How to beat the fatigue of multiple sclerosis

From an email I got.  Ask your doctor about this and not politely. Can your doctor put two and two together and maybe consider the applicability of this to post stroke fatigue? With your doctor doing nothing huge number of survivors are not getting treated for this.

I had massive fatigue immediately post stroke and continuing for years. My doctor stupidly said I needed to get more cardiovascularly fit. He never tested my cardio fitness. Three years after my stroke I had a physical where my resting heart rate was 54 at the age of 53. That means my cardiovascular fitness was that of an athlete, even after doing nothing on it for 3 years. Yet I was still completely fatigued everyday.

 Statistics on stroke fatigue:

At least half of all stroke survivors experience fatigue Or is it 70%?

Or is it 40%?

How to beat the fatigue of multiple sclerosis

In my research, I found 4 main natural compounds that are quite effective at reducing MS-related fatigue:

Thiamine (Vitamin B1) - When patients with MS supplement with thiamine, they see a significant improvement in their fatigue (1).  CoQ10 - Researchers have found that CoQ10 significantly improves fatigue and depression in patients with MS (2-3).  Magnesium - Lower magnesium levels are correlated with higher fatigue scores in MS patients (4). Alpha Lipoic Acid (ALA) - Studies show that ALA improves fatigue and depression in people with MS (5).

What do all these natural compounds have in common?

They all support your mitochondria.

That's why I included all four of them in Optimal Energy.

Optimal Energy is a powerful mitochondrial formula designed to boost your energy.

It also includes 13 other science-backed ingredients proven to boost cellular energy levels.
 

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References:

(1) https://www.ncbi.nlm.nih.gov/pubmed/23861280 July 2013

(2) https://www.ncbi.nlm.nih.gov/pubmed/25603363  2016

(3) https://www.tandfonline.com/doi/abs/10.1179/1476830515Y.0000000002?journalCode=ynns20 January 2015

(4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968354/ 2014

(5) https://www.ncbi.nlm.nih.gov/pubmed/31056714  May 2019

 

Dietary alpha-Lipoic Acid Impacts Brain Development of the Young Pig

We'll never know if this will help in stroke recovery because we have NO leaders to go to to update the stroke strategy and followup these simple questions with research. Myelination  may be impacted if we need myelination post-stroke
http://www.fasebj.org/content/30/1_Supplement/915.10.short

1. Austin T Mudd1,
2. Rosaline Waworuntu2,
3. Brian M Berg2 and
4. Ryan N Dilger1

+ Author Affiliations

1. ¹Neuroscience Program, University of Illinois, Urbana, IL
2. ²Pediatric Nutrition Institute, Mead Johnson Nutrition, Evansville, IN

Abstract

Alpha-lipoic acid (a-LA) is an antioxidant that has been shown to ameliorate age-associated impairments of brain and cardiovascular functions as well as diabetic neuropathy in rodents and humans. While the developing brain is highly metabolic and therefore potentially subject to periods of oxidative stress, relatively little is known about the extent to which antioxidants influence the developing brain. Using the preclinical piglet model, this exploratory study was designed to examine dose response effects of a-LA on growth, cognition and brain development. Beginning at 2 d of age, 31 male pigs received one of three diets formulated to contain: control (CONT) [0 mg a-LA/100g], low a-LA (LOW) [120 mg a-LA/100g], or high a-LA (HIGH) [240 mg a-LA/100g]. From 14 to 28 d of age, pigs were subjected to a spatial T-maze behavioral assessment and neuroimaging procedures were performed upon study completion at 31 d of age. No differences due to diets were observed in measures of small intestine weight or length, or brain volumes. Additionally, there was no observed interactive effect of diet x day for bodyweight measures. Spatial T-maze assessment did not reveal learning differences due to diet, however HIGH-fed piglets exhibited faster (P = 0.02) latency to choice compared with CONT and LOW-fed pigs on d 2 of the reversal phase. Neuroimaging analysis of microstructure using diffusion tensor imaging (DTI) revealed decreased (P = 0.01) fractional anisotropy (FA) in the internal capsule of HIGH-fed pigs, compared with CONT- and LOW-fed pigs. Moreover, internal capsule axial diffusivity values in HIGH-fed pigs were smaller (P < 0.01) than CONT pigs, but were not different from LOW-fed pigs. Tract-based spatial statistics (TBSS), which provide a voxel-wise comparison of FA values along pre-determined fiber tracts, revealed 4,116 voxels in which HIGH-fed pigs exhibited lower (P < 0.05) FA values compared with CONT pigs. Furthermore, TBSS revealed 7,105 voxels with lower (P < 0.05) FA values in HIGH-fed pigs compared with LOW-fed pigs. In both comparisons, the largest voxel-wise FA value differences were localized to areas of the internal capsule, further corroborating DTI observations. No TBSS differences were observed between CONT and LOW-fed pigs. Taken together, the DTI and TBSS data suggest an altered trajectory of brain white matter maturation in HIGH-fed piglets. In conclusion, lack of difference in growth, behavioral assessment, and neuroimaging outcomes between LOW and CONT pigs, indicate low concentrations of a-LA support normal development. Future research is warranted to determine if supplementation of low concentrations of a-LA may confer specific neurodevelopmental benefits to piglets exposed to hypoxia, oxidative or inflammatory stress during development. However, since supplementation at high concentrations may delay brain myelination future research should explore immunohistochemistry staining and/or electron microscopy in conjunction with longitudinal follow-up to better understand the implications of these findings.

Support or Funding Information

Supported by Mead Johnson Nutrition.