performance in the urea cycle, reduces plasma oxygen availability in blood below optimal levels. Elevated ureas decrease oxygen available to non-vascularized tissues by limiting plasma oxygen solubility or plasma oxygen desaturation or both (author). This effect increases hypoxic vulnerability to non-vascularized tissues;
- Cyanide binds hemoglobin receptors reducing oxygen transport.
This can deplete Hydroxocobalamin, B-12,
which has stronger affinity for CN than hemoglobin. Secondly, elevated CN can deplete deplete Nitrite (arginine alphaketoglutarate) and thiosulfates
substrate reserves.
| Component | Role |
|---|---|
| Improves chloride oxidation of stress toxins. Supplies ionic magnesium and sulfur. Aids elimination Nitrate and Ammonium ureas. | |
| Aids reduction of Ammonium ureas. Aids elimination of toxic lipids which accumulate with prolonged stress. | |
| Aids cellular neutralization of stress toxin antibodies that develop in response to toxic exposure. Can replace oxygen as a metabolite during acute stress because of chemical reactive similarity, hence aid acute stress tolerance when reserves are sufficient. |
Vascular tone is limited by inhibition of the following control systems:
- Inhibited signals from the brain to vagus nerve to the organ systems which govern blood pressure;
- Reduced production of vascular neurotransmitters which govern vascular tone, NO donors and alcohols;
- Oxygen deprivation arterial muscles which constrict to maintain vascular tone.
| Component | Role |
|---|---|
| Vascular neurotransmitter which enables vascular constriction reflex (Revici) that apparently depletes under catabolic stress. | |
| Probable Vascular neurotransmitter which enables vascular constriction reflex (Revici) that apparently depletes under catabolic stress. | |
| Salt that aids body compensation for electrolyte disturbances and electrolyte deficiency typical with hypotension. |
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Protocol
This protocol provides four recommendations:
- Restore systemic oxygen availability with Oxygen Multistep Therapy (Ardenne)
- Support secondary detox metabolism with sulfur and selenium preparations
- Titrate vascular tone with vasoregulatory alcohols (n-Butyl & glycerol) and magnesium rich electrolytes
There are multiple effects which result in hypotension. This protocol model divided into levels, based on therapy/nutrient combinations most likely restore normal regulation.
| Level | Primary Mechanism | Therapy Model |
Product
|
|---|---|---|---|
| 1 | Vasoregulator/Electrolyte Deficiency | Nutrients system which restore regulation and electrolytes |
Flow E, Flow C |
| 2 | Oxygen Nutrient Transport Deficiency | Nutrient package to support tissue oxygen delivery |
Oxygen Nutrient Transport Blend (OMST)
|
| 3 | Capillary edema in Brain and Body | Therapy to reset capillary edema switch. See Oxygen Multistep Therapy | |
| 4 | Toxin Disrupted Oxygen Delivery | Advanced Plan Required |
If you do not achieve normal blood pressure on one level, it means that dysfunction from one or more of the other levels is likely preventing recovery.
Level 1 / Vasoregulator & Electrolyte Restoration
This titration provides a ramped support for vascular cofactors which depend on quantitative dysregulation level.
| Supplement | Purpose |
| Flow E, Flow C | Aid kidneys and fluid distribution Magnesium salts & Glycerin. Support electrolytes to maintain fluid |
| Electrolyte Deficiency | Adds working salts and adrenal agents to improve ionized mineral availability. Important with Betaine-HCL to improve digestion. |
Recommend experiment using Flow EC to manage blood pressure during day. Low BP is likely some combination of hypoxia. Flow C and Flow E tend to push metabolism toward Anabolic and will aid sleep.
- Use BP Cuff to take BP
- Use it to manage Dosage by table below
- And take the following number of droppers
Suggested Usage Table:
|
Systolic BP
|
Droppers of Flow E & C
|
Capsules of Electrolyte Deficiency |
|
< 115
|
1
|
1
|
|
< 110
|
2
|
1
|
|
< 105
|
3
|
2
|
|
< 100
|
3
|
2
|
|
< 95
|
4
|
3
|
Dropper: 1 mL is approximately 1 dropper full or about 10 drops.
Level 2 / Oxygen Transport Nutrient Protocol
| Component | Dosage | Role |
|---|---|---|
|
1-3x daily as needed
|
Vitamin Cofactors for oxygen delivery | |
|
1-3x weekly
|
Liposomal supplement delivers intracellular nutrients to support oxygen performance. | |
|
1-3 ml/day
|
Provides secondary oxygenic, 6 valence, nutrients for collateral oxygen support. |
Level 3 / Oxygen Multistep Therapy
Please see our OMST protocol support page for more information.
This protocol supports hypotension which results from:
- Systemic hypoxia – blood pressure is low because the whole body lacks oxygen and the vascular system does not constrict;
- Endothelial Dysfunction – where oxygen delivery to parts of the body which control blood pressure is inhibited limited because blood flow is limited by inflammation of the endothelium. (documented by Manfred von Ardenne)
For Hypotension, consider these options:
- If you do not exercise regularly use OMST 36h to build durability;
- After restoring durability use OMST Hypotension;
- User OMST 15 min quick procedure, or OMST Maintenance to maintain optimal vascular performance.
Please visit our product site for OMST systems and nutrients. You will need to join the site to access pricing information.
Level 4 / Detailed Analysis / Assessment
Limited response to the protocol above suggests oxygen transport and/or desaturation are acutely limited by toxic factors.We offer advanced metabolic with our physiology assessment system. These effects likely reflect multi-system dysfunction and often require detailed intervention.Please consider these additional approaches:
- Contact us for protocol support.
- Evaluate Dysaerobic Imbalance. Use Anabolic Repair Protocol
- Test for nitrate ureas. If elevated Use Nitrate Urea Detox.
- If elevated HbA1c. If elevated use PC Detox to aid glucose metabolism.
** At the time of this writing it appears that Oral Myers Cocktail is no longer available. We are searching for a replacement.
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