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The Oxygen Model of Pain

Majid Ali, M.D.

 

In my clinical work when I see pain, I think oxygen. I think about how dehydration in one person worsens functional oxygen deficits, and how incremental oxidative stress threatens oxygen homeostasis—locally and/or systemically—in another. I think about how sugar roller coasters (rapid hyperglycemic- hypoglycemic shifts) trigger rapid insulin responses, increase adrenaline production, and the intensity of pain. I think about how undetected and unmanaged allergic triggers acting in the bowel and elsewhere cumulatively cause increased acidity (acidosis), feed the fires of free radicals (oxidosis), lead to dehydration, and so set the stage for attacks of pain. All these factors interfere with local and systemic oxygen homeostasis. Specifically, they block oxygen functions in the body, including:

1. Oxygen-driven cellular energetics,

2. Oxygen-driven cellular development and multiplication,

3. Oxygen-driven removal of cellular grease (oxygen’s detergent functions),

4. Oxygen-activation of the enzyme systems of the body,

5. Oxygen-driven cellular detox mechanisms.

I point out that the direct evidence for my Oxygen Model of Pain comes from the efficacy of oxygen therapies— oxygen by mask and hyperbaric oxygen—for controlling headaches and migraine attacks. Specifically, in one double-blind trial breathing 100% oxygen for 15 minutes or less during headache episodes controlled or significantly reduced the pain of acute cluster attacks in all subjects. Not surprisingly, one fourth of the study participants experienced cluster attacks soon after the treatment was stopped —since various elements putting in jeopardy oxygen homeostasis were not addressed. Administration of higher concentrations of oxygen during the postoperative period relieves or reduces the intensity of postoperative pain. It appears to both reduce the release of a pain neurotransmitters called substance P and influence pain inhibitory pathways in the peripheral nerves. Correlation between urinary substance P and bladder pain has been documented.

Mechanisms of Pain

Following are some commonly observed clinical manifestations of biochemical interactions among the pain sensors and modifiers listed above:

1. Coronary chest pain is relieved or mitigated by the administration of oxygen, as are attacks of headache and migraine;

2. Direct oxystatic measures — treatments that restore oxygen homeostasis, including ozone, hydrogen peroxide, singlet oxygen, and related treatments — prevent, diminish or relieve diffuse tissue pain in fibromyalgia;

3. Indirect oxystatic measures— treatments such as prolotherapy with injection of 50% glucose or other suitable agents that stimulate fibroproliferative responses— relieve trigger point pain by evoking local oxystatic inflammatory tissue response;

4. Chronic back pain in many cases can be relieved by effective self-regulatory methods, especially with specific breathing methods (see limbic breathing in The Cortical Monkey and Healing (2000);

5. Pain syndromes accompanying reflex sympathetic dystrophy can be relieved with direct oxystatic therapies combined with indirect oxystatic measures, including restoration of bowel ecology and hepatic detoxification (personal unpublished observations); and

6. Cooling of forehead diminishes sympathetic tone, increases regional blood supply (correcting oxygen deficit), and relieves certain types of pain associated with dysautonomia.

For additional information about the Oxygen Model of Pain, I refer the reader to a companion tutorial entitled "Neurochemistry and Clinical Aspects of Pain."

Neurochemistry of Pain

A large number of pain neurotransmitters are involved in clinical pain syndromes, including: substance P; enkephalins; neurokinin 1, 2, and 3; serotonin; adenosine triphosphate (ATP); nitric oxide; calcitonin; vasoactive intestinal peptides; epinephrine, norepinephrine, and related sympathomimetic agents; glutamic acid, aspartic acid, and related excitatory transmitters; and GABA, glycine, and related inhibitory transmitters.2-4

* Excitatory transmitters increase pain:

        Glutamic acid and aspartic acid,

        Activation of NMDA receptors,

* Inhibitory transmitters prevent or diminish pain.

Next to oxygen and serotonin, substance P (SP) is the best examined of all the pain neurotransmitters, and its relationship with oxygen deficit has been most clearly delineated. It is an 11-residue peptide belonging to the tachykinin sub-family of G-protein-coupled receptors (GPCR). Those receptors form a class of integral membrane proteins. Serotonin in the mammalian brain and receptors of the olfactory epithelium that binds odorants are two other members of this family are receptors.

Oxygen deficit triggers the release of substance P. There are several lines of direct and indirect evidence for it.3 Direct evidence for that comes from experiments in which decreasing concentrations of oxygen were associated with the release of increasing amounts of SP. Specifically, the carotid bodies contain SP — in concentrations ranging from 1.4 to 1.6 ng/mg protein — that is released in response to tissue hypoxia. The amount of SP released from the carotid bodies increases in proportion to the severity of hypoxia. It is noteworthy that the release of SP by hypoxia is a calcium-dependent process, and is primarily mediated by N- and L-type Ca2+ channels.

Related Tutorials

 

Tutorial P1. What Is Pain?

Tutorial P2. The Oxygen Model of Pain

Tutorial P3. Migraine Migraine - Please Say Yes to Detection and No to Diagnosis

Tutorial P4. Migraine Labels That Reveal Nothing and Hide Much

Tutorial.P5. Neurochemistry and Clinical Aspects of Pain

Tutorial P6. A Pathologist’s Migraine

Tutorial P7. A President’s Migraine

Tutorial.P8. A Politician’s Migraine

Tutorial.P9.  Short-term Use of Migraine Attacks With Drugs Concurrent With Nondrug Natural Remedies

 

 

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