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12 Articles in Volume 7, Issue #8
A Clinical Guide to Weaning Off Intrathecal Opioids
Avoiding the Pitfalls of Opioid Reversal with Naloxone
Central Role of Dopamine in Fibromyalgia
CES in the Treatment of Insomnia: A Review and Meta-analysis
Combined Phrenic Nerve Palsy and Cervical Facet Joint Pain
Dextrose Prolotherapy for Unresolved Neck Pain
Low Level Laser Therapy - Part 1
Mistakes Made by Chronic Pain Patients
Near-infrared Therapeutic Laser and Pain Relief
Patulous Eustachian Tube: Part 2
The “Promise” of Pain Medicine: Profession, Oaths, and the Probity of Practice
Three Dimensional Imaging of the Foot

Low Level Laser Therapy - Part 1

Effects at the cellular level increase ATP energy and DNA synthesis and benefit acute and chronic musculoskeletal aches and pains, chronic inflammation, acute soft-tissue injuries, as well as other conditions.
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I am very pleased to introduce you to Dr. Dan Murphy. He is a seasoned clinicist, having been in practice for 30 years. He is extensively published and considered an expert in cervical spine injuries as well as laser therapy. He has published many articles on the neurophysiology of therapeutic laser. In this article, Dr. Murphy elaborates on a few of the unique physiological effects of laser on cellular structures. I am excited to have Dr. Murphy sharing his extensive knowledge with us and look forward to reading more in the near future..

William J. Kneebone, CRNA, DC, CNC, DIHom

In 1997, Douglas Wallace wrote an article for Scientific American titled “Mitochondrial DNA In Aging and Disease.”1 In this article, he notes that an intracellular organelle, the mitochondria, is the power plant of cells because it produces ATP energy. “Mitochondria provide about 90% of the energy that cells, and thus tissues, organs, and the body as a whole need to function.” Every cell in the body contains hundreds of mitochondria that produce the energy that the body requires.

Each mitochondria contains many copies of DNA, called mitochondrial DNA, or mtDNA. Mitochondrial DNA is separate and distinct from the cell’s copy of nuclear DNA. An individual’s mtDNA comes from, and is identical to, the mother’s mtDNA. Mitochondrial DNA (mtDNA) codes for 13 proteins (enzymes) required for the production ATP energy.

A simplified mechanism of the mitochondrial contribution to the production of ATP energy is illustrated in Figure 1 (after Audesirk2). Note that the primary producer of ATP energy is the “electron transport system” of the mitochondria. This is important in the understanding of laser physiology. Wallace further notes: “Anything able to compromise ATP production in mitochondria could harm or even kill cells and so cause tissues to malfunction and symptoms to develop.”1

The inner membrane of the mitochondria contains 4 protein complexes called the respiratory chain. Electrons from food pass through these protein complexes with the help of Coenzyme Q10, interacting with oxygen and hydrogen to produce water and ATP energy. When discussing low powered laser therapy, it is important to understand that the terminal enzyme of the mitochondrial respiratory chain, the “cytochrome c oxidase” enzyme, also functions as a photoacceptor.3,4

“As the respiratory chain participates in energy production, toxic by-products known as oxygen free radicals are given off. These oxygen derivatives carry an unpaired electron and are highly reactive, and can attack all components of cells, including respiratory chain proteins and mitochondrial DNA. Anything that impedes the flow of electrons through the respiratory chain can increase their transfer to oxygen molecules and promote the generation of free radicals.”1 Conversely, anything that improves the flow of electrons through the respiratory chain will increases the production of ATP while reducing the generation of free radicals. This is the key to low-level laser therapy.

Wallace notes: “The mitochondrial theory of aging holds that as we live and produce ATP, our mitochondria generate oxygen free radicals that inexorably attack our mitochondria and mutate our mitochondrial DNA.”1 The accumulation of mitochondrial DNA mutations reduce ATP energy output below optimal levels. “In so doing, the mutations and mitochondrial inhibition could contribute to common signs of normal aging, such as loss of memory, hearing, vision, and stamina.”1

In support of the writings of Wallace is the 2004 book edited by Rainer Straub and Eugenio Mocchegiani. These authors note: “One of the most accepted theories of aging is the free radical theory of aging. The overproduction of free radicals can induce cell death. Aging, as stated in free radical theory of aging, is characterized by an increased production of free radicals in several tissues or a decreased antioxidant defense leading to chronic oxidative stress.”5 The mitochondria are the major source for the production of free radicals.

As noted, the mitochondrial production of ATP is coupled with the production of Oxygen Free Radicals (Reactive Oxygen Specie,s or ROS). This is undesirable because ROS are major contributors to many diseases, including cancer. Additional support for the deleterious nature of free radical production comes from the authoritative 2006 text by Singh, titled Oxidative Stress, Disease and Cancer. The preface of this text states: “The ability of cells to reduce oxygen to produce energy is fundamental to aerobic life.

“Unfortunately, production of energy by reduction of dioxygen leads to the generation of reactive oxygen species that cause oxidative stress.

“It is now well established that oxidative stress causes extensive damage to cellular components, which can lead to a number of diseases, including cancer.”6

A recent article by Pieczenik and Neustadt states: “A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction.”4

Figure 1. Simplified mechanism of mitochondrial contribution in the production of ATP.

Tiina Karu wrote the chapter “Low-Power Laser Therapy” in the book Biomedical Photonics Handbook in 2003.7 She notes that low-level laser therapy probably works because the laser light is absorbed by the mitochondria photoreceptors, which enhances cellular metabolism. She also notes that the primary reaction of laser light is in the mitochondria, which results in increased ATP energy. “The mechanism of low-power laser therapy at the cellular level is based on the increase of oxidative metabolism of mitochondria, which is caused by electronic excitation of components of the respiratory chain.”7 In her most recent book, Karu notes that the primary component of the mitochondrial respiratory chain being influenced by laser phototherapy is the terminal enzyme of the mitochondrial respiratory chain, the “cytochrome c oxidase” enzyme.3

Karu states: “It is known that even small changes in ATP level can significantly alter cellular metabolism.”7 The elevated levels of ATP energy increase the rate of DNA synthesis.

Consequently, the increased levels of ATP energy and DNA synthesis will benefit acute and chronic musculoskeletal aches and pains, inflamed oral tissues, help to heal skin and mucosal ulcerations; treat edema, burns, and dermatitis; relieve pain and treat chronic inflammation as well as autoimmune diseases. Laser therapy is also used in sports medicine and rehabilitation clinics (to reduce swelling and hematoma, relieve pain, improve mobility, and to treat acute soft-tissue injuries). It was shown in the 1980s that laser radiation altered the firing pattern of nerves, which is connected with pain therapy. In 1988, Rochkind et al.8 noted that the ability of laser irradiation to affect the action potential was dependent upon the wavelength: the effect was strong at 540 nm and 632.8 nm; while laser radiation at 660, 830, 880, 904, and 950 nm had no effect.

The 2002 book by Jan Turner and Lars Hode, titled Laser Therapy Clinical Practice and Scientific Background, contains 1,281 references. These authors note:

Last updated on: February 25, 2011