ALS, or amyotrophic lateral sclerosis, is also known as motor neuron disease because it affects exclusively motor neurons that control the body's voluntary and skeletal muscles. While there is no cure, evidence continues to mount that mitochondrial failure is a primary cause. If researchers can identify a cause, a cure may be around the corner. Because creatine is closely involved with mitochondrial function, the nutrient has come under scrutiny as a potential treatment.
Mitochondria
Mitochondria are often referred to as the "powerhouse" of cells. These organelles residing within cells convert glucose into ATP, or adenosine triphosphate, in a process called oxidative phosphorylation. ATP is the major source of fuel for the heart, brain and skeletal muscles. During oxidative phosphorylation, electrons pass between cells using special proteins as carriers in what's known as the electron transport chain. This basic biochemisty sets the stage for understanding creatine's role as a potential ALS treatment. The dynamics are detailed in a web-based tutorial published by Washington University Department of Chemistry.
Electron Transport Chain
The electron transport chain is crucial for fueling muscles and makes it possible for chemical messengers to reach from the brain all the way to the toes. Researchers reporting in the November 2008 issue of "Molecular Medicine" explain that in ALS, toxins target the mitochondrial electron transport chain, contributing greatly to the disease's cause and progression. In particular, the inefficient transfer of electrons produces a barrage of reactive oxygen species or ROS that turn mitochondria into the primary ROS producers in the cell. The result is motor neuron death leading to the muscle weakness and paralysis characteristic of ALS.
Creatine's Role
Creatine is consumed in the diet and synthesized in the body. The major dietary source of creatine is meat protein. Fully 95 percent of creatine is found in skeletal muscle. Creatine is moved by protein carriers into the electron transport chain, where it plays a major role in oxidative phosphorylation, the process that produces ATP, the major source of cellular energy. Creatine metabolism provides nearly half of the energy during the first 10 seconds of a muscle contraction. Research published in the November 2004 issue of "CNS Drugs" describes this process and how creatine supplementation improves athletic performance.
Creatine in ALS Patients
Because of the criticality of creatine in the electron transport chain and its success in improving muscle strength in athletes, researchers tested creatine supplementation in ALS patients hoping for the same benefit. The researchers published their results in the October 2008 issue of "Amyotrophic Lateral Sclerosis." One hundred seven ALS patients were randomized to receive either daily treatment of 5 g of creatine or placebo for nine months. Although the creatine did not improve muscle function as hoped, it did improve survival. The authors reported that research into the survival benefits of creatine is ongoing.
References
- Washington University Department of Chemistry: Oxidative Phosphorylation
- "Neurmolecular Medicine"; Creatine and Its Potential Therapeutic Value for Targeting Cellular Energy Impairment in Neurodegenerative Diseases; Peter Adhihetty and Flint Beal; November 2008
- "CNS Drugs"; The Role of Creatine in the Management of Amyotrophic Lateral Sclerosis and Other Neurodegenerative Disorders; Amy Ellis and Jeffrey Rosenfeld; November 2004
- "Amyotrophic Lateral Sclerosis"; Creatine Monohydrate in ALS: Effects on Strength, Fatigue Rrespiratory Status and ALSFRS; Jeffrey Rosenfeld et al.; October 2008
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