| 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
On 1/9/07 I
decided to go back
to something I tried for awhile a couple of years. The reason is
outlined 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.
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