| There are many reasons for this page. While there is
much information on Muscular Dystrophy on the Internet and
various other places. I wanted to provide a place where
much of that information could be located easily.
Let me make it perfectly clear that I am neither a doctor or any other
type of health care professional. My only
knowledge comes from the fact that I have a form of MD
called Friedrich's Ataxia. I have spent some time
looking for information and possible treatments which I
will share with anyone here.
I invite anyone to share any knowledge they may have
with visitors to this site. Simply email me
If you read as much as I have from the conventional
medical field you tend to lose hope of a treatment or
cure.
My feelings are do as much as you can. I never accept
what the doctors tell me and I do things they say I
can't do. My younger brother never let his condition
stop him as long as he could keep going he did and
attempted things even I didn't consider.
Do you have a poem or story? Send
it
here
I'm afraid there was no way to make this short as there
is lots of information here. Some may apply to many
people and some only to me. I have to make another point
here...I use homeopathic remedies, some people have a
very difficult time accepting that and if you are one of
the people are unwilling to consider them I would
suggest that you not even read any further.
I asked the homeopath one day who is helping me what
advice I could give people with one of the forms of MD?
His answer was "Get to a good
homeopath as soon as possible"
Alternatives
Personally I have tried a few other types of treatment.
This page will deal with some of those possibilities. If
any of these links go off of this domain they open in a
new window. Close that window to return here. These are unconventional or
alternative sources
 Have you ever heard of LDN (Low
Dose Naltrexone)? Info here I am conducting my own
trial here
A couple of studies I just
became aware of thanks to PubMed
a service of the U.S. National Library of Medicine. I
was told about them by Andreas M. Papas PhD, President YASOO
Health Inc.
Fredreichs
Ataxia
|
Fredreichs
Ataxia |
Hart
PE, Lodi R, Rajagopalan B, Bradley JL, Crilley JG,
Turner C, Blamire
AM, Manners D, Styles P, Schapira AH, Cooper JM.
Antioxidant treatment of
patients with Friedreich ataxia: four-year
follow-up. Arch Neurol. 2005
Apr;62(4):621-6.
BACKGROUND:
Decreased mitochondrial respiratory chain function
and increased oxidative stress have been
implicated in the pathogenesis of Friedreich
ataxia (FRDA), raising the possibility that energy
enhancement and antioxidant therapies may be an
effective treatment.
OBJECTIVE:
To evaluate the long-term efficacy of a combined
antioxidant and mitochondrial enhancement therapy
on the bioenergetics and clinical course of FRDA.
DESIGN:
Open-labeled pilot trial over 47 months.Patients
Seventy-seven patients with clinical and
genetically defined FRDA.Intervention A combined
coenzyme Q(10) (400 mg/d) and vitamin E (2100
IU/d) therapy of 10 patients with FRDA over 47
months.
MAIN OUTCOME
MEASURES: Clinical assessment using
echocardiography and the International Cooperative
Ataxia Rating Scale and cardiac and skeletal
muscle bioenergetics as assessed using phosphorus
P 31 magnetic resonance spectroscopy.
RESULTS:
There was a significant improvement in cardiac and
skeletal muscle bioenergetics that was maintained
throughout the 47 months of therapy.
Echocardiographic data revealed
significantly increased fractional shortening at
the 35- and 47-month time points. Comparison with
cross-sectional data from 77 patients with FRDA
indicated the changes in total International
Cooperative Ataxia Rating Scale and kinetic scores
over the trial period were better than predicted
for 7
patients, but the posture and gait and hand
dexterity scores progressed as predicted.
CONCLUSION:
This therapy resulted in sustained improvement in
mitochondrial energy synthesis that was associated
with a slowing of the progression of certain
clinical features and a significant improvement in
cardiac function.
|
Cooper
JM, Schapira AH. Friedreich's Ataxia: disease
mechanisms, antioxidant
and Coenzyme Q10 therapy. Biofactors.
2003;18(1-4):163-71. Review.
Mitochondria clearly play a central role in the
pathogenesis of Friedreich's Ataxia. The most
common genetic abnormality results in the
deficiency of the protein frataxin, which is
targeted to the mitochondrion. Research since this
discovery has indicated that mitochondrial
respiratory chain dysfunction, mitochondrial iron
accumulation and oxidative damage are
important components of the disease mechanism.
While the role of frataxin is not known, evidence
is currently pointing to a role in either
mitochondrial iron handling or iron sulphur centre
synthesis. These advances in our understanding of
the disease mechanisms are enabling therapeutic
avenues to be explored, in particular the use of
established drugs such as antioxidants and
enhancers of respiratory chain function. Vitamin E
therapy has been shown to be beneficial in
patients with ataxia with vitamin E deficiency,
and CoQ10 therapy was effective in some patients
with ataxia associated with CoQ10 deficiency. A
combined therapy involving long term treatment
with high
doses of vitamin E and coenzyme Q10 has jointly
targeted two of the major features of Friedreich's
Ataxia; decreased mitochondrial respiratory chain
function and increased oxidative stress. This
therapy clearly showed a rapid and sustained
increase in the energy generated by the FRDA heart
muscle,
nearly returning to normal levels. The
improvements in skeletal muscle energy generation
parallel those of the heart but to a lower level.
While this therapy appeared to slow the predicted
progression of some clinical symptoms a larger
placebo controlled study is required to confirm
these observations. Other antioxidant strategies
have involved the use of
Idebenone, selenium and N acetyl cysteine but only
the use of Idebenone has involved structured
trials with relatively large patient numbers.
Idebenone clearly had an impact upon the cardiac
hypertrophy in the majority of patients, although
there have not been any other significant benefits
reported to date.
|
MS
|
MS |
Nordvik I, Myhr KM,
Nyland H, Bjerve KS. Effect of dietary
advice and n-3
supplementation in newly diagnosed MS patients.
Acta Neurol Scand. 2000
Sep;102(3):143-9.
OBJECTIVE:
To investigate whether supplementation with fish
oil given together with dietary advice and vitamin
supplementation influenced the clinical outcome in
newly diagnosed multiple sclerosis (MS) patients.
MATERIAL AND
METHODS: Sixteen consecutive, newly
diagnosed patients with multiple sclerosis were
recruited to an open intervention study. They were
given dietary advice and supplemented with 0.9
g/day of long-chain marine fatty acids and
vitamins. The patients were followed for 2 years
with
respect to dietary habits, blood parameters and
neurological assessment including exacerbation
rate.
RESULTS:
There was a significant reduction in the mean
annual exacerbation rate and the mean Expanded
Disability Status
Scale (EDSS) as compared to pre-study values. The
plasma total phospholipid n-3 fatty acids
increased and n-6 fatty acids decreased
significantly.
CONCLUSIONS:
The results suggest that fish oil supplementation
given together with vitamins and dietary advice
can improve clinical outcome in patients with
newly diagnosed MS.
|
Stewart TM, Bowling
AC. Polyunsaturated fatty acid supplementation in
MS.
Int MS J. 2005 Nov;12(3):88-93.
This article focuses on polyunsaturated fatty acid
(PUFA) supplementation, which is a popular form of
complementary and alternative therapy among people
with MS. Owing to their popularity, clinicians
should be knowledgeable about the PUFA supplements
that are widely available, and the efficacy and
safety data from clinical studies. Small-scale
studies have
demonstrated trends towards some beneficial
effects. PUFA supplementation is generally well
tolerated, although some specific supplements are
best avoided and some clinical situations warrant
caution. A review of the efficacy and safety data
suggests that PUFA supplementation may be a
promising approach. Large-scale trials are
required to confirm the benefits.
|
|
