Improved nutritional status is of utmost importance in mitigating the detrimental effects of ALS.

[HysteryDiagnosis]

So say the experts. Homeopathy is not mentioned, nor is any oily substances derived from snakes. Voodoo is mentioned but only briefly whereas alternative medicine is nowhere to be seen.

http://www.ncbi.nlm.nih.gov/pubmed/19782443

Clin Nutr. 2009 Dec;28(6):604-17. Epub 2009 Sep 25.
Nutritional and exercise-based interventions in the treatment of amyotrophic lateral sclerosis.

Patel BP, Hamadeh MJ.

School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada M3J 1P3.
Abstract

BACKGROUND & AIMS: Disease pathogenesis in amyotrophic lateral sclerosis (ALS) involves a number of interconnected mechanisms all resulting in the rapid deterioration of motor neurons. The main mechanisms include enhanced free radical production, protein misfolding, aberrant protein aggregation, excitotoxicity, mitochondrial dysfunction, neuroinflammation and apoptosis. The aim of this review is to assess the efficacy of using nutrition- and exercise-related interventions to improve disease outcomes in ALS.

METHODS: Studies involving nutrition or exercise in human and animal models of ALS were reviewed.

RESULTS: Treatments conducted in animal models of ALS have not consistently translated into beneficial results in clinical trials due to poor design, lack of power and short study duration, as well as differences in the genetic backgrounds, treatment dosages and disease pathology between animals and humans. However, vitamin E, folic acid, alpha lipoic acid, lyophilized red wine, coenzyme Q10, epigallocatechin gallate, Ginkgo biloba, melatonin, Cu chelators, and regular low and moderate intensity exercise, as well as treatments with catalase and l-carnitine, hold promise to mitigating the effects of ALS, whereas caloric restriction, malnutrition and high-intensity exercise are contraindicated in this disease model.

CONCLUSIONS: Improved nutritional status is of utmost importance in mitigating the detrimental effects of ALS.

[Schema Thing]

1. who would guess that malnutrition could be contraindicated

in fighting a disease?




Or is there a usage of the word "malnutrition" that I'm unaware of?

[HysteryDiagnosis]

2. It ain't about malnutrition when you are talking about using key specific nutrients

such as CoQ10, L-carnitine, and others to elicit a response, it's about using naturally occurring substances at levels which would otherwise be thought of as wasteful or even harmful. Certain medical conditions are linked to a lack of certain beneficial nutrients and many drugs will cause the depletion of certain essential nutrients/enzymes/cofactors.

[Schema Thing]

7. I was referring to this statement:

"whereas caloric restriction, malnutrition and high-intensity exercise are contraindicated in this disease model."


It seems nonsensical, or rather sort of "duh" unless "malnutrition" actually IS indicated as effective treatment for some disease models.

[HysteryDiagnosis]

8. Yes, that is a duh statement..... don't know how that got by the eds. n/t

[tabatha]

3. Thanks. Many of your posts make me do further research.

But how many people use "lyophilized red wine"?

[HysteryDiagnosis]

5. Not enough. Here are a couple of papers you may or may not have seen, they

are very important imho.

http://www.ncbi.nlm.nih.gov/pubmed/20112300
Mol Nutr Food Res. 2010 Apr;54(4):447-56.
Dietary omega-3 fatty acid supplementation for optimizing neuronal structure and function.

Heinrichs SC.

Department of Psychology, Regis College, Weston, MA 02390, USA. [e-mail]
Abstract

Direct actions of omega-3 polyunsaturated fatty acids (PUFAs) on neuronal composition, neurochemical signaling and cognitive function constitute a multidisciplinary rationale for classification of dietary lipids as "brain foods." The validity of this conclusion rests upon accumulated mechanistic evidence that omega-3 fatty acids actually regulate neurotransmission in the normal nervous system, principally by modulating membrane biophysical properties and presynaptic vesicular release of classical amino acid and amine neurotransmitters.

The functional correlate of this hypothesis, that certain information processing and affective coping responses of the central nervous system are facilitated by bioavailability of omega-3 fatty acids, is tentatively supported by developmental and epidemiological evidence that dietary deficiency of omega-3 fatty acids results in diminished synaptic plasticity and impaired learning, memory and emotional coping performance later in life.

The present review critically examines available evidence for the promotion in modern society of omega-3 fatty acids as adaptive neuromodulators capable of efficacy as dietary supplements and as potential prophylactic nutraceuticals for neurological and neuropsychiatric disorders.

PMID: 20112300


http://www.ncbi.nlm.nih.gov/pubmed/20233652
J Nutr Biochem. 2010 May;21(5):364-73. Epub 2010 Mar 16.
Mechanisms of n-3 fatty acid-mediated development and maintenance of learning memory performance.

Su HM.

Department of Physiology, National Taiwan University College of Medicine, Taipei, Taiwan. [e-mail]
Abstract

Docosahexaenoic acid (DHA, 22:6n-3) is specifically enriched in the brain and mainly anchored in the neuronal membrane, where it is involved in the maintenance of normal neurological function. Most DHA accumulation in the brain takes place during brain development in the perinatal period. However, hippocampal DHA levels decrease with age and in the brain disorder

Alzheimer's disease (AD), and this decrease is associated with reduced hippocampal-dependent spatial learning memory ability. A potential mechanism is proposed by which the n-3 fatty acids DHA and eicosapentaenoic acid (20:5n-3) aid the development and maintenance of spatial learning memory performance. The developing brain or hippocampal neurons can synthesize and take up DHA and incorporate it into membrane phospholipids, especially phosphatidylethanolamine, resulting in enhanced neurite outgrowth, synaptogenesis and neurogenesis.

Exposure to n-3 fatty acids enhances synaptic plasticity by increasing long-term potentiation and synaptic protein expression to increase the dendritic spine density, number of c-Fos-positive neurons and neurogenesis in the hippocampus for learning memory processing. In aged rats, n-3 fatty acid supplementation reverses age-related changes and maintains learning memory performance. n-3 fatty acids have anti-oxidative stress, anti-inflammation, and anti-apoptosis effects, leading to neuron protection in the aged, damaged, and AD brain. Retinoid signaling may be involved in the effects of DHA on learning memory performance. Estrogen has similar effects to n-3 fatty acids on hippocampal function. It would be interesting to know if there is any interaction between DHA and estrogen so as to provide a better strategy for the development and maintenance of learning memory.

Copyright 2010 Elsevier Inc. All rights reserved.

[tabatha]

4. I don't know what the difference is between

Cu in food (Cocoa is high, and I drink that) and Cu chelators.

Also, many of the nutrients mentioned above are contained in the multi-vitamin I take, again from the same manufacturer, where epigallocatechin gallate is from green tea.

http://www.ultimatelife.com/CatDefense2.htm

I think the guy who founded this company did his research.

[HysteryDiagnosis]

6. A Cu chelator would be a material that helps Cu exit the body, apparrently there

is a Cu overload in ALS.

http://www.ncbi.nlm.nih.gov/pubmed/21292280
J Neurol Sci. 2011 Feb 1.
Patterns of levels of biological metals in CSF differ among neurodegenerative diseases.

Hozumi I, Hasegawa T, Honda A, Ozawa K, Hayashi Y, Hashimoto K, Yamada M, Koumura A, Sakurai T, Kimura A, Tanaka Y, Satoh M, Inuzuka T.

Department of Neurology and Geriatrics, Gifu University, Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan.
Abstract

We measured the levels of some biological metals: copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), and zinc (Zn) in the cerebrospinal fluid (CSF) in patients with neurodegenerative diseases (52 patients with amyotrophic lateral sclerosis (ALS)), 21 patients with Alzheimer's disease (AD), and 20 patients with Parkinson's disease (PD) by inductively coupled plasma mass spectrometry (ICP-MS).

The diagnoses were additionally supported by neuroimaging techniques for AD and PD. In ALS, the levels of Mg (p<0.01 significant difference), Fe, Cu (p<0.05), and Zn (p<0.10) in CSF were higher than those in controls. Some patients showed very high levels of Cu and Zn before the critical deterioration of the disease.

In AD, the levels of Cu and Zn in CSF were significantly higher in patients with late-onset AD (p<0.01). In PD, we found significantly increased levels of especially Cu and Zn in particular (p<0.01) and Mn (p<0.05) in CSF. A multiple comparison test suggested that the increased level of Mg in ALS and that of Mn in PD were the pathognomonic features. These findings suggest that Cu and Zn in particular play important roles in the onset and/or progression of ALS, AD, and PD.

Therefore, Cu-chelating agents and modulators of Cu and Zn such as metallothionein (MT) can be new candidates for the treatment of ALS, AD, and PD.

Copyright © 2011. Published by Elsevier B.V.