Here are a couple of articles I am posting in response to your question about diet and MS. I have known for years that John Hopkins uses a high fat diet to stop seizures in children. Something is going on in the brains to rewire these kids so that the seizures stop.
It has been awhile since I read about this treatment, but I do remember that after a year or so of the diet , which restricts carbohydrates to almost zero, the children are able to eat normally and get no more seizures.
This might also go along with those on this board that believe insulin has a causal proponent to MS.
This article is about a high fat, ketogenic diet, and how it helps ALS symptoms. I would prefer that the paper was telling about humans, but for now it is about rats with the disease.
The restriction of carbohydrates and the consumption of more fats, especially high omega 3 fats, may help other nerve diseases too.
Eskimos in Alaska do not get MS, as far as I know, and they eat a very high fat diet since their main source of meat is salmon and whale blubber.
They would be getting high doses of Vitamin D from the fish, as well as high omega 3's.
Please note that I am not talking about eating doughnuts, ice cream candy, etc made with Trans Fats. Rather the good fats such as olive oil and fish fats.
Here is the first article.
Medical News Today
A High Caloric Diet May Prevent The Progression Of Amyotrophic Lateral Sclerosis
19 Apr 2006
A recent study directed by the Mount Sinai School of Medicine suggests a ketogenic- high caloric diet may prevent
the progression of Amyotrophic Lateral Sclerosis (ALS). This study, which appears in the April 2006 issue of
BMC Neuroscience, is the first to draw a correlation between diet and neuronal cell death, the cause of ALS.
ALS is an adult-onset neurodegenerative disorder in which spinal and cortical motor neurons die causing
relentlessly progressive weakness and wasting of skeletal muscles through the body.
"ALS is such a devastating disease for those individuals diagnosed with the disorder," said Giulio Maria Pasinetti,
M.D., Ph.D., Professor of Psychiatry and Neuroscience, Director of the Neuroinflammation Research Center at
The Mount Sinai School of Medicine and lead author of this study. "The findings assert the significance of certain
high caloric dietary intake in the prevention of ALS. In view of any available therapeutic application for the
disease, this new evidence might bring hope to those affected."
The cause of neuronal death in ALS is uncertain but study researchers say mitochondrial dysfunction plays an
important role. Ketones promote mitochondrial energy production and membrane stabilization. Mitochondiral membrane
dysfunction, loss of oxidative stress control, generation of excessive free radicals, neurofilament accumulation,
and excitotoxicity are all implicated in the onset of ALS.
About the Study
Mount Sinai School of Medicine investigators used a mouse model to examine the affects of a ketogenic diet (KD)
on the progression of ALS. ALS mice were fed a high caloric - ketogenic diet (KD) and motor performance, longevity,
and motor neuron counts were measured in treated and diseased mice. Because mitochondrial dysfunction plays a
central role in neuronal cell death in ALS, the effect that the principal ketone body, D-â-3 hydroxybutyrate (DBH),
has on mitochondrial ATP generation and neuroprotection were studied.
Blood ketones were > 3.5 times higher in KD fed animals compared to controls. KD fed mice lost 50% of baseline
motor performance 25 days later than the disease controls. The interaction between diet and change in weight was
significant; KD mice weighed 4.6g more than the disease control group at study endpoint. In spinal cord sections
obtained at the study endpoint, there were more motor neurons in KD fed animals. DBH prevented rotenone mediated
inhibition of mitochondrial complex I but not malonate inhibition of complex II. Rotenone neurotoxicity in spinal
cord motorneuron was also inhibited by DBH.
This is the first study showing that diet, specifically a high caloric - KD, may slow the progression of the
clinical and biological manifestations of ALS in a mouse model. This may be due to the ability of ketone bodies
to promote ATP synthesis and bypass inhibition of complex I in the mitochondrial respiratory chain.
About the Mount Sinai School of Medicine
Located in Manhattan, Mount Sinai School of Medicine is internationally recognized for ground-breaking clinical
and basic-science research, and innovative approaches to medical education. Through the Mount Sinai Graduate School
of Biological Sciences, Mount Sinai trains biomedical researchers with an emphasis on the rapid translation of
discoveries of basic research into new techniques for fighting disease. One indication of Mount Sinai's leadership
in scientific investigation is its receipt during fiscal year 2005 of $174.1 million in research support from the
NIH. Mount Sinai School of Medicine also is known for unique educational programs such as the Humanities in
Medicine program, which creates opportunities for liberal arts students to pursue medical school, and instructional
innovations like The Morchand Center, the nation's largest program teaching students and physicians with
"standardized patients" to become not only highly skilled, but compassionate caregivers. Long dedicated to
improving its community, the School extends its boundaries to work with East Harlem and surrounding communities
to provide access to health care and educational programs to at risk populations.
Contact: Mount Sinai Press Office
The Mount Sinai Hospital / Mount Sinai School of Medicine
Article URL: http://www.medicalnewstoday.com/medical ... wsid=41783
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