The Lesser Known Cousin
Acetyl-L-Carnitine: The Lesser Known Cousin
Acetyl-L-carnitine (ALC) is the powerful but lesser known cousin of L-carnitine (LC),
a natural cellular amino acid synthesized by the body. LC is required
for the conversion of fat, one of three types of cellular fuel, to
chemical energy. LC functions as a vehicle to transport subunits of
fat, fatty acids, into the specialized cellular structures, the mitochondria,
for conversion to a chemical form of energy. A deficiency in LC, common
in vegetarians (vegans), aging, and those who use certain prescribed
drugs, results in a tired physical and mental state.
is it different?
Structurally, the difference between the acetyl-L-carnitine (ALC) and L-carnitine (LC) is that ALC is an LC molecule
that also contains an attached acetic acid group. This structural difference
is small, but it produces a considerable difference in the biochemical properties
of the molecule and, consequently, in its effects on metabolism. Acetyl-L-carnitine can substitute
for L-carnitine in fat metabolism; however, as described below, recent studies have
resulted in identification of several biological characteristics that are unique
to acetyl-L-carnitine .
acetyl group on acetyl-L-carnitine can be donated to a specific acceptor molecule,
choline, to form the neurotransmitter acetylcholine, which helps
restore nerve function. This activity is believed to be at least
partly responsible for the improved mental function that results
from acetyl-L-carnitine supplementation in patients with cognitive disorders,
including Alzheimer's disease, Parkinson's disease, Chronic Fatigue
Syndrome, and other disorders of the nervous system. Additional
studies supporting a neuroprotective role for acetyl-L-carnitine are those demonstrating
an improvement in symptoms of peripheral nerve damage common to
acetyl group can also be utilized for the production of energy
in the Krebs cycle. This donation increases the availability of
an important cofactor (CoA) required for the conversion of carbohydrates
to energy. Sufficient amounts of carnitine, derived from acetyl-L-carnitine, are
necessary to transport, toxic, non-metabolizable, short-chain fatty
acids, out of the mitochondria, and thus to free up the cofactor,
CoA. A deficiency in acetyl-L-carnitine promotes a corresponding decrease in this
cofactor, and consequently impaired energy production from both
fats and carbohydrates, thus affecting energy levels in all cells
of the body.
but not LC, has been demonstrated to protect the nervous system,
partly because it more readily is transported into the nervous
system. Recent studies with humans have indicated many of the age-associated
disorders involving the nervous system, such as depression, impaired
cognition, and decreased mental alertness, may be at least partially
a response to a deficiency in ALC.
but not LC, protects the mitochondria. A recent finding demonstrated
that a deficiency in ALC affects the structure and energy-producing
capacity of the mitochondria. The mitochondria are responsible
for producing virtually all the energy required by the cell. Therefore
any subtle change in their structure can have a tremendous effect
on the cell's energy reserves. ALC has been demonstrated to revitalize
mitochondria by restoring levels of a key mitochondrial component,
a phospholipid known as cardiolipin, which is susceptible to age-associated
reduction in levels. Cardiolipin can be envisioned as the glue
that secures and organizes, or better yet, orchestrates, the energy-producing
machinery of the mitochondria.
acetic acid group on ALC allows it to enter the mitochondria more
readily than LC and consequently more rapidly perform its beneficial
effects An additional enzyme must act on LC before it can enter
can it affect physical and mental state?
These characteristics raise some questions. First, why would a deficiency in
a fat-burning chemical affect our physical as well as mental state? The two
systems of the body requiring the most energy are the muscular and nervous
systems. It has been estimated that for normal function and health, the brain
requires every day the amount of energy present in a quarter pound of sugar.
A lack of energy in brain and muscle tissues will be exhibited as impaired
physical and mental activity. If the deficiency persists for a sufficient period
of time, it can lead to disease.
the brain normally does not use fat for energy, (it prefers glucose
from carbohydrates), except under conditions of fasting or starvation,
it nevertheless can be adversely affected by a deficiency in ALC, because
of all 5 of the numbered items described above.
does it come from?
Although the cells of the body do produce this important chemical, it is widely
believed that the major source of the compound is derived from the diet. Meat,
lamb especially, is the major dietary source of ALC, and the basis for why
vegans can be deficient in ALC, since plants contain insignificant amounts.
with animals have recently demonstrated a gradual decline in plasma
levels of ALC with age, which correlates with age-associated energy
decline. Additional studies with humans have indicated a steady decline
in ALC, beginning with the fourth decade of life. This too is correlated
with energy decline. This decline in plasma ALC may be a reflection
of inefficient absorption from the diet and/or reduced synthesis. Both
are believed to be responsible for the lower levels of ALC as we age.
In view of the age-associated decline in the ability of the body to
synthesize and absorb ALC, use of dietary supplements to ensure adequate
ALC is a growing trend in healthy aging.
years, scientists have theorized that, in view of the biochemical
properties of acetyl-L-carnitine (ALC; also abbreviated as ALCAR),
it should have a beneficial effect on brain function. Many clinical
trials in the U.S. and Europe have looked into the ability of ALC
to slow the progression of natural cognitive impairment associated
with old age. Studies have varied in length from 3 to 12 months,
and doses from 1.5 to 3 grams/day.
of different study parameters, interpretation of the combined
results is a challenging endeavor. However, in a recently published
study, a group at Imperial College University in London has conducted
a "meta-analysis," which gathers data from a large
number of studies and uses statistical techniques to reach overall
conclusions. The result demonstrated a beneficial effect of ALC,
compared to placebo, in protecting against age-related cognitive
impairment. In addition, ALC was well tolerated. For
further information, click
Research Update column highlights articles related to recent scientific
inquiry into the process of human aging. It is not intended to promote
any specific ingredient, regimen, or use and should not be construed
as evidence of the safety, effectiveness, or intended uses of the
Juvenon product. The Juvenon label should be consulted for intended
uses and appropriate directions for use of the product.