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ALC Reverses Neuroendoctrine Aging
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.
Restoring Nerve Growth Factor Function
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 receptorsystem). 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.
Restoring
Mitochondrial Enzyme Activity and Cardiolipin to more Youthful Levels
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
facilitates 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 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
improvesthe 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
Alzheimers Disease [persons afflicted with Alzheimers Disease
exhibited significantly less deterioration in Mental Functionfollowing
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. theReceptors 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 oneside 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
Sheathsthat 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 thedepletion 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)
thatoccurs 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].
References
De Falco, F. A., et al. Effect of the chronic treatment with L-acetyl
carnitine in Downs syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimers disease. Nutr Rev.
50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a
short-term study on CSF neurotransmitters and neuropeptides. Alzheimer
Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration
and Alzheimers disease. Annals of the New York Academy of Sciences
(USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress
of Alzheimers Disease? Annals of the New York Academy of Sciences
(USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the
efficacy of a pharmacological aid. Drugs under Experimental and
Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly
demented elderly patients. International Journal of Clinical
Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of
acetyl-L-carnitine in Alzheimers disease. Neurobiol Aging. 16:1-4,
1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine
in patients with Alzheimers dementia. Current Medical Research and
Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl
levocarnitine in patients with Alzheimers disease. Arch Neurol.
49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients
treated with acetyl-L-carnitine. International Journal of Clinical
Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl l-carnitine treatment in
Alzheimers disease. Neurology. 41(11):1726-1732, 1991.
More on L-Carnitine Deficiency
We know already that L-Carnitine
deficiency, by denying the mitochondria the needed fatty acids,
decreases energy output, but let's look at the other side of this
energy equation. If you aren't burning fat, you must be storing it.
This obviously leads to a variety of health problems, namely fatty
build-ups. L-Carnitine supplementation can help prevent fatty
build-ups in the heart and liver (especially likely if you are a
regular consumer of alcoholic beverages). Putting it all together, L-Carnitine
emerges as a great supplement: it helps increase energy, burn fat
(making it excellent addition to a weight loss program), and supports
heart and liver health all at the same time!
Certain medications
interact with L-carnitine: Some interactions may increase the need for
L-carnitine ( ), other interactions may be negative ( ) and indicate
L-carnitine should not be taken without first speaking with your
physician or pharmacist, others may require further explanation ( ).
Refer to the individual drug article for specific details about an
interaction.
Note: the following list only includes the generic or class name of a
medication—to find a specific brand name, use the Safetychecker index.
Allopurinol
Anticonvulsants
AZT
Doxorubicin
Gabapentin
Phenobarbital
Valproic Acid
Acetyl L-Carnitine
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
Reduces Brown Spots, which are a Universal Sign of Aging
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
Reduced Deterioration of Brain Cells Associated with Aging
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.
ALC
Reduces Risk of Alzheimer's Disease and May Slow Progression
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
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.
Restores
NMDA Receptors
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.
ALC
Reverses Neuroendoctrine Aging
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.
Restoring
Nerve Growth Factor Function
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 receptorsystem). 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.
Restoring
Mitochondrial Enzyme Activity and Cardiolipin to more Youthful Levels
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
facilitates 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 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
improvesthe 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
Alzheimers Disease [persons afflicted with Alzheimers Disease
exhibited significantly less deterioration in Mental Functionfollowing
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. theReceptors 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 oneside 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
Sheathsthat 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 thedepletion 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)
thatoccurs 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].
References
De Falco, F. A., et al.
Effect of the chronic treatment with L-acetyl carnitine in Downs
syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimers disease. Nutr Rev.
50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a
short-term study on CSF neurotransmitters and neuropeptides. Alzheimer
Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration
and Alzheimers disease. Annals of the New York Academy of Sciences
(USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress
of Alzheimers Disease? Annals of the New York Academy of Sciences
(USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the
efficacy of a pharmacological aid. Drugs under Experimental and
Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly
demented elderly patients. International Journal of Clinical
Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of
acetyl-L-carnitine in Alzheimers disease. Neurobiol Aging. 16:1-4,
1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine
in patients with Alzheimers dementia. Current Medical Research and
Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl
levocarnitine in patients with Alzheimers disease. Arch Neurol.
49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients
treated with acetyl-L-carnitine. International Journal of Clinical
Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl l-carnitine treatment in
Alzheimers disease. Neurology. 41(11):1726-1732, 1991.
L-CARNITINE:
THE BEAT GOES ON - L-CARNITINE AND HEART HEALTH
by Lynn Hinderliter CN, LDN
Of the
nutrients that support the health of the heart, in first place I
position Coenzyme Q10 , and second on the list I would place L-Carnitine.
I have been recommending it for many years now, but we live in
exciting times nutritionally, and new research is continually being
published that underscores its vital part in the cardiovascular
system, and for other health conditions. In fact, it is a little hard
to limit an article on l-Carnitine JUST to the heart, because this
substance has been positively linked to improvements in health
problems as superficially far removed as obesity and Parkinsonism.
Vegetarians
are likely to be deficient in L-Carnitine, since the best source is
red meat. I would urge parents to be very reluctant to raise their
children as vegetarians from birth, because of the effect a deficiency
of Carnitine could have on the growth pattern and development of the
child. (Arch Fr Pediatr. 1984 Dec;41(10):715-9.) When one considers
the problems attached to congenital defects in Carnitine metabolism,
such as heart damage, its importance in the developing body is clear.
First,
however, what it is. The prefix "L" would lead one to suppose that it
is an amino acid - but strictly speaking, although its structure is
similar to amino acids , it is more closely related to the B vitamins,
and it plays no role in protein structures. It is considered a
nonessential nutrient in the sense that the body can manufacture it
from other nutrients present in the body (Lysine, Methionine, B6 among
others, with Vitamin C being a limiting factor), but it is highly
essential in its actions. In the diet it is found mostly in muscle
meats ( as the name would suggest, coming from the Latin root for
meat), and while it is rare for an actual clinical deficiency to
exist, sub-optimal levels can lead to many problems associated with
diabetes, obesity, cardiovascular disease and possibly Alzheimer and
muscular dystrophy.
The reason
L-Carnitine can be involved in such a wide range of problems, and the
reason for its extreme importance in the maintenance of heart health,
is its influence on the destiny of the massive amounts of
carbohydrates in the average American diet. Excess carbs are stored as
fat, and Carnitine facilitates the burning of fat for energy by making
it possible for the long chain fatty acids it transports to enter the
cell . After all, if the fatty acids cannot reach the mitochondria
where they are transformed to cellular energy, it stands to reason
they are going to be deposited in places where the body will suffer
from their presence, as happens in fatty liver disease, fatty build-up
in the heart, and your plain old everyday variety obesity, where fatty
build-up occurs in the muscles..
My hero Dr.
Whitaker compares the heart deficient in Carnitine to a car without a
fuel pump! However, as you can plainly see, the heart is not the only
organ that can benefit from more efficient burning of fats for energy:
Carnitine has its uses in the following conditions: angina,
myocardial infarction, recovery from heart surgery, hypertension and
high cholesterol levels, also high triglycerides, Alzheimer's, liver
disease (including alcohol induced liver problems) diabetes, diabetic
neuropathy male infertility, diabetic neuropathy, Parkinson's and many
other more obscure afflictions.
In his
book, The Carnitine Miracle, Robert Crayhon MS, CN says " Nearly
one-third of all deaths related to heart disease occur because of
arrhythmias. Carnitine is a valuable nutrient for the control of
arrhythmias ..." and he goes on to recommend also taurine, magnesium
and fish liver oils. This combination, he states, has eliminated every
case of arrhythmia he has seen in his practice.
A Jan 1998
article by Dr. Richard Podell M.D. touches on the excellent research
which enables him to say that he is now able to recommend L-Carnitine
as standard treatment for intermittent claudication, an
extremely painful condition that causes great pain in the legs during
exercise. He based this on studies in Italy using a Carnitine
derivative where double-blind, placebo controlled research with 245
patients showed not only that Carnitine helped the condition, but that
the more severe the problem, the greater the degree of relief. The
initial dose was 500mg twice a day, and the highest dose used (
incremental increases) where no improvement occurred at lower doses
was 1500mg twice a day.
It is very
useful and helpful for people trying to lose weight, but only if their
diet is deficient in Carnitine. To quote from a release by the Lonza
Group ( who manufacture L-Carnitine):" Studies in obese people have
shown that only low calorie diets together with exercise will
guarantee long term weight loss. Both of these measure induce a
deficiency in L-Carnitine. Sub-optimal levels of L-Carnitine may also
cause fatigue and strongly impair beta-oxidation. Clinical studies
demonstrate the effectiveness of supplementary L-Carnitine for weight
management, the improvement of exercise performance and maintenance of
a healthy heart."
As a less
scientific side-note, when people are on a low carbohydrate diet, we
have found that supplementary L-Carnitine lessens the irritability and
nervousness that such an extreme change in body chemistry often
brings.
The average
amount of Carnitine found in the daily diet is app. 50 mgs:
therapeutic levels range from 500 to 2000 mgs. Deficiencies may be due
to a genetic error in Carnitine synthesis, or to low levels of lysine,
high levels of homocysteine, or vegetarianism . There do not appear to
be any side effects from its use even at high dosages, but it is wise
to increase Vitamin C supplementation, since some studies show that
high amounts of Carnitine cause loss of Vitamin C from the body. It is
available as Acetyl-l Carnitine, L-Carnitine (these are the preferred
forms) and is also marketed as DL-Carnitine, which in my opinion
should be avoided since some experts say it interferes with the body's
use of natural L-Carnitine.
Athletes
have known about Carnitine's ability to burn fat for energy for some
time, but heart disease sufferers are just beginning to realize the
benefits that come from using a substance that provides the heart with
its main fuel: the heart gets two thirds of its energy from burning
fat! Less pain and more endurance can be associated with supplementing
with L-Carnitine, with no downside. It works synergistically with
Coenzyme Q 10.
L-Carnitine
may be upsetting to the stomach, so make sure to take it with a
meal. Dr. Podell also urges caution if a person has any kidney or
liver problems, or is pregnant or lactating.
Lactic acid
build-up can really be a villain, not just for athletic performance
but for energy production generally: particularly unfortunate are its
repercussions on brain function. Fortunately there is a nutrient so
effective at addressing it that it has also been developed as a
"drug". That nutrient is Acetyl-L-Carnitine (ALC), which can be
produced in the liver from 2 amino acids (Lysine and Cysteine) but is
often not available in sufficient quantities because its synthesis
requires several vitamins which our diets are often inadequate to
provide: B6, Folic acid, Pantothenic acid, Biotin and C.
The Acetyl
form of Carnitine is more expensive than plain vanilla L-Carnitine,
but also more effective for energy related problems because it is
better assimilated, and also has been shown to pass the blood/brain
barrier more efficiently. (This, of course, accounts for the studies
that have found an influence on Alzheimer's, where lactic acid
build-up in the brain is being studied as a causative factor - more
here).
ALC has
been shown to boost the activity of an enzyme, carnitine
acetyltransferase, which increases the burning of fatty acids for fuel
in the mitochondria. It is therefore helpful at 2 levels, one as a
remover of waste, and 2 as a provider of fuel - both positively
affecting energy levels. Whether this is the case throughout the body,
or mainly in the brain, has not yet been determined.
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