from summary prepared under contract for the ReGenesis Medical
Center/ Dec 2000)
I am not a medical doctor. All material provided at this website
is for informational purposes only. Readers are encouraged to
confirm the information contained herein with other sources.
Patients and consumers should review the information carefully
with their professional health care provider. The information
is not intended to replace medical advice offered by physicians.
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special, exemplary, or other damages arising therefrom.
In Multiple Sclerosis,
the nerve fibers of the brain and spinal cord gradually lose
their protective fatty covering, myelin. Just like a wire that
looses it insulation, a nerve affected by MS develops a short
circuit. Scarred patches called plaques may develop throughout
the brain and spinal cord. Even before this happens, MS can cause
swelling and lack of oxygen to these tissues and can produce
many different symptoms. The accumulated Central Nervous System
(CNS) damage from years of repetition of this process eventually
results in disability.
afflicts both sexes but is more prevalent in women, given the
greater female tendency to anemia. There is a higher incidence
of MS in people of Northern European descent.
not all of them typical of MS ( some similar to symptoms of porphyria),
have been associated with MS. These include:
System (CNS) Damage and Disability
Pallor and Local Cyanosis (bluish nail beds)
to Mild Abdominal Distress During Flares
During Flares (can also be diarrhea instead)
Loss During Flares
During Last Trimester of Pregnancy
Reddish Urine During Flares
Induced Rash Following Flares
Strong Craving For Salt
To Low Blood Pressure
Flashes of Light in the Peripheral Vision
Regarding this last
symptom, a prominent Immunologist who specializes in `MS has
stated that an immune system attack on the CNS cannot cause this
symptom. It has long been known, however, that the acute porphyrias
can cause this symptom by causing spasms of the retinal artery.
All forms of MS are
exacerbated by things like stress hormones, alcohol, infection
byproducts, etc., all provocateurs of heme synthesis by the liver.
It also appears that `MS occurs with greater frequency in areas
high in environmental toxins.
MS is caused primarily
by autoimmune and environmental inducers which may include viral
infections and genetic susceptibility. However, biochemical hereditary
factors may also be responsible for some form of a new MS subtype.
These factors affect the body's iron metabolism and the heme
biosynthesis pathway. Heme synthesis commences in the liver in
response to the presence of toxins requiring neutralization (stress
hormones, alcohol, sulfonamide medications, infection byproducts,
barbiturates, etc.). The nervous system damage from hereditary
and biochemical factors of MS may be related to a derangement
of heme synthesis in the liver during periods of anemia.
The increased prevalence
of `MS in women compared with men is due to genetic defects of
iron metabolism and/or the effect of sex hormones on the heme
biosynthesis pathway in subjects with a predisposition for MS.
The ultimate cause
of this illness appears to be an inherited reduced ability to
absorb iron resulting in a tendency to chronic anemia. The impact
of low iron availability during heme synthesis by the liver may
cause a derangement of the heme biosynthetic pathway that promotes
CNS damage in a manner similar to that seen in the acute porphyrias.
The mechanism responsible
for MS-induced damage to the CNS is rather difficult to explain
in simple terms. It will suffice to state that the neurotoxic
process causing central nervous system (CNS) damage in MS patients
with intermittent iron deficiency may be due to a genetic defect
but may also occur in persons who become anemic for other reasons.
This may provoke onset of autoimmune MS as the immune system
may mistakenly target CNS components, like myelin, as it attempts
to clear the damage left behind by this process. Characterization
of the putative HBMS gene and its product may therefore also
explain the establishment of classical MS.
of Central Nervous System Damage by MS
CNS damage is evoked by a disproportion between the porphyrin
precursors, such as delta aminolevulinic acid and porphobilinogen
(reducing agents) and uroporphyrin-1 isomers (antioxidants).
Uroporphyrin-1 is deficient as a result of iron deficiency, leaving
the central nervous system vulnerable to the oxidative damage
of the precursors.
between acute porphyrias and MS
The main difference
is that MS results only in CNS damage whereas in the acute porphyrias,
the peripheral and/or central nervous systems are also affected.
Another differentiating characteristic between this `MS and the
acute porphyrias is that porphyrin precursor levels, delta Aminolevulinic
Acid (ALA) and Porphobilinogen (PBG), need not be elevated for
the damage to occur. It is suspected that it is the proportion
of precursors in relation to Uroporphyrins that is cogent.
MS is sometimes is
misdiagnosed with porphyria because of the similarities of symptoms
and damage caused to the Central Nervous System. Porphyria is
a broad term referring to any of several hereditary disturbances
in the liver's heme-making processes. Heme synthesis commences
in the liver in response to the presence of toxins requiring
neutralization (stress hormones, alcohol, sulfonamide medications,
infection byproducts, barbiturates, etc.). The acute porphyrias
Symptoms, beyond those
commonly associated with `MS have been observed such as hive-like
skin rash following sun exposure, abdominal pain and digestive
for Multiple Sclerosis
There are several
medications for treating chronic-progressive multiple sclerosis
(often known as secondary progressive multiple sclerosis ). Approved
for relapsing forms of multiple sclerosis are medications such
as Betaseron, Avonex, and Copaxone. Very favorable results have
been completed with Betaseron. Besides utilizing these medications,
chemotherapies such as methotrexate or Iniuran have also been
successfully utilized for certain forms of multiple sclerosis.
The exact mechanism
responsible for the development of MS is not fully understood.
Since, autoimmune, environmental and biochemical genetic factors
may be responsible, present research is focused on the possible
connection of these factors to the heme biosynthesis pathway
and to possible disturbances in porphyrin metabolism. Understanding
the relationship of heme synthesis to Central Nervous System
(CNS) damage may also help explain its control over MS. For "hereditary
biochemical multiple sclerosis" (HBMS) present research
is focused on identifying a gene that may be responsible.
treatments for Multiple Sclerosis
MS appears to occur
with greater frequency in areas with high levels of toxins and
heavy metals, thus suggesting the importance of environmental
triggers. Therefore, for patients whose MS may have resulted
from environmental triggers (i.e. infections, hormones, heavy
metal intoxication), or even from autoimmune and genetic factors
(also affecting the heme biosynthesis pathway), iron supplementation
may be a helpful form of treatment (if the patient is not suffering
from Hemochromatosis, a dangerous hereditary condition that causes
over absorption of iron). EDTA and other forms of chelation therapy
(to remove heavy metals), as well as Hyperbaric Oxygen treatments,
may also be helpful.
Summaries on Chronic Illnesses
heart disease | |
stroke | diabetes |
| high blood
| | high cholesterol | | Alzheimer's | |
arthritis | |
| poor circulation | | brain injury | | multiple sclerosis | | cerebral palsy | | life extension | | memory
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