MULTIPLE SCLEROSIS
AND
GLUTATHIONE CONNECTION
AND
GLUTATHIONE CONNECTION
What is MS
Multiple sclerosis (abbreviated MS, also known as disseminated sclerosis or encephalomyelitis disseminata) is
an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are
damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms.[1] Disease
onset usually occurs in young adults, and it is more common in females.[1] It has a prevalence that ranges
between 2 and 150 per 100,000.[2] MS was first described in 1868 by Jean-Martin Charcot.[3]
MS affects the ability of nerve cells in the brain and spinal cord to
communicate with each other. Nerve cells communicate by sending
electrical signals called action potentials down long fibers called axons,
which are wrapped in an insulating substance called myelin. In MS, the
body's own immune system attacks and damages the myelin. When myelin
is lost, the axons can no longer effectively conduct signals.[4]
The name multiple sclerosis refers to scars (scleroses—better known as
plaques or lesions) particularly in the white matter of the brain and spinal cord,
which is mainly composed of myelin.[3]
Almost any neurological symptom can appear with the disease, and often
progresses to physical and cognitive disability.[4] MS takes several forms,
with new symptoms occurring either in discrete attacks (relapsing forms)
or slowly accumulating over time (progressive forms).[6] Between attacks,
symptoms may go away completely, but permanent neurological problems
often occur, especially as the disease advances.[6]
Classification
Progression of MS subtypesSeveral subtypes, or patterns of progression, have
been described. Subtypes use the past course of the disease in an attempt to
predict the future course. They are important not only for prognosis but also for
therapeutic decisions. In 1996 the United States National Multiple Sclerosis Society standardized four subtype
definitions:[6]
1.relapsing remitting,
2.secondary progressive,
3.primary progressive, and
4.progressive relapsing.
The relapsing-remitting subtype is characterized by unpredictable relapses followed by periods of months to
years of relative quiet (remission) with no new signs of disease activity. Deficits suffered during attacks may
either resolve or leave sequelae, the latter being more common as a function of time.[1] This describes the
initial course of 80% of individuals with MS.[1] When deficits always resolve between attacks, this is sometimes
referred to as benign MS,[8] although patients will still accrue some degree of disability in the long term.[1] The
relapsing-remitting subtype usually begins with a clinically isolated syndrome (CIS). In CIS, a patient has an
attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis.[1][9] However only 30 to
70% of persons experiencing CIS later develop MS.[9]
Nerve axon with myelin sheath Secondary progressive MS (sometimes called "galloping MS") describes around
65% of those with an initial relapsing-remitting MS, who then begin to have progressive neurologic decline
between acute attacks without any definite periods of remission.[1][6] Occasional relapses and minor remissions
may appear.[6] The median time between disease onset and conversion from relapsing-remitting to secondary
progressive MS is 19 years.[10]
The primary progressive subtype describes the approximately 10–15% of individuals who never have remission
after their initial MS symptoms.[11] It is characterized by progression of disability from onset, with no, or only
occasional and minor, remissions and improvements.[6] The age of onset for the primary progressive subtype is
later than for the relapsing-remitting, but similar to mean age of progression between the relapsing-remitting and
the secondary progressive. In both cases it is around 40 years of age.[1]
Progressive relapsing MS describes those individuals who, from onset, have a steady neurologic decline but
also suffer clear superimposed attacks. This is the least common of all subtypes.[6]
Atypical variants of MS with non-standard behavior have been described; these include Devic's disease, Balo
concentric sclerosis, Schilder's diffuse sclerosis and Marburg multiple sclerosis. There is debate on whether
they are MS variants or different diseases.[12] Multiple sclerosis also behaves differently in children, taking
more time to reach the progressive stage.[1] Nevertheless they still reach it at a lower mean age than adults.[1]
Multiple sclerosis signs and symptoms
- A person with MS can suffer almost any neurological symptom or sign,
including changes in sensation such as loss of sensitivity or tingling,
pricking or numbness (hypoesthesia and paraesthesia), muscle weakness,
clonus, muscle spasms, or difficulty in moving; difficulties with coordination
and balance (ataxia); problems in speech (dysarthria) or swallowing
(dysphagia), visual problems (nystagmus, optic neuritis including
phosphenes, [13][14] or diplopia), fatigue, acute or chronic pain, and
bladder and bowel difficulties.[1]
- Cognitive impairment of varying degrees and emotional symptoms of
depression or unstable mood are also common.[1] Uhthoff's phenomenon,
an exacerbation of extant symptoms due to an exposure to higher than usual
ambient temperatures, and Lhermitte's sign, an electrical sensation that runs
down the back when bending the neck, are particularly characteristic of MS
although not specific.[1] The main clinical measure of disability progression
and symptom severity is the Expanded Disability Status Scale or EDSS.[15]
- Symptoms of MS usually appear in episodic acute periods of worsening (called
relapses, exacerbations, bouts, attacks, or "flare-ups"), in a gradually progressive deterioration of neurologic
function, or in a combination of both.[6] Multiple sclerosis relapses are often unpredictable, occurring without
warning and without obvious inciting factors with a rate rarely above one and a half per year.[1] Some attacks,
however, are preceded by common triggers. Relapses occur more frequently during spring and summer.[16]
- Viral infections such as the common cold, influenza, or gastroenteritis increase the risk of relapse.[1]
- Stress may also trigger an attack.[17]
Causes
Most likely MS occurs as a result of some combination of genetic, environmental and infectious factors,[1] and
possibly other factors like vascular problems.[19] Epidemiological studies of MS have provided hints on possible
causes for the disease. Theories try to combine the known data into plausible explanations, but none has proved
definitive.
Autoimmunology MS is currently believed to be an immune-mediated disorder mediated by a complex
interaction of the individual's genetics and as yet unidentified environmental insults.[4] Damage is believed to
be caused by the patient's own immune system. The immune system attacks the nervous system, possibly as a
result of exposure to a molecule with a similar structure to one of its own.[4]
Lesions
The name multiple sclerosis refers to the scars (scleroses – better known as plaques or lesions) that form in the
nervous system. MS lesions most commonly involve white matter areas close to the ventricles of the
cerebellum, brain stem, basal ganglia and spinal cord; and the optic nerve. The function of white matter cells is
to carry signals between grey matter areas, where the processing is done, and the rest of the body. The
peripheral nervous system is rarely involved.[4]
More specifically, MS destroys oligodendrocytes, the cells responsible for creating and maintaining a fatty
layer—known as the myelin sheath—which helps the neurons carry electrical signals.[4] MS results in a thinning
or complete loss of myelin and, as the disease advances, the cutting (transection) of the neuron's extensions or
axons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.[4] A repair
process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes cannot
completely rebuild the cell's myelin sheath.[27] Repeated attacks lead to successively fewer effective
remyelinations, until a scar-like plaque is built up around the damaged axons.
Inflammation
Apart from demyelination, the other pathologic hallmark of the disease is inflammation. According to a strictly
immunological explanation of MS, the inflammatory process is caused by T cells, a kind of lymphocyte.
Lymphocytes are cells that play an important role in the body's defenses.[4] In MS, T cells gain entry into the
brain via the previously described blood–brain barrier. Evidence from animal models also point to a role of B
cells in addition to T cells in development of the disease.[29]
The T cells recognize myelin as foreign and attack it as if it were an invading virus. This triggers inflammatory
processes, stimulating other immune cells and soluble factors like cytokines and antibodies. Leaks form in the
blood–brain barrier, which in turn cause a number of other damaging effects such as swelling, activation of
macrophages, and more activation of cytokines and other destructive proteins.
Glutathione And Multilple Sclerosis
- Many studies have compared groups of MS patients to healthy individuals. Among other things, they have
measured levels of reactive metabolites (break-down products of oxidation) and of protective enzymes,
especially GSH (Glutathione).
- An Italian group headed by Vince Calabrese drew samples of cerebrospinal fluid (CSF) through spinal taps. CSF
analysis is a good indicator of brain metabolism. They found that GSH-peroxidase levels in the cerebrospinal
fluid of MS patients were consistently low. Their conclusion was that in MS, the fundamental activity of anti-
oxidation is abnormal and that oxidative stress plays a causative role.
- Another study looking at CSF was performed by the Swedes G. Ronquist and G. Frithz who tested spinal taps
from a large number of patients including those with stroke, seizures, brain tumors and MS. The cerebrospinal
fluid of MS patients was found to be almost entirely lacking in GSH.
- There is further evidence of the involvement of free radical elevation and GSH depletion in MS. Helen
Langemann in Switzerland measured GSH levels within MS plaques themselves. Without exception, they were
depleted.
- Researchers led by I. Singh at the University of South Carolina examined the fundamental tissue abnormality in
multiple sclerosis. The actual myelin breakdown occurs to a large part because of the release of strong
inflammatory chemicals called cytokines. These cytokines generate huge numbers of free radicals. Pre-treating
neurological tissues with NAC (N-acetycysteine) to raise glutathione levels protected these tissues from
demyelination. Conversely, when GSH was chemically depleted, the demyelination grew worse.
-Simpler studies demonstrating decreased blood levels of GSH peroxidase in MS patients have been repeated
by many Scandinavian, Italian and North American researchers. These levels as well can be inversely correlated
with the degree of severity of the attack.
PLEASE NOTE:
This page is meant to be an informative overview of MS, once you understand what the body is undergoing in
this disease process you need to go to :
This page will give you the information you require to know that REPLENISHING GLUTATHIONE is completely
necessary for a person that suffers from MS. The most efficient method of replenishing Glutathione in the body
is by consuming
GSH-Immunity® The Choice of Professionals!
Multiple sclerosis (abbreviated MS, also known as disseminated sclerosis or encephalomyelitis disseminata) is
an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are
damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms.[1] Disease
onset usually occurs in young adults, and it is more common in females.[1] It has a prevalence that ranges
between 2 and 150 per 100,000.[2] MS was first described in 1868 by Jean-Martin Charcot.[3]
MS affects the ability of nerve cells in the brain and spinal cord to
communicate with each other. Nerve cells communicate by sending
electrical signals called action potentials down long fibers called axons,
which are wrapped in an insulating substance called myelin. In MS, the
body's own immune system attacks and damages the myelin. When myelin
is lost, the axons can no longer effectively conduct signals.[4]
The name multiple sclerosis refers to scars (scleroses—better known as
plaques or lesions) particularly in the white matter of the brain and spinal cord,
which is mainly composed of myelin.[3]
Almost any neurological symptom can appear with the disease, and often
progresses to physical and cognitive disability.[4] MS takes several forms,
with new symptoms occurring either in discrete attacks (relapsing forms)
or slowly accumulating over time (progressive forms).[6] Between attacks,
symptoms may go away completely, but permanent neurological problems
often occur, especially as the disease advances.[6]
Classification
Progression of MS subtypesSeveral subtypes, or patterns of progression, have
been described. Subtypes use the past course of the disease in an attempt to
predict the future course. They are important not only for prognosis but also for
therapeutic decisions. In 1996 the United States National Multiple Sclerosis Society standardized four subtype
definitions:[6]
1.relapsing remitting,
2.secondary progressive,
3.primary progressive, and
4.progressive relapsing.
The relapsing-remitting subtype is characterized by unpredictable relapses followed by periods of months to
years of relative quiet (remission) with no new signs of disease activity. Deficits suffered during attacks may
either resolve or leave sequelae, the latter being more common as a function of time.[1] This describes the
initial course of 80% of individuals with MS.[1] When deficits always resolve between attacks, this is sometimes
referred to as benign MS,[8] although patients will still accrue some degree of disability in the long term.[1] The
relapsing-remitting subtype usually begins with a clinically isolated syndrome (CIS). In CIS, a patient has an
attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis.[1][9] However only 30 to
70% of persons experiencing CIS later develop MS.[9]
Nerve axon with myelin sheath Secondary progressive MS (sometimes called "galloping MS") describes around
65% of those with an initial relapsing-remitting MS, who then begin to have progressive neurologic decline
between acute attacks without any definite periods of remission.[1][6] Occasional relapses and minor remissions
may appear.[6] The median time between disease onset and conversion from relapsing-remitting to secondary
progressive MS is 19 years.[10]
The primary progressive subtype describes the approximately 10–15% of individuals who never have remission
after their initial MS symptoms.[11] It is characterized by progression of disability from onset, with no, or only
occasional and minor, remissions and improvements.[6] The age of onset for the primary progressive subtype is
later than for the relapsing-remitting, but similar to mean age of progression between the relapsing-remitting and
the secondary progressive. In both cases it is around 40 years of age.[1]
Progressive relapsing MS describes those individuals who, from onset, have a steady neurologic decline but
also suffer clear superimposed attacks. This is the least common of all subtypes.[6]
Atypical variants of MS with non-standard behavior have been described; these include Devic's disease, Balo
concentric sclerosis, Schilder's diffuse sclerosis and Marburg multiple sclerosis. There is debate on whether
they are MS variants or different diseases.[12] Multiple sclerosis also behaves differently in children, taking
more time to reach the progressive stage.[1] Nevertheless they still reach it at a lower mean age than adults.[1]
Multiple sclerosis signs and symptoms
- A person with MS can suffer almost any neurological symptom or sign,
including changes in sensation such as loss of sensitivity or tingling,
pricking or numbness (hypoesthesia and paraesthesia), muscle weakness,
clonus, muscle spasms, or difficulty in moving; difficulties with coordination
and balance (ataxia); problems in speech (dysarthria) or swallowing
(dysphagia), visual problems (nystagmus, optic neuritis including
phosphenes, [13][14] or diplopia), fatigue, acute or chronic pain, and
bladder and bowel difficulties.[1]
- Cognitive impairment of varying degrees and emotional symptoms of
depression or unstable mood are also common.[1] Uhthoff's phenomenon,
an exacerbation of extant symptoms due to an exposure to higher than usual
ambient temperatures, and Lhermitte's sign, an electrical sensation that runs
down the back when bending the neck, are particularly characteristic of MS
although not specific.[1] The main clinical measure of disability progression
and symptom severity is the Expanded Disability Status Scale or EDSS.[15]
- Symptoms of MS usually appear in episodic acute periods of worsening (called
relapses, exacerbations, bouts, attacks, or "flare-ups"), in a gradually progressive deterioration of neurologic
function, or in a combination of both.[6] Multiple sclerosis relapses are often unpredictable, occurring without
warning and without obvious inciting factors with a rate rarely above one and a half per year.[1] Some attacks,
however, are preceded by common triggers. Relapses occur more frequently during spring and summer.[16]
- Viral infections such as the common cold, influenza, or gastroenteritis increase the risk of relapse.[1]
- Stress may also trigger an attack.[17]
Causes
Most likely MS occurs as a result of some combination of genetic, environmental and infectious factors,[1] and
possibly other factors like vascular problems.[19] Epidemiological studies of MS have provided hints on possible
causes for the disease. Theories try to combine the known data into plausible explanations, but none has proved
definitive.
Autoimmunology MS is currently believed to be an immune-mediated disorder mediated by a complex
interaction of the individual's genetics and as yet unidentified environmental insults.[4] Damage is believed to
be caused by the patient's own immune system. The immune system attacks the nervous system, possibly as a
result of exposure to a molecule with a similar structure to one of its own.[4]
Lesions
The name multiple sclerosis refers to the scars (scleroses – better known as plaques or lesions) that form in the
nervous system. MS lesions most commonly involve white matter areas close to the ventricles of the
cerebellum, brain stem, basal ganglia and spinal cord; and the optic nerve. The function of white matter cells is
to carry signals between grey matter areas, where the processing is done, and the rest of the body. The
peripheral nervous system is rarely involved.[4]
More specifically, MS destroys oligodendrocytes, the cells responsible for creating and maintaining a fatty
layer—known as the myelin sheath—which helps the neurons carry electrical signals.[4] MS results in a thinning
or complete loss of myelin and, as the disease advances, the cutting (transection) of the neuron's extensions or
axons. When the myelin is lost, a neuron can no longer effectively conduct electrical signals.[4] A repair
process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes cannot
completely rebuild the cell's myelin sheath.[27] Repeated attacks lead to successively fewer effective
remyelinations, until a scar-like plaque is built up around the damaged axons.
Inflammation
Apart from demyelination, the other pathologic hallmark of the disease is inflammation. According to a strictly
immunological explanation of MS, the inflammatory process is caused by T cells, a kind of lymphocyte.
Lymphocytes are cells that play an important role in the body's defenses.[4] In MS, T cells gain entry into the
brain via the previously described blood–brain barrier. Evidence from animal models also point to a role of B
cells in addition to T cells in development of the disease.[29]
The T cells recognize myelin as foreign and attack it as if it were an invading virus. This triggers inflammatory
processes, stimulating other immune cells and soluble factors like cytokines and antibodies. Leaks form in the
blood–brain barrier, which in turn cause a number of other damaging effects such as swelling, activation of
macrophages, and more activation of cytokines and other destructive proteins.
Glutathione And Multilple Sclerosis
- Many studies have compared groups of MS patients to healthy individuals. Among other things, they have
measured levels of reactive metabolites (break-down products of oxidation) and of protective enzymes,
especially GSH (Glutathione).
- An Italian group headed by Vince Calabrese drew samples of cerebrospinal fluid (CSF) through spinal taps. CSF
analysis is a good indicator of brain metabolism. They found that GSH-peroxidase levels in the cerebrospinal
fluid of MS patients were consistently low. Their conclusion was that in MS, the fundamental activity of anti-
oxidation is abnormal and that oxidative stress plays a causative role.
- Another study looking at CSF was performed by the Swedes G. Ronquist and G. Frithz who tested spinal taps
from a large number of patients including those with stroke, seizures, brain tumors and MS. The cerebrospinal
fluid of MS patients was found to be almost entirely lacking in GSH.
- There is further evidence of the involvement of free radical elevation and GSH depletion in MS. Helen
Langemann in Switzerland measured GSH levels within MS plaques themselves. Without exception, they were
depleted.
- Researchers led by I. Singh at the University of South Carolina examined the fundamental tissue abnormality in
multiple sclerosis. The actual myelin breakdown occurs to a large part because of the release of strong
inflammatory chemicals called cytokines. These cytokines generate huge numbers of free radicals. Pre-treating
neurological tissues with NAC (N-acetycysteine) to raise glutathione levels protected these tissues from
demyelination. Conversely, when GSH was chemically depleted, the demyelination grew worse.
-Simpler studies demonstrating decreased blood levels of GSH peroxidase in MS patients have been repeated
by many Scandinavian, Italian and North American researchers. These levels as well can be inversely correlated
with the degree of severity of the attack.
PLEASE NOTE:
This page is meant to be an informative overview of MS, once you understand what the body is undergoing in
this disease process you need to go to :
This page will give you the information you require to know that REPLENISHING GLUTATHIONE is completely
necessary for a person that suffers from MS. The most efficient method of replenishing Glutathione in the body
is by consuming
GSH-Immunity® The Choice of Professionals!
GLUTATHIONE, MASTER ANTIOXIDANT / ANTI INFLAMMATORY
