Naviaux et. al.: Metabolic features of chronic fatigue syndrome

Research 1st

Research 1st

Severe ME, POTS & MCAS.
Messages
768
gregh286 said:
lipid groups with over 80% metabolic impact in the study.
Click to expand...

Well spotted.

Chronic presence of deranged lipids in adult humans are potentially dangerous and contribute significantly in autoimmune and chronic inflammatory diseases (such as Rheumatoid Arthritis) to dying prematurely from Myocardial Infaction (Heart Attack).

Some with ME (who privately test) are also finding out they have a chronic inflammatory disease state.

Lipids also have a protective effect, so we don't want them too low, or too high. Too low, and the Mitochondria won't work, too high and you run a risk of premature:

Vascular Dementia
Adverse Cardiac and Neurological events inc TIA + Stroke

Two potentially useful blood tests I would suggest when inflammation and 'ME' are present are Lp-PLA2 + Oxidised LDL. (I would also add HS-CRP into the mix for cardiovascular 'risk', as usually, CRP alongside ESR doesn't show anything much in ME unless an acute infection or other autoimmune disease has developed).

In case you're interested, I've linked some research below.




Lp-PLA2

Test Explanation:
https://labtestsonline.org/understanding/analytes/lp-pla2/tab/test/

Research:
Association between Lp-PLA2 and coronary artery disease: focus on its relationship with lipoproteins and markers of inflammation and hemostasis.
http://www.ncbi.nlm.nih.gov/pubmed/16115490

Elevated Lp-PLA2 levels add prognostic information to the metabolic syndrome on incidence of cardiovascular events among middle-aged nondiabetic subjects.
http://www.ncbi.nlm.nih.gov/pubmed/17431184

Enhanced expression of Lp-PLA2 and lysophosphatidylcholine in symptomatic carotid atherosclerotic plaques.
http://www.ncbi.nlm.nih.gov/pubmed/18356547

Relationship of lipoprotein-associated phospholipase A2 and oxidized low density lipoprotein in carotid atherosclerosis.
http://www.ncbi.nlm.nih.gov/pubmed/19359705

The correlation of human serum Lp-PLA2 and hs-CRP and stability of coronary atherosclerotic plaques
http://www.ncbi.nlm.nih.gov/pubmed/19954057

Lp-PLA(2) as a marker of cardiovascular diseases.
http://www.ncbi.nlm.nih.gov/pubmed/20425250

Plasma Lp-PLA2 in acute coronary syndrome: association with major adverse cardiac events in a community-based cohort.
http://www.ncbi.nlm.nih.gov/pubmed/20675983

Antioxidant and inflammatory aspects of lipoprotein-associated phospholipase A₂ (Lp-PLA₂): a review.
http://www.ncbi.nlm.nih.gov/pubmed/21955667

Temporal profile and prognostic value of Lp-PLA2 mass and activity in the acute stroke setting.
http://www.ncbi.nlm.nih.gov/pubmed/22153151

Lipoprotein-associated phospholipase A2 (Lp-PLA2): a review of its role and significance as a cardiovascular biomarker.
http://www.ncbi.nlm.nih.gov/pubmed/22401038

http://www.ncbi.nlm.nih.gov/pubmed/22499993
Evidence supporting a key role of Lp-PLA2-generated lysophosphatidylcholine in human atherosclerotic plaque inflammation.

Lp-PLA2 is associated with structural valve degeneration of bioprostheses.
http://www.ncbi.nlm.nih.gov/pubmed/24328921

Baseline elevated Lp-PLA2 is associated with increased risk for re-stenosis after stent placement.
http://www.ncbi.nlm.nih.gov/pubmed/24580749

Increased serum level of Lp-PLA2 is independently associated with the severity of coronary artery diseases: a cross-sectional study of Chinese population.
http://www.ncbi.nlm.nih.gov/pubmed/25879827

Association of Lp-PLA2-A and early recurrence of vascular events after TIA and minor stroke.
http://www.ncbi.nlm.nih.gov/pubmed/26311748


Oxidised LDL:

Research:

Oxidized Low-Density Lipoprotein
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315351/

Role of Oxidised LDL in Atherosclerosis
http://www.ncbi.nlm.nih.gov/pubmed/11795267

Measuring Circulating Oxidized Low-Density Lipoprotein to Evaluate Coronary Risk
http://circ.ahajournals.org/content/103/15/1930

Oxidized LDL, a critical factor in atherogenesis
http://cardiovascres.oxfordjournals.org/content/68/3/353

Oxidized LDL and HDL: antagonists in atherothrombosis
http://www.fasebj.org/content/15/12/2073.abstract

Circulating Oxidized LDL Is a Useful Marker for Identifying Patients With Coronary Artery Disease
http://atvb.ahajournals.org/content/21/5/844.full

The Dynamics of Oxidized LDL during Atherogenesis
http://www.hindawi.com/journals/jl/2011/418313/
 
voner

voner

Senior Member
Messages
592
Marky90 said:
Just got through the paper


.....Fourth: They concluded that ME is a hypometabolic state, with a profile similar to the medically recognised survival state of "dauer", which occurs when humans experience extreme circumstances where it may die if it not change its metabolism. E.g. in extremely cold conditions, or in states of extreme hunger. ME could in other words be a evolutionary conserved hypometabolic state remniscent of this, that for some reason occurs in response to other triggers together with genetic predispositions.
Click to expand...

So, the term "evolutionary conserved " means that it is a metabolic response eons old???
 
Forbin

Forbin

Senior Member
Messages
966
If this means our cells are trying to achieve some kind of state of suspended animation, I may have to change my avatar. :)

fry.jpg
 
Research 1st

Research 1st

Severe ME, POTS & MCAS.
Messages
768
deleder2k said:
Premature, but can this point us in any direction in terms of treatment?
Click to expand...

Yes, in basic form you need to switch off the CDR, but we don't know if this is possible, in case the pathogens in the patients, then worsen the disease. Dr Cheney proposed ages ago, that the 'effect' of extreme exhaustion in 'CFS' may well be protective, e.g. by making you able to do nothing, this is happening for a reason and keeping you alive.

He may well be correct.

So before we have out cutting edge treatment that enables us to go down a gym, we need to see that it's safe to turn off the CDR, as previously mentioned.. for this we need cutting edge pathogen studies, in the correct group of patients, with this proposed Novel defect discovered, they would indeed, by the correct group (what we've always lacked).

Hopefully in the next few years, scientists, doctors and even Government Health Agencies (enablers of harm to ME CFS sufferers) giving charlatan F48.0 psychiatrists a planet wide exclusion zone they must stick to, to avoid further harm to the patients.

Ideally, the Moon.
 
voner

voner

Senior Member
Messages
592
I thought this quote from the paper was worth citing..

....The low sphingolipid profile in CFS appears to be an adaptive response that is opposite to the increased sphingolipids observed in metabolic syndrome (11) and the acute cell danger response (CDR) (7) and ultimately may represent a fundamental response to oppose the spread of persistent viral and intracellular bacterial infections....
Click to expand...
 
G

Groggy Doggy

Guest
Messages
1,130
Hi @Ben Howell

"Eighty subjects were from California". Can we find out if there is a relationship to where the subjects lived/worked (number of months) and known government reported toxic areas?

Here is a map, that can be used to identify sources of toxic waste. The data is derived from US Gov't sources. If we were able to get a data feed from Terradex and reference it with subject self reports (geographic locations) then we could see if the toxic chemical exposures had any impact on the study participants. If there was a relationship, then we could look at specific chemicals that are detailed about each site.

http://whatsdown.terradex.com/

Maybe Ron is already doing this research? It might be a conflict of interest, since one of the offending sites was formerly occupied by Hewlett Packard (OptoElectronic Division) located in Palo Alto, on Page Mill Road; the land is owned (maybe still is owned?) by Stanford University.

http://www.toxicsites.us/site.php?epa_id=CAD980884209


Thanks!!

GD
 
Never Give Up

Never Give Up

Collecting improvements, until there's a cure.
Messages
971
Groggy Doggy said:
Hi @Ben Howell

"Eighty subjects were from California". Can we find out if there is a relationship to where the subjects lived/worked (number of months) and known government reported toxic areas?

Here is a map, that can be used to identify sources of toxic waste. The data is derived from US Gov't sources. If we were able to get a data feed from Terradex and reference it with subject self reports (geographic locations) then we could see if the toxic chemical exposures had any impact on the study participants. If there was a relationship, then we could look at specific chemicals that are detailed about each site.

http://whatsdown.terradex.com/

Maybe Ron is already doing this research? It might be a conflict of interest, since one of the offending sites was formerly occupied by Hewlett Packard (OptoElectronic Division) located in Palo Alto, on Page Mill Road; the land is owned (maybe still is owned?) by Stanford University.

http://www.toxicsites.us/site.php?epa_id=CAD980884209


Thanks!!

GD
Click to expand...
I believe the subjects were from in and around Santa Rosa, CA.
 
voner

voner

Senior Member
Messages
592
Another interesting quote from the paper:

.....Flavin Adenine Dinucleotide (FAD) Was Decreased. Plasma FAD was decreased in both males and females with CFS (Tables 2 and 3). FAD is synthesized from riboflavin (vitamin B2) and ATP. The gastrointestinal absorption, distribution, and transporter-medi-ated uptake of FAD are carefully regulated during health and disease (19). FAD is mobilized from tissues, increased in the plasma, and renal secretion is increased under conditions of stress or infection (20). FAD is an important cofactor for fatty acid oxidation and sterol synthesis and is required for activation and oxidation of vitamin B6 (pyridoxine); lipoic acid metabolism (E3 subunit) needed for pyruvate, alpha-ketoglutarate, and branched chain amino acid oxidation; vitamin A activation; 5-methyltetrahydrofolic acid synthesis; niacin and NAD synthe-sis; and glutathione reduction.....
 
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