(Cell Power) has been shown to protect brain cells against aging related degeneration and improve mood, memory, and cognition. Prevents age relation impairment of eyesight. Increases muscle mass and convertS body fat into energy. The most important effect of acetyl-l-Carnitine is to maintain the function of the cell's energy powerhouse, the mitochondria. It maintains the immune competence and reduces the aging pigment lipofuscin. It prevents the aging process in the skin. It alleviates depression and improves the quality of sleep. It also increases testosterone levels.
Acetyl-L-Carnitine is the O-acetyl derivative of Carnitine (often manufactured and supplemented) synthetically - ALC is also naturally present in the body (i.e. it is endogenous) and occurs naturally in small amounts in some foods. Approximately 7.5% - 10.2% of the body’s total Carnitine content is in the form of ALC.
Note that ALC may provide health benefits above and beyond those derived from Carnitine supplementation (according to the Sigma Tau pharmaceutical corporation).
ALC may retard some aspects of the Aging Process:
ALC may prevent the decline in the number of Glucocorticoid Receptors in the Brain that occurs in tandem with the progression of the Aging Process.
ALC may significantly reduce Lipofuscin deposits in the Brain and Heart tissue.
ALC may inhibit the increase in the size of the Adipocytes of the Subcutaneous Tissue of the Skin that occurs in tandem with the progression of the Aging Process.
ALC may inhibit damage to mitochondrial DNA (mtDNA) - the principal detrimental process implicit in the Mitochondrial DNA Theory of Aging.
ALC may retard the natural decline in the number of NMDA Receptors (N-Methyl-D-Aspartate Receptors) that occurs in tandem with the Aging Process.
ALC may improve the reaction times of Cerebral Insufficiency patients.
ALC may significantly reduce Lipofuscin deposits in Heart tissue and may improve the function of the Mitochondria in the Heart.
ALC (2,000 -4,000 mg per day) may improve walking distance without Pain in Intermittent Claudication patients.
ALC may counteract the toxic effects of Ischemia on the Brain.
ALC may protect the Brain from many of the toxic after-effects of Stroke.
ALC may enhance the transport of Fatty Acids into the Mitochondria (for subsequent use in the production of Energy) and facilitates the clearance of toxic levels of Fatty Acids from the Mitochondria.
ALC may inhibit the ability of Alcohol (ethanol) to cause Gastric Ulcers.
ALC may improve Hearing ability in elderly Age-Related Hearing Loss Patients (by retarding and reversing damage to mitochondrial DNA in the Ears’ Cochlea).
ALC may inhibit and reverse damage to mitochondrial DNA (mtDNA) in the Ears’ Cochlea.
ALC (1,500 mg per day) may help to prevent Cataracts (by preventing Simple Sugars from causing Cross-Linking [glycosylation] of the body's endogenous Proteins within the Eyes).
ALC may be useful for the prevention of Glaucoma. It may inhibit the Cross-Linking (glycosylation) that has been implicated in the damage that occurs to the Optic Nerve in Glaucoma patients.
ALC may inhibit the Cross-Linking (glycosylation) of the Optic Nerve.
ALC may inhibit the loss of Sight, degeneration of Neurons and damage to the Retina associated with Retinopathy (including diabetic Retinopathy).
ALC may prevent the age-related impairment of Sight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain).
ALC may stimulate the Immune System:
ALC may enhance the ability of Macrophages to function as Phagocytes.
ALC is a potent Antioxidant.
ALC may improve Athletic Performance.
ALC may lower total serum Cholesterol levels.
ALC (1,000 - 2,000 mg per day) may increase Energy levels in Chronic Fatigue Syndrome (CFS) patients. ALC (1,500 mg per day) may prevent Simple Sugars from causing the Cross-Linking [glycosylation] of the body's endogenous Proteins (within the Eyes and possibly in other areas of the body also). ALC may enhance the function of Cytochrome C Oxidase (an essential enzyme of the Electron Transport System (ETS). ALC may improve the Energy metabolism of Neurons and other Cells (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranesof Neurons into the Mitochondria). ALC enhances Energy production in every Cell of the body.
ALC may enhance the performance of people who Exercise (when ALC is administered prior to Exercise). ALC may alleviate Fatigue. ALC may inhibit the damage caused by Hypoxia. ALC transports Lipids into the Mitochondria of Cells.
ALC may improve Stamina.
Nervous System: Ailments
- ALC may alleviate Age Associated Memory Impairment (AAMI):
- ALC may improve Creativity in persons afflicted with AAMI.
- ALC may improve Memory in persons afflicted with AAMI.
- ALC may improve Mood in persons afflicted with AAMI.
ALC (2,500 - 3,000 mg per day) may inhibit the deterioration in Mental Function associated with Alzheimer’s Disease and may retard the progression of Alzheimer’s Disease - ALC may increase Alertness in Alzheimer's Disease patients. - ALC may inhibit the toxicity of Amyloid-Beta Protein (ABP) to Neurons. - ALC may improve Attention Span in Alzheimer's Disease patients. - ALC may improve Short-Term Memory in Alzheimer's Disease patients.
ALC (1,500 – 3,000 mg per day) may be useful for the treatment of Amyotrophic Lateral Sclerosis (due to its ability to improve the function of Motor Nerves).
ALC (500 - 3,000 mg per day) may alleviate Depression: -ALC may alleviate Major Depression) especially in the elderly. -ALC may improve Attention Span and Memory in Down’s Syndrome patients.
ALC may be useful for the treatment of Drug Dependence caused by Alcohol (ethanol):
- ALC may reduce the craving for Alcohol in Alcoholics.
- ALC may reduce the severity of the withdrawal symptoms experienced by reforming Alcoholics.
ALC may enhance the recovery of Hemiplegia (Paralysis of one side of the body) patients and improves their Mood and Attention Span.
ALC (2,000 mg per day) may be useful for the treatment of Multiple Sclerosis (due to its ability to inhibit the further degradation of Myelin Sheaths which occurs in Multiple Sclerosis patients).
ALC may inhibit the degeneration of Neurons that is implicit in Neuropathy (including diabetic Neuropathy) and may inhibit the ability of various Pharmaceutical Drugs to cause (peripheral) Neuropathy.
ALC is being researched as a possible treatment for Parkinson's Disease.
ALC may improve the function of (i.e. it may reduce the over-excitability of) Motor Nerves in Spasticity patients.
ALC may inhibit the excessive release of Cortisol in response to Stress and may inhibit the depletion of Luteinizing Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
Nervous System: Enhancement
ALC may improve Alertness in normal, healthy people and in Alzheimer's Disease patients..
ALC may increase Attention Span.
ALC (1,500 mg per day) may improve (eye to hand) Coordination in healthy persons by 300% to 400%.
ALC may improve Learning ability.
ALC may improve Memory (both Short-Term Memory and Long-Term Memory):
ALC may improve Spatial Memory (an aspect of Short-Term Memory that involves remembering one’s position in space). ALC may improve Mood in up to 53% of healthy subjects. ALC may improve the quality of Sleep and may reduce the quantity of Sleep required. ALC may improve Verbal Fluency.
High concentrations of ALC are naturally present in various regions of the Brain:-
ALC may counteract the toxic effects of Ischemia on the Brain. ALC may reverse the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine). ALC may normalize Circadian Rhythms. ALC may improve the Interhemispheric Flow of Information across the Corpus Callosum of the Brain. ALC may facilitate the regeneration of Cranial Nerves after injury. ALC may retard 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 may enhance the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors. - ALC may prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death).
ALC may retard the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.ALC may retard the age-related deterioration of the Hippocampus and may help to prevent age-related Neuron loss in the Hippocampus. ALC may reduce the formation of Lipofuscin in the Brain’s Neurons.ALC may inhibit (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process. ALC may improve Nerve Conduction Velocity. ALC may rejuvenate and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain. A single dose of ALC has been shown to increase the number of functional NMDA Receptors. - ALC may protect the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process.
ALC may retard the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.
ALC may retard age-related and crushing injury-related damage to Neuromuscular Junctions.
ALC may stimulate and maintain the growth of new Neurons within the Brain (both independently of Nerve growth Factor (NGF) and as a result of preserving NGF) and may help to prevent the death of existing Neurons: - ALC may facilitate the repair of damaged Peripheral Nerves.
- ALC may enhance the function of Motor Nerves.
ALC may facilitate the binding of Dopamine to Dopamine Receptors in the Striatum.
ALC (2,000 mg per day) may alleviate Peyronie’s Disease.
ALC may retard some aspects of the Aging Process in the Skin:
- ALC may inhibit the increase in the size of the Adipocytes of the Subcutaneous Tissue of the Skin that occurs in tandem with the progression of the Aging Process.
Acetyl-L-Carnitine may Enhance the Function of these Substances
ALC increases tissue levels of Carnitine.
ALC may increase Brain levels of Choline Acetylase.
ALC may enhance the function of Cytochrome C Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.
ALC may increase (free) Insulin-like Growth Factor-1 (IGF-1) levels.
ALC may increase the responsiveness of Neurons to Neurotrophic Factors:
- ALC may retard the decline in Nerve Growth Factor (NGF) that occurs with the progression of the Aging Process.
ALC may normalize Beta-Endorphin levels.
ALC may prevent the depletion of Luteinizing Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC may increase the night-time secretion of Melatonin by the Pineal Gland.
ALC may increase plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and may prevent the depletion of Testosterone caused by exposure to excessive Stress.
ALC may increase the body's levels of circulating Thyrotrophin.
ALC may facilitate the body's production of Acetyl Coenzyme A by donating its Acetyl group to Acetyl Coenzyme A, thereby regenerating Acetyl Coenzyme A from Coenzyme A.
ALC may facilitate the production of Adenosine Triphosphate (ATP).
ALC may stimulate the production of Cardiolipin.
ALC “shuttles” Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC may facilitate both the release and synthesis of Acetylcholine.
- 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 may mimic the function of Acetylcholine.
- ALC may increase the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC may enhance the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
ALC may inhibit and reverse damage to mitochondrial DNA (mtDNA).
ALC may facilitate the uptake of Choline into the Cerebral Cortex of the Brain.
ALC may Counteract these Potentially Toxic Substances
ALC may help to protect Neurons from the excitotoxic effects of excessive Glutamic Acid.
ALC may inhibit Xanthine Oxidase (XO) activity (in Skeletal Muscles).
ALC may reduce Stress-induced Cortisol release.
ALC may inhibit the release of Substance P.
ALC may inhibit the ability of MPP+ to damage Neurons.
ALC may prevent MPTP-induced damage to dopaminergic Neurons in the Brain.
ALC may reduce the neurotoxicity caused by exposure to the excitotoxin N-methyl-D-aspartate (NMDA).
ALC may help to protect Neurons from the toxic effects of Ammonia.
ALC may reduce the neurotoxic effects associated with Cisplatin treatment.
ALC may inhibit the Brain, Heart, Kidney and Liver damage caused by excessive consumption of Alcohol (ethanol):
- ALC may reduce the craving for Alcohol in Alcoholism patients and may reduce the severity of the withdrawal symptoms in Alcoholism patients who cease Alcohol consumption.
- ALC may improve Mental Function where Alcohol (ethanol)-induced cognitive Impairment exists.
- ALC may inhibit the ability of Alcohol to cause Gastric Ulcers.
ALC may counteract Ecstacy-induced damage to NMDA Receptors.
These Substances may Enhance the Function of ALC
Carnitine Acetyltransferase catalyzes the conversion (acylation) of Carnitine to ALC.
Carnitine is a component of ALC - 7.5% to 10.2% of the body’s total Carnitine content is present in the form of ALC.
These Factors may Interfere with ALC
The body's (especially the Brain's) level of ALC declines in tandem with the Aging Process.
Dietary Sources of ALC
Small amounts of ALC are present in (cow’s) Milk. The quantity of ALC in Milk is too small to exert therapeutic effects.
Toxic Effects of ALC
No toxicity has been found to be associated with ALC even when supplemented in large dosages.
As a precautionary measure, women should not supplement with ALC during Pregnancy or Lactation (Although ALC has never been found to be toxic to women during Pregnancy or Lactation, its effects on pregnant/lactating women have not yet been clinically studied. The only real reason for it to be avoided during Pregnancy/Lactation is the lack of clinical studies to support its use or non-use).
ALC vs. L-Carnitine?
ALC is generally claimed to be superior in terms of its therapeutic effects compared to its unacetylated sister compound, L-Carnitine:
- Some scientists have recently claimed that there may perhaps be no advantage to taking the (more expensive) ALC form of Carnitine over the more economical unacetylated form of Carnitine (L-Carnitine).
- Dr. Brian Leibovitz (who authored the book “Carnitine, Vitamin BT”) claims that because the Sigma Tau corporation owns the patents on ALC for pharmaceutical purposes, they have concocted a myth that only ALC is clinically effective in many situations.
- Some acknowledged leaders of the life extension movement are presently taking half of their daily ALC dose in the form of L-Carnitine and the other half of their dose in the form of ALC until this debate is settled.
When ingested orally, ALC dissolves in the Stomach and is then absorbed by the Jejunum and enters blood circulation.
ALC readily permeates the Blood-Brain Barrier.
The bioavailability of ALC is not affected by the Aging Process, i.e. the degree to which it is assimilated does not decline in older persons.
Endogenous ALC Levels
The average mean plasma ALC concentration of most people is 6.3 nmol/L.
Using Supplemental ALC
Smart Drugs Synergism
ALC is synergistic with many Smart Drugs and its dosage should be reduced accordingly if it is used in conjunction with Smart Drugs.
Duration of Action
Cognitive enhancement derived from ALC supplementation persists for 30 days or longer after the cessation of ALC supplementation.
The optimal timing for Acetyl-L-Carnitine supplements is in the morning (in order to derive the stimulatory effects of ALC throughout the day and to avoid its stimulatory effects during the night) - if administered at night-time, supplemental ALC may suppress Serotonin and Melatonin activity.
ALC supplements should be taken on an empty Stomach (30 - 45 minutes prior to breakfast or lunch) with Water or juice.
The therapeutic dosage of ALC for young people without cognitive impairment is 500 - 2,000 mg per day (many people obtain its effect using the lower dosage of 500 mg per day).
The therapeutic dosage of ALC for older people without severe cognitive impairment is 1,500 - 2,500 mg per day.
The therapeutic dosage of ALC for people affected by Alzheimer’s Disease is 2,500 - 3,000 mg per day.
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