Carnitine is a constituent of red meat as well as milk products and eggs, it is not present in vegetables. It is also a metabolic by-product from the degradation of lysine. Carnitine was given its name based on its source; carni (meat as in chili con carni, chili with meat), i.e., carnitine in the chili comes from meat. Early on it was considered as a vitamin since the definition of a vitamin is a substance required in small amounts that cannot be synthesized in the body. Carnitine fits this definition as it applies to infants, but not so well for adults because infants are unable to synthesize carnitine but adults can when adequate lysine is consumed.
One has to look long and hard to find what the carnitine content of foods is (see end reference.) Since this is difficult, the natural assumption is that carnitine must be synthesized by the body in adequate amounts which in most cases it is. After careful seeking the source or precursor, which turns out to be the amino acid lysine, researchers assumed that all is well if one consumes adequate lysine. Therein lies the rub. Lysine is not too abundant in cereal grains, beans, celery and such. To make matters worse, carnitine also is absent from these foodstuffs. If you were a pig consuming an all vegetable diet (corn and soybeans), the herdsman would insist in supplementing your diet with synthetic lysine or if not too expensive, carnitine.
Perhaps we shouldn't worry about carnitine anyway. This obscure biochemical isn't all that complex in structure and it appears that its primary role is to shuttle fats into the mitochondria so that they can be metabolized. In fact, since it is only essential for long chain fatty acid metabolism, perhaps we should leave it alone and just let the fatty acids accumulate in the cell cytosol as they must do if they can't be metabolized. Alas, we are coming to understand that when one set in action a sequence of events in biochemical processes, the outcome is far from predictable.
In carnitine's checkered past, it was discovered that in a set of identical twins, they had a problem with cramps when they consumed meals high in fat, or when they fasted, or underwent exercise. Since most of us do these things and since most of us have cramps from time to time, perhaps the body is trying to tell us something, if only we would listen.
For a while let's forget about ourselves and turn our attention to the pig nutritionist and see what this animal (the pig not the nutritionist) has to tell us. Adult pigs (called hogs for the educationally deprived) have adequate levels of the enzymes necessary to synthesize carnitine. However, the newborn does not. Thus, carnitine is an essential nutrient! Where does the baby get its carnitine? From mom's pap, where-else. So if mom isn't delivering enough milk or if the herdsman chooses to use a ubiquitous milk replacer, the baby pig may be falling short of its requirements. Maybe this isn't such a problem, but let's see what happens in the baby pig model and then by a stretch of the imagination see what happens in Homo sapiens.
In pigs, those deficient in carnitine had lowered rates of gain, i.e., they don't grow as fast as they could or should. The need for energy makes an adequate amount of carnitine stored in the piglet important, hence the dependence on mom. In addition, carnitine has an influence on insulin and insulin-like growth factor-1 which translates to an effect on muscle fiber development, which in turn can mean the difference between fatty tissues or muscle. From the hog farmer's standpoint, when carnitine is supplemented in the diet, he has pigs that grow-up to have carcasses that are less fatty, have a higher lean content and when the 220 or so pound hog is slaughtered he gets a premium for the quality. This translates to money in the pocket.
Not so for couch potatoes and future ones. Look about at the more that few overweight, poorly muscled youth and wonder if we have predisposed a generation of young adolescents to a fate which is truly worse than death. All the accompanying consequences of being overly "fat".
Once the die is cast, it is difficult to reverse nature. There is a belief in some circles that fat cells once formed in the young, are with us for life and while they can be engorged with fat or depleted dependent on diet and environmental considerations, they are there to spring forth in all their beauty when extra calories are consumed. Frightening isn't it? And when the recommendations of our current day Cassandras who unfortunately are untrue to their name, are believed, we will have to wait and see. But while we wait, there's more.
Parents are worried about Reye's syndrome, and have been advised by the medical profession that aspirin and other salts of salacylic acid may under certain circumstances directly cause the disease. Seems that as children exposed to virus infections sometimes lapse into conditions that are described as being; feverish, confused, in a stupor, vomiting and a number of other symptoms of Reyes, that the problem is due to having been given aspirin or one of the related compounds. So, in good faith, people have switched from aspirin to other pharmaceuticals to diminish the effects of fever, &c. All this when the medical profession isn't sure exactly what Reye's syndrome actually is or what causes it. Here is where carnitine enters the scene. (L-Carnitine, Academic Press, 1992, pp 91). "Episodes of metabolic encephalopathy (brain damage), hypoglycaemia (inadequate control of blood sugar levels), defective synthesis of ketones (fat metabolism), hepatomegaly (enlargement of the liver), with fatty degeneration of the liver(see comment regarding aflatoxin in notes) are characteristic of Reye's syndrome, one of the major causes of sudden infant death (Howat et al, 1985). Some of these infants were shown to have dicarboxlic aciduria, with adipic, suberic, and sebacic acids in their urines (Rhead et al, 1983). Total carnitine content was markedly low in their tissues (Stanley et al, 1983)."
The questions that haven't been asked are: 1) were these children suckling on mom's pap? 2) were they on a high carbohydrate, low protein diet and one lacking in meat as a source of protein? 3) were the children overly fat or were they skinny? 4) Would carnitine supplemented to the diet have avoided the problem or been therapeutic? Alas, nowhere do the answers to these questions appear, and certainly not in those pages on the Internet provided as a public service by a number of non-profit and governmental agencies.
What's a parent to do? Avoiding aspirin and the like is a stop gap measure, in fact it appears that the incidence of Reye's is increasing. Perhaps the answer is too easy. First, supply human milk rather that those substitutes that are so readily available. Second, include meat (red meat) in the diet at an early age (after all mankind is called an omnivore for a reason). And third, pediatricians should routinely monitor carnitine in infants on a routine basis.
Will this reduce the incidence of Reye's syndrome? Possibly. But the child (like the baby piglets) will have better nutrition and how can that be all that bad.
>From a biochemical standpoint, carnitine plays an essential role in energy metabolism. In long chain fatty acids metabolism, it serves as shuttle between the cell sap and the mitochondria inner-workings permitting breakdown of the long carbon chain into two carbon fragments. But probably the more important role is in maintaining a balance between the concentration of a compound called acyl CoA in the cell compartments. For sugars to be metabolized, they are sequentially degraded to smaller fragments until carbon dioxide is produced, along the way energy is conserved. Acyl CoA is an important intermediate in transfer of energy. Accordingly, it is important that the concentration of Acyl CoA be regulated and this function falls on carnitine which in forming a complex with Acyl CoA permits it being shuttled among cell compartments. Without carnitine, cell metabolism would soon grind to a halt and as goes the cell, so goes the tissue and the body, i.e., death!
Others have stretched the value of carnitine to include everything from hardening of the arteries, plaque, Altzheimers, muscle wasting in the elderly and you name it, it's been proposed by the snake oil salesmen as good for what ails. To diminish their pitch and add a precautionary note; just because something appears to be "non-toxic" in the dosage given, doesn't mean it can't wreck havoc on some other part of the biological enigma we call the body. Truly we need to know more about carnitine and it's multi-variant roles. But, do you want to do a one rat experiment where the rat is you?
In the meantime, perhaps we should reconsider our diet as more than just something that taste good or is popular at the moment. Fueling the body is important and the role (and source) of protein is more important than would first appear. Shortchanging your own system is up to you, but what about the unborn, the infant and the growing child.
These thoughts, provoked about carnitine, were inspired by an article, where-else, but in a "farmer's magazine", Feed Management, October 1999 by Phillip Lobo. For his reading audience he cites song and verse to recent research (for pigs). Too bad there aren't companion articles for Homo sapiens.
When our medical and biochemical specialist, which I suppose includes human nutritionist as well, seek information on the Internet they will be overwhelmed by promoters of vitamins and minerals as well as other nutriceuticals These are offered as the fountain of youth and solutions to nefarious ills. Beware!
In the case of carnitine, two sites that offer factual information are: Journal of Nutrition and Los Angeles AIDS web site.
If you look to recent peer reviewed scientific papers, you will be greatly disappointed as the information contained is of recent research findings and typically ignores results of twenty or so years ago. And the bastion of the educational system, textbooks, are written with much glitz and graphics but ignore the basic principles that need be taught. Human nutrition is much too important.
Notes: Aflatoxin is one of the most potent carcinogens known to man. First instances of the metabolic effect of aflatoxin were in reports that moldy peanuts (ground-nuts in South Africa) caused a condition termed fatty liver in turkeys. Obviously, the aflatoxin was interfering with fat metabolism and resulting in the accumulation of fat in the liver cells. This is not unlike the condition known for Reye's syndrome. While much attention has been paid to the role of aflatoxin in carcinogenesis, little is known about its role in interfering with lipid metabolism and fatty acid transport across membranes. This is just one more instance where events triggered by one imbalance in the body cascades through other systems.
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