Acetyl-L-carnitine (ALC) is a biochemical substance made by all organisms except bacteria. Every cell of every plant, animal,
yeast, mold, mushroom, and protozoan makes acetyl-L-carnitine molecules and uses them in the extraction of energy from fats.
In the body, ALC and L-carnitine are interconvertible.
ALC’s essential role in fat metabolism
Cells are constantly breaking down fat molecules and making new ones. This is how cells
- maintain and repair their internal and external membranes;
- adjust the structure of these membranes in response to changing conditions;
- take advantage of the energy contained in dietary fats.
A fat molecule typically consists of three fatty acids bonded to a glycerol bridge. The process of breaking down fats starts
with enzymes that pull the fatty acids off of their glycerol bridges. The free fatty acids are then sent to subcellular organelles
called ‘mitochondria’ for further processing.
Mitochondria, however, are bounded by a protective barrier — a double membrane that prevents inappropriate molecules from
entering and disrupting the specialized processes that take place inside. Even appropriate molecules may require assistance in passing through this barrier. In particular, many of our dietary fatty acids (the longer-chain
ones) are unable to enter a mitochondrion in their free form.
To enable long-chain fatty acids to pass through this barrier, cells ‘tag’ them with a carrier substance called ‘L-carnitine’
— an enzyme attaches a molecule of L-carnitine to each fatty acid. A transporter protein in the inner membrane will now recognize
the carnitine-fatty-acid construct and allow it to pass through the membrane into the interior of the mitochondrion.
Once a fatty acid molecule is inside the mitochondrion, its L-carnitine tag is stripped off and the fatty acid is taken up
by a processing complex that breaks it into small pieces, exposes the pieces to oxygen atoms, and siphons off the energy released
during the resulting chemical reactions, storing it for future use.
What happens to the L-carnitine tags? Some of them are directly transported back out through the mitochondrial membranes into
the cell-at-large; these are now ready to transport more fatty acid molecules into the mitochondria. Others of the L-carnitine
molecules are converted to acetyl-L-carnitine which is efficiently ferried out of the mitochondria by membrane proteins. Thus,
acetic acid molecules use L-carnitine to ‘hitch a ride’ out of the mitochondria so that they can be used in the many ‘acetylation’
processes that take place in cells. Once outside the mitochondria, acetyl-L-carnitine can be deacetylated back to L-carnitine for reuse as a fatty acid transporter.
What we can’t tell you
In the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration
have adopted censorship as a method for intensifying their control over the supplement industry and its customers.
Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments,
even if they are, in fact, effective.
Accordingly, we will limit our discussion of Acetyl-L-Carnitine to a brief summary of relevant research,
and let you draw your own conclusions about what medical conditions it may be effective in treating.
ALC as a treatment for aging: the theory behind it
‘Aging’ is a catch-all term that covers many different medical ailments — weakening bones, muscles, and skin; stiffening blood
vessels and connective tissue; failing memory, cognition, and sensory organs; loss of cancer suppression; etc. Thousands of
medical names have been given to different variations of these ailments — names such as ‘osteoporosis, arthritis, Alzheimer’s,
atherosclerosis, pancreatic cancer, macular degeneration, etc. But these age-related ailments share some fundamental causes,
- structural damage by free radicals inside and outside of cells
- protein damage from cross-linking sugars
- growing numbers of incorrectly regulated genes
- skewed proportions of molecules in biological membranes
- biochemical feedback loops that stray from stable patterns.
These (and several other fundamental causes of aging) take place throughout the body, and they affect all the structures inside
and outside the cells. Among the structures they affect are the mitochondria — the subcellular organelles that extract energy
from fats and carbohydrates. As mitochondria extract energy from these substances, they store the energy in the form of ATP
molecules, which are distributed to all parts of all cells in the body.
As cells age, their mitochondria age. The mitochondrial membranes develop skewed proportions of the various molecules they
are made of — particularly the lipid molecules which are made from fatty acids. This disrupts the functions of complex nanomachinery
which resides in the membranes. Some of these nanomachines transport molecules into and out of the mitochondria; others perform
the actual extraction of energy from broken-down fats and carbohydrates, and channel this energy into the production of molecules
Thus, a skewed membrane composition causes disrupted nanomachine function, which leads to a defective transport of raw materials
and to a decline in ATP production. As the transport system fails and the wrong kinds of molecules are allowed into the mitochondria,
the composition of the membranes becomes even more skewed. The energy-extracting nanomachines are forced into non-optimal
positions in the membranes and they become less efficient; an increasing percentage of the energy they produce is wasted instead
of being stored; and the mitochondria, and the cells they belong to, become starved for energy. The wasted energy is simply
dissipated as heat instead of being used for maintaining biological structures and for enabling damaged cells to be replaced.
The current view is that ALC supplementation increases the amount of L-carnitine available for tagging fatty acids in cells.
This, in turn, alters the distribution of fatty acids transported into mitochondria. A better fatty acid mix restores the
proper proportions of lipid molecules in the mitochondrial membranes. With an improved membrane environment, the nanomachines
embedded in the membranes perform better. As a result, the efficiency of energy production in mitochondria is enhanced, enabling
more of the energy extracted from food to be stored as ATP instead of being wasted as heat. The subject is too complex to
describe here in more detail than this, but the ‘bottom line’ is that ALC rejuvenates mitochondria, and the boost in useful
energy that results from this enables cells to behave more youthfully, too.
Potential uses of ALC
Since ALC plays a central role in the production of energy in cells of all kinds, an increase in ALC availability would be
expected to ameliorate many different kinds of ailments that involve cellular energy deficiency or impaired fat metabolism.
Athletic individuals could reasonably expect that ALC consumption would lead to accelerated fat metabolism and increased endurance
But ALC also has effects that seem to be independent of its involvement in energy production. For example, ALC enhances the
production of the neurotransmitter acetylcholine, it stimulates the synthesis of protein, and it affects the fluidity of biological
membranes. The mechanisms are poorly understood, but we can nevertheless exploit them to alter the performance of our bodies
Medical conditions which have responded well to ALC supplements include:
- Alzheimer’s, Parkinson’s, and other neurodegenerative diseases
- Hepatic neuropathy and encephalopathy
- macular degeneration
- HIV-related lipodystrophy
- increased fat metabolism and endurance during exercise
- diabetes and diabetic neuropathy
- Peripheral neuropathy due to HIV or cancer chemotherapy
- high blood pressure
- recovery from heart attacks
- recovery from strokes
- age-related memory decline
- low libido and erectile dysfunction
- MS-related fatigue
- noise-induced hearing loss
- Peyronie’s disease
- Rett syndrome cardiac failure
- Nerve injury
- Peripheral neuropathy
- eye-lens stiffening
Several of these ALC applications have been receiving much attention recently. Let’s look briefly at these.
Alzheimer’s and Parkinson’s
The first clinical study of ALC for treating Alzheimer’s Disease was reported in 1983. Wouldn’t you think that by now, a quarter of a century later, the medical world would have settled the question of whether
or not this substance should be a standard weapon against this disease? Well, it hasn’t, for reasons that are controversial.
Cynics claim that the medical profession downplays all dietary supplements because physicians are being bribed by the makers
of prescription drugs. Others claim that mainstream medicine shies away from supplements because they give inconsistent results
in human clinical trials — and that these trials of supplements are conducted sloppily, on low budgets, in contrast to prescription
drugs, which are tested in high-budget trials.
Be that as it may, many studies of ALC in cell culture, lab animals, and in humans have demonstrated unequivocal anti-Alzheimer’s
effects. As summarized in one medical review, “improvements were noted in spatial learning tasks, timed tasks of attention,
discrimination-learning tasks, and tasks of personal recognition.”
Several mechanisms have been suggested through which ALC produces its anti-Alzheimer’s effects. These include anti-oxidant
action, prevention of apoptosis (cell-death by caused by signalling molecules), and prevention of toxicity due to amyloid proteins.
ALC has received attention from Parkinson’s researchers, too. The beneficial action of ALC in Parkinson’s Disease has been shown both in animal models and in humans. The mechanisms suggested by researchers to explain the anti-Parkson’s effects are vague and involve preventing oxidative
Brain rejuvenation and nerve repair
ALC enhances the effects of the Nerve Growth Factor — a substance made in the nervous system that stimulates nerve growth.
Tissue culture and lab animal experiments show that ALC causes heightened production of the receptor with which nerve cells
detect and respond to Nerve Growth Factor. This results in faster repair of damaged nerve cells and the replacement of brain neurons that have been lost through trauma or aging.
Blood pressure and heart protection
Two potential cardiovascular benefits of ALC supplementation were recently shown in clinical studies. First, a significant
lowering of blood pressure was seen in patients with coronary artery disease who were given combination of ALC with alpha-lipoic
acid for 8 weeks. And second, it was found that heart attacks will cause less damage to the heart if the subjects (lab animals, in these studies)
have been treated with ALC a few hours prior to the attacks.
It is often stated by promoters of acetyl-L-carnitine that, for use as a supplement, this form of carnitine is superior to
L-carnitine itself because it has a higher bioavailability. However, the absolute oral bioavailability of acetyl-L-carnitine
has not been determined in humans. It may well be higher than that of L-carnitine (which varies dramatically and inversely
with dosage). Regardless of what the percentage bioavailability of ALC turns out to be, it does what we want it to do: it raises blood
concentrations of ALC, making more of it available to cells throughout the body. In fact, 2 g/day of an oral ALC supplement
will increase blood levels to 143% of the pre-dose value.
Furthermore, ALC readily crosses the blood-brain-barrier. Its measurable effects on energy production and on neurotransmitter production in nerve cells have inspired numerous studies
of its ability to reverse the mental symptoms of aging and neurodegenerative diseases.
Dosages and co-supplements
Oral dosages of 1-3 g/day have been used in clinical trials for the medical conditions for which ALC has been studied. In
Alzheimer’s studies, for example, a typical dosage would be 500 mg taken three times per day. Much higher doses have been studied informally as an anti-aging treatment, with no apparent ill effects.
Since acetyl-L-carnitine enhances mitochondrial energy production, and since destructive free radicals are always a by-product
of this process, it is important to scavenge these free radicals before they can damage the mitochondria and other cellular
structures. The standard way to accomplish this scavenging is to use a second supplement — the antioxidant alpha-lipoic acid. A reasonable dosage would be 100 mg of alpha-lipoic acid three times per day.
Anyone who is considering the use of ALC for treating or preventing Alzheimer’s, Parkinson’s, or other neurodegenerative disease,
should also consider the simultaneous use of a curcumin-containing product like LifeLink’s Primeric™. The mechanism of action of curcumin is unrelated to that of ALC, which means that the combination may benefit from synergism.
Are Acetyl-L-Carnitine supplements useful for the conditions and purposes mentioned above?
We aren’t allowed to tell you, so you should take a look at some of the references cited here,
and then decide for yourself.