THE ALS DIET - Semantic Scholar

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THE ALS DIET David A Steenblock, BS, MS, DO 26381 Crown Valley Parkway, Suite 130 Mission Viejo, CA 92691 1-800-300-1063 Amyotrophic lateral sclerosis (ALS) is characterized by brain and spinal cord motor neuron degeneration that cause progressive weakness and atrophy of the body’s skeletal muscles. Most sufferers have chronic neck and/or back injuries that have damaged the peri-spinal (around the spine) blood vessels creating a spinal cord that is barely getting enough oxygen. A primary contributor to ALS is endotoxins from bacteria, yeast and parasites in the intestinal tract that pass into the blood and lymph and finally reach the cerebrospinal fluid. Once in the cerebrospinal fluid these endotoxins are phagocytized (grabbed up) by the microglia that surround the motor neurons. Once these endotoxins get into the microglia they make them “go crazy” and begin churning out a tremendous quantity of noxious chemicals that injure and kill motor neurons. Many other toxic compounds can also enter the body, reach the microglia, and overwhelm them. The goal of our treatment program is to rid the body and intestine of these poison producing bacteria, strengthen and heal the inner lining of the intestines, repair the damaged blood vessels leading into the spinal cord, remove the inflammation within the spinal cord and support the motor neurons return to health. If followed religiously this program should result in impressive improvements. The program is a three week intensive program carried out in my office and includes the use of stem cell rich bone marrow (aspirate) to repair the gut, the tissues around the spine and the

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spinal motor neurons. This booklet will present some of the leading research on diet, foods and supplements that can help reduce the destruction to motor neurons.


The Ketogenic Diet and ALS A. The Mitochondria Within all our cells are little energy factories called mitochondria that produce high energy

molecules called ATP (adenosine triphosphate). The first phase of energy production is called Complex I which is blocked by the kind of mutant SOD1 that characterizes ALS. It has since been found that ketones can restore complex I function so that the mitochondria can continue producing energy for the muscles.

Dr. Zhao and his coworkers showed a ketogenic diet

produced a 3.5 fold increase in circulating ketones in the blood of mice models of ALS compared to control mice that were given standard laboratory diets. The ketones that were increased in the animals included acetone, acetoacetate and hydroxybutyrate (D-3-β hydroxybutyrate). The ketogenic mice maintained their muscle strength longer than the standard diet-fed mice and had significantly more motor neurons at the end of the study than the control mice. As the experiment continued, the ketogenic mice also lost weight at a slower rate than the control mice. Hydroxybutyrate has the highest ketone content and was found to correct the defects and override inhibiting agents by improving mitochondrial respiration and ATP production. This improvement also reduced free radical production and neuronal die-off. This significantly reduced the number of dying motor neurons in the ketogenic fed mice compared to the control mice, whose neurons showed degeneration and death from the mitochondrial defects. 1

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The ketone, hydroxybutyrate, has the potential of slowing down the rate of motor deterioration and death that is caused by SOD1-induced complex I inhibition.

In addition, with both familial and sporadic or acquired ALS, the level of glutathione, the main antioxidant in every cell, are usually lower. With d-β-hydroxybutyrate as an energy alternative in the ketogenic diet, glutathione levels are higher. The researchers suggest that mitochondrial dysfunction is caused by reductions in glucose-derived pyruvate that alter glutamate metabolism and lower glutamate and glutathione levels.2 In addition to the ketogenic di