Polly: Carnitine transports long-chain fatty acids into the cell mitochondrion so that they can be burned. Often it is prescribed to help burn off the very long chain fatty acids that accumulate in certain diseases, including some cases of autism. Symptoms of carnitine deficiency are poor muscle tone, problems walking and severe hypoglycemia.
Sharon: An interesting anomaly on Jennifer is that she tolerates a small addition of Carnitor (prescription carnitine) 1.6ml 2xday, but when our doctor tried to double that to 3.0ml 2xday… she went into a spiral of nine days of grand mal seizures (???) Why such a reaction with the increase? Jennifer does not show a deficiency, but does show at times a mild carnitine-wasting problem. Currently, Jennifer is showing a great deal of “ thickening” fat deposits around the trunk. This is why we tried to increase the Carnitor. Although it was working to dissipate the fat, it wasn’ t worth the seizure activity.
Note: Jennifer does not have autism or fibromyalgia, but she has a lot of hypothyroid symptoms. She has not been treated with thyroid because her blood tests were normal. Her doctor suspects a mitochondrial disorder and hence he suggested the use of carnitine, even though the child does not have a carnitine deficiency. The package insert warns that carnitine can cause seizures.
Polly: Carnitine, under the right circumstances, may be useful. It can actually protect one from seizures because it helps the body dispose of ammonia. Yet, excessive carnitine can induce seizures. Likely, this is due to a reduction in carbon dioxide production. Carnitine, by encouraging the oxidation of fats, will suppress glucose oxidation and will therefore reduce the production of carbon dioxide. (Glucose oxidation produces more carbon dioxide than does the oxidation of fats. ) Carbon dioxide is very important. It helps get oxygen delivered to the tissue and helps protect one from seizures. One mother on the Internet wrote that making sure her son wasn’ t hungry helped him tolerate the carnitine. Perhaps her strategy made a little more glucose available, which helped protect her son.
Another possible problem with carnitine is that the carnitine transport system changes the proportion of unsaturated to saturated fats that are burned. More unsaturates will be burned which could be damaging to the mitochondria.  It appears to be a matter of balance again not too much and not too little. A safer approach would be to only use carnitine if a child’ s carnitine levels measured moderately low and if it seemed to benefit the child. The thyroid hormone levels should probably be adjusted before considering a supplement of carnitine. In some cases, correcting a hypothyroid problem can increase carnitine levels to normal.  Thyroid should also increase production of carbon dioxide, which would help protect one from seizures.
Nutrients that support the formation of carnitine by the liver and kidneys include lysine, methionine, B6, C, niacin and iron.  The methylation provided by SAMe is important in the formation of carnitine too.  Several antiseizure medications may lower carnitine. These are phenytoin (Dilantin) and valproic acid (Depakote, Depakene). A supplement of carnitine may be necessary when using these drugs.
The use of coconut oil should provide some protection from seizures. At least in rats, it has been shown that several different saturated oils, especially the lauric acid found in coconut oil, is protective against seizures.  The saturated fatty acid palmitic acid in coconut oil may also be useful. The palmitic acid in coconut oil suppresses the formation of lactic acid. Lactic acid, by competition, can reduce the carbon dioxide in the blood. (Many of the autistic children have lactic acidosis.)
The short chain saturated fatty acids in coconut oil do not need carnitine to be burned. This provides protection. Raymond Peat, PhD, explains this in an article on coconut oil found at his website, //www.efn.org/~raypeat/index.html. The following is an excerpt:
Coconut oil is unusually rich in short and medium chain fatty acids. Shorter chain length allows fatty acids to be metabolized without use of the carnitine transport system. Mildronate, which I discussed in an article on adaptogens, protects cells against stress partly by opposing the action of carnitine, and comparative studies showed that added carnitine had the opposite effect, promoting the oxidation of unsaturated fats during stress, and increasing oxidative damage to cells. I suspect that a degree of saturation of the oxidative apparatus by shortchain fatty acids has a similar effect that is, that these very soluble and mobile short-chain saturated fats have priority for oxidation, because they don’ t require carnitine transport into the mitochondrion, and that this will tend to inhibit oxidation of the unstable, peroxidizable unsaturated fatty acids.