The November 2003 Issue of Reader's Digest features a headline "The Pill That Ends Aging." I suggest you pick up this issue and read it carefully. This story features two of Young Again's (now supplementspot) featured supplements: Acetyl L-Carnitine or ALC and Alpha Lipoic Acid or ALA. The benefits of supplementing with the proper dose of both alpha-lipoic acid (ALA) and acetyl-L-carnitine seem endless, and we have summarized them in the following article. The Reader's Digest is accurate except it gives the impression this is a new discovery. .......

Here is a summary of the Amazing list of ALCAR benefits

Acetyl L-Carnitine (ALC) is a cognitive enhancer and neuroprotective agent that protects against a wide range of age-related degenerative changes in the brain and nervous system. ALC is an ester of carnitine that modulates cellular concentrations of free coenzyme A and acetyl-coenzyme A, two compounds integrally involved in numerous cellular functions, including the transfer of fatty acids across mitochondrial membranes for energy production.

ALC is found in various concentrations in the brain and its levels are significantly reduced with aging. ALC also significantly reduces damaged fats, such as lipofuscin, in the brains of aged rats. In addition to accumulating in the aging brain, lipofuscin also accumulates in the skin as "aging spots," those brownish pigmented blemishes that accumulate in the backs of hands of many people over fifty. The reduction of these deposits following consumption of ALC may be evidence of a slowing in the aging process in the brain.

ALC also has the ability to cross into the brain where it acts as a powerful antioxidant, preventing the deterioration of brain cells that normally occurs with age. Because of this protective effect, ALC may be beneficial in the prevention and treatment of free- radical mediated diseases, such as Alzheimer's and Parkinson's disease.

Alzheimer's Disease: As mentioned earlier, Alzheimer's disease primarily effects cholinergic function. ALC has been shown to promote both the release and synthesis of acetylcholine. Additionally, ALC promotes high affinity uptake of choline, which declines significantly with age.

Parkinson's Disease: In addition to ALC's cholinergic- enhancing properties, researchers have shown that ALC has numerous beneficial effects on dopaminergic neurons. The decline of the dopaminergic neurotransmission system is most evident in Parkinson's disease patients. ALC has been shown to improve age-related changes of dopamine receptors, including improved release and binding of dopamine. Research has shown that ALC can prevent dopaminergic neuron death caused by MPTP, a neurotoxin that mimics neurological symptoms similar to Parkinson's disease by selectively killing dopaminergic neurons.

Restoring NMDA Receptors: The NMDA (N-Methyl-D- Aspartic acid) receptor system is one of the most important receptor systems involved with cognitive function and memory. NMDA receptors are widely distributed in the brain, and their effects are mediated by excitatory amino acids like glutamate. It has been shown that the density of NMDA receptors declines with age. Damage to the NMDA receptors is also the most severe adverse effect of the street drug, Ecstasy (MDMA). Treatment with ALC restores NMDA receptor numbers to a significant degree. In fact, even a single dose of ALC can significantly increase the number of available NMDA receptors.

Reversing Neuroendocrine Aging: One of the most important, and often overlooked, receptor systems is that of lucocorticoids. The hypothalamus in the brain is the site of negative feedback between the pituitary and adrenal gland. This is the center that regulates the production of glucocorticoids (principally, cortisol) by the adrenals. The number of glucocorticoid receptors in the hypothalamus declines significantly with age, and this results in an imbalance in the hypothalamus-pituitary- adrenal (HPA) axis. ALC treatment has been shown to prevent this age-related decline in receptor number. Because these receptors are central to neuroendocrine aging, their decrease is considered a consistent marker for aging. It appears that ALC may have substantial potential for helping to slow the degradation of this principlemarker of neuroendocrine aging.

One of the most exciting areas of brain research has been the functions of Nerve Growth Factor (NGF). NGF mediates many 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. 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. ALC has the ability to partially reverse both of these changes, and has even been shown topositively effect both neuronal survival and growth. ALC's ability to enhance NGF effects suggests a tremendous potential for this natural compound in many diseases and conditions affecting the brain and nervous system.

A group of Italian scientists (Paradies, et al, 1994) evaluated the effect of dietary ALC on the mitochondrial membranes of young and old rats. They found that the activity of the enzyme, cytochrome c oxidase, declined about 30% in the old rats, compared to the young. This may explain the reduction in ATP formation (and reduced energy) with age. The scientists found that dietary ALC restored cytochrome c oxidase activity in old rats to that of the younger animals. Furthermore, in a follow-up study, they found that the activity of another enzyme, the ADP carrier protein adenine nucleotidase (ANT) also decreases with age. Decreased ANT can also result in reduced production of ATP. The scientists again found that ALC restored ANT activity to more youthful levels.

Finally, the same scientists found that mitochondrial levels of cardiolipin, a key lipid subfraction, were also much improved. In fact, they hypothesized that this dramatic improvement in cardiolipin fraction was the key element in its other demonstrated benefits.

ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.

ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).

ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

ALC improves the reaction times of persons afflicted with Cerebral Insufficiency.

ALC (2-4 grams per day) improves walking distance without Pain in persons afflicted with Intermittent Claudication.

ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.

ALC enhances the ability of Macrophages to function as Phagocytes.

ALC given prior to exercise increased the maximum running speed of animals.

ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).

ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).

ALC inhibits the damage caused by Hypoxia.

ALC transports Lipids into the Mitochondria of Cells.

ALC improves Memory in persons afflicted with Age Associated Memory Impairment.

ALC improves Mental Function where Alcohol induced cognitive Impairment exists.

Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer's Disease and slows the progression of Alzheimer’s Disease [persons afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the ministration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].

ALC increases Alertness in persons afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].

ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.

ALC improves Attention Span in persons afflicted with Alzheimer's Disease.

ALC improves Short Term Memory in persons afflicted with Alzheimer's Disease.

High concentrations of ALC are naturally present in various regions of the Brain.

ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).

ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].

ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.

ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.

ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.

ALC improves Attention Span and Memory in persons afflicted with Downs Syndrome.

ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.

ALC enhances the recovery of persons afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.

ALC retards the age-related deterioration of the Hippocampus [research - rats].

Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].

ALC improves both Short-Term Memory and Long- Term Memory.

ALC improves Mood [ALC improves Mood in 53% of healthy subjects].

ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].

ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.

ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].

ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.

ALC rejuvenates and increases the number of N- Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:

ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].

ALC is presently being researched as a treatment for Parkinson's Disease.

ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).

ALC improves the quality of Sleep and reduces the quantity of Sleep required.

ALC improves the function of (reduces the over- excitability of) Motor Nerves in persons afflicted with Spasticity.

ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering ones position in space).

ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.

ALC improves Verbal Fluency.

ALC enhances the function of Cytochrome Oxidase (also called Complex IV) -an essential enzyme of the Electron Transport System.

ALC normalizes Beta-Endorphin levels.

ALC reduces Stress-induced Cortisol release [research - animals].

ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.

ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.

ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].

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