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This article first appeared in the by A.S. Gissen The reversible formation of ALC in the
body modulates cellular concentrations of free coenzyme A and acetyl-coenzyme
A, compounds integrally involved in numerous cellular functions including
energy production. By exchanging across sub-cellular membranes, ALC serves as
a pool of acetyl groups to regenerate acetyl-CoA from free coenzyme A. While
this natural role for ALC in cellular metabolism has been well established
for decades, research in recent years has hoisted ALC from its somewhat
mundane role in energy production to nutritional cognitive enhancer and
neuroprotective agent extraordinaire. Indeed, taken in its entirety, ALC has
become one of the premiere “anti-aging” compounds under scientific
investigation, especially in relation to brain and nervous system
deterioration. ALC is found in various concentrations
in the brain, and its levels are significantly reduced with aging.(1) In
numerous studies in animal models, ALC administration has been shown to have
the remarkable ability of improving not only cognitive changes, but also
morphological (structural) and neurochemical changes. Initially, these
effects were thought to stem from ALC’s ability to donate its acetyl group to
help form acetylcholine, or its ability to mimic acetylcholine, a
neurotransmitter known to have an important role in memory and related
cognitive functions. In fact, it is now known that ALC has
varied effects on cholinergic activity, including promoting the release(2)
and synthesis(3) of acetylcholine. Additionally, ALC promotes high affinity
uptake of choline, which declines significantly with age.(4) While these
cholinergic effects were first described almost a quarter of a century
ago,(5) it now appears that this is only the tip of the ALC iceberg. In
recent years research on the neurological and other effects of ALC has
exploded, primarily due to pharmaceutical interest in this fascinating
compound. This large volume of research has expanded ALC from acetylcholine
mimic to a safe and naturally occurring compound with varied effects on
numerous age-related degenerative changes in the brain. The discovery that ALC has effects on
brain systems other than the cholinergic system complicated the scientific
picture of ALC. This is because it was generally believed that ALC functioned
simply as an enhancer of cholinergic activity by promoting the production, or
mimicking the effect, of acetylcholine. Before we examine these varied
effects, however, let's examine what is now known about ALC’s effects on the
cholinergic system. The cholinergic system has been extensively researched
because of its central role in memory, as well as the evidence that
cholinergic dysfunction plays a large role in age-related memory loss. This
is most evident in Alzheimer’s disease, which effects primarily cholinergic
function. As mentioned earlier, ALC effects both acetylcholine synthesis and
release. Additionally, long-term ALC treatment has shown the ability to
restore the decrease in cholinergic receptors in some brain areas. One study
found that the functioning of the cholinergic synapse was disturbed due to
altered properties of the neuronal membrane, resulting in the functional
impairment of cholinergic receptors. Old rats treated with ALC were found to
have improved acetylcholine release due to a preservation of the neuronal
membrane structure and the functioning of the receptors embedded within the
membrane.(6) Indeed, these varied effects have shown that long-term ALC
treatment reduces the significant age-related difference in receptor-mediated
acetylcholine release. This has not gone unnoticed, and ALC has been studied
in Alzheimer’s disease patients with promising results. While ALC’s cholinergic-enhancing
properties are exciting, it now appears that ALC possesses broader
neuroprotective and neuroenhancing properties than previously thought. For
instance, it is now known that ALC has effects on the dopaminergic system.(7)
The decline of this neurotransmission system is most evident in Parkinson’s
disease patients. ALC has shown the ability to improve age-related changes of
dopamine receptors, including improved release and binding of dopamine.
Additionally, ALC can prevent dopaminergic neuron death by the neurotoxin
MPTP.(8) MPTP causes neurological symptoms similar to Parkinson’s disease by
selectively killing dopaminergic neurons. Thus, it appears that ALC can have
numerous beneficial effects on dopaminergic neurons. One of the most important receptor
systems involved with cognitive function and memory is the NMDA receptor
system. NMDA (N-Methyl-D-Aspartic acid) receptors are widely distributed in
the brain, and their effects are mediated by excitatory amino acids like
glutamate. These receptors are unique because receptor function is mediated
not only by the interaction between receptor and excitatory amino acid, but
is dependent on the membrane potential. Thus, activation of these receptors
requires additional synaptic inputs. While this may sound confusing, the
point is that NMDA receptors have a “conditional” nature to their activation,
which is highly unusual. This underlies the central role that NMDA receptors
are now believed to play in the synaptic plasticity associated with learning
and memory. Indeed, a rapidly growing body of evidence suggests that
excitatory amino acids, through their interaction with NMDA receptors, are
involved many aspects of neuronal activity. It has been established that the
density of NMDA receptors declines with age and that treatment with ALC
restores to a significant degree these receptor numbers.(9) In fact, even a
single dose of ALC can significantly increase the number of available NMDA
receptors. One of the most important, and often
overlooked, receptor system is that of glucocorticoids. The hippocampus in
the brain is the site of negative feedback between the pituitary and adrenal
gland, and this helps to regulate the production of glucocorticoids by the
adrenals. The number of glucocorticoid receptors in the hippocampus declines
significantly with age,(10) and this is thought to result in perturbations in
the hypothalamus-pituitary-adrenal (HPA) axis. ALC treatment has been shown
to prevent this age-related decline in receptor number.(11) Because these
receptors are central to neuroendocrine aging, and their decrease is
considered a consistent marker for aging, it appears that ALC may have
substantial potential for helping to slow down neuroendocrine aging. One of the most exciting areas of brain
research has been into the functions of Nerve Growth Factor (NGF). NGF
mediates much of its effects through a receptor system (NGF receptor system).
Unfortunately, aging is associated with a significant drop in the number of
NGF receptors in certain brain regions, as well as a decrease in the amount
of NGF produced. ALC has shown the ability to partially reverse both of these
changes, and has even been shown to have independent stimulatory effects on
neuronal survival and growth.(12) Because NGF is important for the growth and
continued maintenance of neurons, the age-related decline in NGF function is
thought to be directly involved in brain aging. The administration of NGF’s
are under investigation for the treatment of brain injury and damage, and
ALC’s ability to enhance NGF effects may have tremendous potential in many
diseases and conditions affecting the brain and nervous system. Taken as a whole, ALC represents a
novel supplement with tremendous potential. Because it also increases tissue
levels of carnitine, as well as providing many benefits not found with
carnitine supplementation, ALC represents an alternative to carnitine with
enhanced properties and benefits. Most human studies examining ALC have
utilized doses from 500-2500 milligrams daily in divided doses. Younger,
healthy persons would probably want to take 500-1000 milligrams daily, while
those with cognitive deficit due to aging or injury may wish to take
1500-2500 milligrams daily. While no serious side effects have been noted in
animal or human studies, ALC may cause symptoms of over-stimulation or
headache in some sensitive individuals. However, these symptoms are not
common and are usually caused by beginning with a high dose. One last
consideration is ALC’s stability. Unlike carnitine, it is recommended that
ALC be kept refrigerated to ensure potency. Thus, while ALC can be shipped
without refrigeration, manufacturers must be sure to refrigerate raw material
and finished product during storage to prevent premature degradation of the
product. Customers, to further protect their investment, should preferably
refrigerate ALC after receipt. ALC truly represents one of the most
promising and well researched cognitive-enhancing compounds available today.
The fact that its non-toxic, occurs naturally in the body, and positively
affects so many different neurological functions makes its potential both
exciting and amazing. References: |
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