L Carnitine, a safe abundant substance, significantly improves recovery of function after acute spinal cord injury
During acute injury to the spinal cord damage occurs primarily from two sources. The first source is the insult itself, including mechanical trauma and loss of blood flow to the damaged region of the cord. In the hours following the initial injury cell death continues and spreads. The spread of the damage is due largely to the actions of the directly injured cells. Damaged cells begin to run out of energy resulting in their death and eventually to damage of adjacent intact cells. Dying cells produce an excess of free radicals (reactive oxygen compounds) that can diffuse readily to surrounding cells causing progressive and spreading death of adjacent cells. As a result a focal region of damage can spread and become more global within hours up to a few days after the initial injury. A method to intervene during this spreading destructive cycle could prevent much of the secondary damage and most importantly loss of function could be minimized.
Recent research at the University of Kentucky indicates that a common dietary supplement, L Carnitine can prevent much of the secondary damage during acute spinal cord injury by preventing damaged cells from becoming energy deficient. L Carnitine facilitates the transport of fuel molecules into the mitochondria where most of the cellular energy is produced. The details of this biochemistry are a bit beyond the scope of this brief review but can be found online or any basic biochemistry text.
An encouraging aspect of this neuroprotective treatment is L Carnitine is very safe with few side effects if taken in recommended doses. In rare instances it can produce relatively mild side effects such as nausea, vomiting, stomach upset, heartburn, diarrhea, and seizures. It is a naturally occurring compound found in meat and dairy products and can be synthesized within our bodies from two readily available amino acids,lysine and methionine.
At present there are few interventions that can be safely administered to lessen the spreading of tissue damage after spinal cord injury, or stroke within the brain. Innocuous agents that can ameliorate the neurological outcome of devastating injury should be welcomed with open arms by clinicians, and incorporated into potential combinatorial therapies being developed by experimental neuroscientists.
Press Release: ScienceDaily (Sep. 28, 2011)
Commonly Used Supplement May Improve Recovery from Spinal Cord Injuries
A commonly used supplement is likely to improve outcomes and recovery for individuals who sustain a spinal cord injury (SCI), according to research conducted by University of Kentucky neuroscientists.
Sasha Rabchevsky, associate professor of physiology, Patrick Sullivan, associate professor of anatomy and neurobiology, and Samir Patel, senior research scientist -- all of the UK Spinal Cord and Brain Injury Research Center (SCoBIRC) -- have discovered that in experimental models, severe spinal cord injury can be treated effectively by administering the supplement acetyl-L-carnitine or ALC, a derivative of essential amino acids that can generate metabolic energy, soon after injury.
The researchers previously reported that following spinal cord injury, the mitochondria, or energy-generation components of cells, are overwhelmed by chemical stresses and lose the ability to produce energy in the form of the compound adenosine triphosphate (ATP). This leads to cell death at the injury site and, ultimately, paralysis of the body below the injury level.
Rabchevsky, Sullivan and Patel have recently demonstrated that ALC can preserve the vitality of mitochondria by acting as an alternative biofuel providing energy to cells, thus bypassing damaged mitochondrial enzymes and promoting neuroprotection.
Results soon to be published show that systemic administration of ALC soon after a paralyzing injury promoted the milestone recovery of the ability to walk. Unlike the animal control group given no ALC, which regained only slight hindlimb movements, the group treated with ALC recovered hindlimb movements more quickly and were able to stand on all four limbs and walk a month later. Critically, such remarkable recovery was correlated with significant tissue sparing at the injury site following administration of ALC.
Because ALC can be administered orally, and is well-tolerated at relatively high doses in humans, researchers believe that their discovery may be translated easily to clinical practice as an early intervention for people with traumatic spinal cord injuries.
Initial funding for these studies was provided by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT). Based on their findings, the research team has been awarded additional grant funding from the National Institutes of Health (NIH) and the Craig H. Neilsen Foundation, with the aim of enabling the investigators to study the beneficial effects of combining ALC with an antioxidant agent known as N-acetylcysteine amide (NACA). The results were reported at the recent National Neurotrauma Society Symposium in July 2011, and will be presented again at the Society for Neuroscience meeting in November 2011.
When translated into clinical practice, this research is expected to offer a viable pharmacological option for promoting neuroprotection and maximizing functional recover following traumatic spinal cord injury.
