Migraines and Clus­ter Headaches are the same. They occur when oxy­gen deliv­ery is too low. Usu­al­ly from stress.

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:

1. Why you get migraines;
2. Why stress trig­gers migraines;
3. 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: All B vit­a­mins; Group 16 ele­ments, Oxy­gen, Sul­fur, Sele­ni­um Agents which inhib­it auto­nom­ic bal­ance: All tox­ins which inhib­it tis­sue oxy­gen deliv­ery (cause hypox­ia); Stress of any sort which exceeds cur­rent autoreg­u­la­to­ry per­for­mance of the ANS which cre­ate con­di­tions which lock metab­o­lism into dys­reg­u­la­tion.

Lack of oxy­gen to artery smooth mus­cles

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.

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:

1. Sys­temic and local oxy­gen deliv­ery per­for­mance
2. Stress tol­er­ance cofac­tors (neu­tral­iza­tion & elim­i­na­tion)

Oxy­gen per­for­mance is a result of sev­er­al fac­tors (von Ardenne):

1. Adap­tive deliv­ery to demand vari­ant tis­sues;
2. Unim­ped­ed blood flow to vas­cu­lar­ized tis­sue;
3. Plas­ma sat­u­ra­tion for deliv­ery to non-vas­cu­lar­ized tis­sue;
4. Avail­able reserves of oxy­gen deliv­ery nutri­ent sub­strates;

Stress Tol­er­ance Cofac­tors

1. Avail­abil­i­ty of Group 6 Chalco­gen Nutri­ents Sul­fur & Sele­ni­um / (Revi­ci)
2. Oxy­gen Trans­port Cofac­tors, includ­ing B Vit­a­mins & Oxy­genic Min­er­als, Mg
3. Vas­cu­lar Tone Mod­u­la­tors, n‑Butyl & glyc­erol

The goal of this pro­to­col is to opti­mize sup­port of under­ly­ing com­pen­sa­tion sys­tems. There are sev­er­al func­tion­al meth­ods:

1. Opti­mize oxy­gen avail­abil­i­ty to reg­u­la­to­ry struc­tures / Hypoten­sion (Requires strong heart)
2. Nutri­ents that sup­port Oxy­gen Trans­port
3. Detox­i­fi­ca­tion of agents which inhib­it oxy­gen trans­port (Pri­ma­ry and Sec­ondary)
4. Opti­mize oxy­gen avail­abil­i­ty to vas­cu­lar struc­tures / 36h
5. 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;

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.

Vas­cu­lar tone is lim­it­ed by inhi­bi­tion of the fol­low­ing con­trol sys­tems:

1. Inhib­it­ed sig­nals from the brain to vagus nerve to the organ sys­tems which gov­ern blood pres­sure;
2. Reduced pro­duc­tion of vas­cu­lar neu­ro­trans­mit­ters which gov­ern vas­cu­lar tone, NO donors and alco­hols;
3. Oxy­gen depri­va­tion arte­r­i­al mus­cles which con­strict to main­tain vas­cu­lar tone.

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Protocol

This pro­to­col pro­vides four rec­om­men­da­tions:

1. Restore sys­temic oxy­gen avail­abil­i­ty with Oxy­gen Mul­ti­step Ther­a­py (Ardenne)
2. Sup­port sec­ondary detox metab­o­lism with sul­fur and sele­ni­um prepa­ra­tions
3. 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.

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.

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.

1. Use BP Cuff to take BP
2. Use it to man­age Dosage by table below
3. And take the fol­low­ing num­ber of drop­pers

Sug­gest­ed Usage Table:

Drop­per: 1 mL is approx­i­mate­ly 1 drop­per full or about 10 drops.

Level 2 / Oxygen Transport Nutrient Protocol

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:

1. If you do not exer­cise reg­u­lar­ly use OMST 36h to build dura­bil­i­ty;
2. After restor­ing dura­bil­i­ty use OMST Hypoten­sion;
3. 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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